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ORGANIC SPECTROSCOPY

Read all about Organic Spectroscopy on ORGANIC SPECTROSCOPY INTERNATIONAL 

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DR ANTHONY MELVIN CRASTO Ph.D

DR ANTHONY MELVIN CRASTO Ph.D

DR ANTHONY MELVIN CRASTO, Born in Mumbai in 1964 and graduated from Mumbai University, Completed his Ph.D from ICT, 1991,Matunga, Mumbai, India, in Organic Chemistry, The thesis topic was Synthesis of Novel Pyrethroid Analogues, Currently he is working with AFRICURE PHARMA, ROW2TECH, NIPER-G, Department of Pharmaceuticals, Ministry of Chemicals and Fertilizers, Govt. of India as ADVISOR, earlier assignment was with GLENMARK LIFE SCIENCES LTD, as CONSUlTANT, Retired from GLENMARK in Jan2022 Research Centre as Principal Scientist, Process Research (bulk actives) at Mahape, Navi Mumbai, India. Total Industry exp 32 plus yrs, Prior to joining Glenmark, he has worked with major multinationals like Hoechst Marion Roussel, now Sanofi, Searle India Ltd, now RPG lifesciences, etc. He has worked with notable scientists like Dr K Nagarajan, Dr Ralph Stapel, Prof S Seshadri, etc, He did custom synthesis for major multinationals in his career like BASF, Novartis, Sanofi, etc., He has worked in Discovery, Natural products, Bulk drugs, Generics, Intermediates, Fine chemicals, Neutraceuticals, GMP, Scaleups, etc, he is now helping millions, has 9 million plus hits on Google on all Organic chemistry websites. His friends call him Open superstar worlddrugtracker. His New Drug Approvals, Green Chemistry International, All about drugs, Eurekamoments, Organic spectroscopy international, etc in organic chemistry are some most read blogs He has hands on experience in initiation and developing novel routes for drug molecules and implementation them on commercial scale over a 32 PLUS year tenure till date Feb 2023, Around 35 plus products in his career. He has good knowledge of IPM, GMP, Regulatory aspects, he has several International patents published worldwide . He has good proficiency in Technology transfer, Spectroscopy, Stereochemistry, Synthesis, Polymorphism etc., He suffered a paralytic stroke/ Acute Transverse mylitis in Dec 2007 and is 90 %Paralysed, He is bound to a wheelchair, this seems to have injected feul in him to help chemists all around the world, he is more active than before and is pushing boundaries, He has 100 million plus hits on Google, 2.5 lakh plus connections on all networking sites, 100 Lakh plus views on dozen plus blogs, 227 countries, 7 continents, He makes himself available to all, contact him on +91 9323115463, email amcrasto@gmail.com, Twitter, @amcrasto , He lives and will die for his family, 90% paralysis cannot kill his soul., Notably he has 38 lakh plus views on New Drug Approvals Blog in 227 countries......https://newdrugapprovals.wordpress.com/ , He appreciates the help he gets from one and all, Friends, Family, Glenmark, Readers, Wellwishers, Doctors, Drug authorities, His Contacts, Physiotherapist, etc He has total of 32 International and Indian awards

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Etelcalcetide, AMG 416, KAI-4169, velcalcetide


H-L-Cys-OH

S— S

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2

WP_000398

AMG 416 IS  (Ac-D-Cys(L-Cys-OH)-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2)

Etelcalcetide (AMG 416, KAI-4169, velcalcetide)

The main chain has 7 amino acids, all in the D-configuration. The side-chain cysteine residue is in the L-configuration. The molecular formula of AMG 416 (free base) is C38H73N21O10S2, and has a calculated average molecular mass of 1048.3 Da.

D-Argininamide, N-acetyl-D-cysteinyl-D-alanyl-D-arginyl-D-arginyl-D-arginyl-D-alanyl-, disulfide with L-cysteine, hydrochloride (1:?)

N-Acetyl-D-cysteinyl-D-alanyl-D-arginyl-D-arginyl-D-arginyl-D-alanyl-D-argininamide disulfide with L-cysteine hydrochloride

http://www.amgenpipeline.com/pipeline/

WO 2011/014707. , the compound may be represented as follows:

H-L-Cys-OH

S— S

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2

The main chain has 7 amino acids, all in the D-configuration and the side-chain cysteine residue is in the L-configuration. The amino terminal is acetylated and the carboxyl-terminal is amidated. This compound (“AMG-416”) has utility for the treatment of secondary hyperparathyroidism (SHPT) in hemodialysis patients. A liquid formulation comprising AMG-416 may be administered to a subject intravenously. The hydrochloride salt of AMG-416 may be represented as follows:

H-L-Cys-OH

S— S

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2 · x(HCl)

Therapeutic peptides pose a number of challenges with respect to their formulation. Peptides in general, and particularly those that contain a disulfide bond, typically have only moderate or poor stability in aqueous solution. Peptides are prone to amide bond hydrolysis at both high and low pH.

Disulfide bonds can be unstable even under quite mild conditions (close to neutral pH). In addition, disulfide containing peptides that are not cyclic are particularly prone to dimer formation. Accordingly, therapeutic peptides are often provided in lyophilized form, as a dry powder or cake, for later reconstitution.

A lyophilized formulation of a therapeutic peptide has the advantage of providing stability for long periods of time, but is less convenient to use as it requires the addition of one or more diluents and there is the potential risk for errors due to the use of an improper type or amount of diluent, as well as risk of contamination. In addition, the lyophilization process is time consuming and costly.

H-L-Cys-OH

S— S

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2

Generic Name:Etelcalcetide
Synonym:KAI-4169
CAS Number:1262780-97-1
N-acetyl-D-cysteinyl-S-(L-cysteine disulfide)-D-alanyl-D-arginyl-D-arginyl-D-arginyl-D-alanyl-D-argininamide
Mechanism of Action:Activates calcium sensing receptor on parathyroid glands reducing PTH synthesis and secretion
Indication: secondary hyperparathyroidism associated with chronic kidney disease
Development Stage: Phase III
Developer:KAI Pharmaceuticals/Amgen Inc.

H-L-Cys-OH

S— S

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2 · x(HCl)

1334237-71-6.png

HYDROCHLORIDE

Generic Name:Etelcalcetide Hydrochloride
AMG 416, KAI-4169, previously also known as velcalcetide hydrochloride
CAS :1334237-71-6
Chemical Name:N-acetyl-D-cysteinyl-D-alanyl-D-arginyl-D-arginyl-D-arginyl-D-alanyl-D-argininamide disulfide with L-cysteine hydrochloride
Mechanism of Action:Activates calcium sensing receptor on parathyroid glands reducing PTH synthesis and secretion
Indication: secondary hyperparathyroidism associated with chronic kidney disease
Development Stage: Phase III
Developer:KAI Pharmaceuticals/Amgen Inc.

Method for preparing etelcalcetide and its salts, particularly hydrochloride. See WO2014210489, for a prior filing claiming stable liquid formulation of etelcalcetide. Amgen, following its acquisition of KAI Pharmaceuticals, and Japanese licensee Ono Pharmaceuticals are developing etelcalcetide, a long-acting iv isozyme-selective peptide-based protein kinase C epsilon inhibitor and agonist of the calcium-sensing receptor, for treating secondary hyperparathyroidism (SHPT) in patients with end-stage renal disease receiving dialysis.

In August 2015, an NDA was submitted seeking approval of the drug for SHPT in patients with chronic kidney disease (CKD) on hemodialysis (HD) in the US.

In September 2015, Amgen filed an MAA under the centralized procedure in the EU for the approval of etelcalcetide for treating SHPT in patients with CKD on HD therapy.

KAI is also investigating a transdermal patch formulation of the drug for treating primary HPT.

Secondary hyperparathyroidism in patients with chronic kidney disease receiving dialysis
AMG 416 is a peptide agonist of the human cell surface calcium-sensing receptor (CaSR). It is being investigated as a treatment for secondary hyperparathyroidism in patients with chronic kidney disease receiving dialysis.
Etelcalcetide is a novel calcimimetic agent that suppresses the secretion of parathyroid hormone and is in clinical development for the treatment of SHPT in patients with CKD on hemodialysis. Etelcalcetide is administered intravenously three times per week at the end of each dialysis session. It acts by binding to and activating the calcium-sensing receptor on the parathyroid gland, thereby causing decreases in parathyroid hormone (PTH). Sustained elevations in PTH are known to be associated with significant clinical consequences for patients with CKD.
The submission includes data from three Phase 3 studies, all of which met the primary endpoints, including two pooled placebo-controlled trials in more than 1,000 patients and a head-to-head study evaluating etelcalcetide compared with cinacalcet.
About Secondary HyperparathyroidismSHPT is a common and serious condition that is often progressive among patients with CKD, and it affects many of the approximately two million people throughout the world who are receiving dialysis, including 450,000 people in the U.S. The disorder develops early in the course of CKD and usually manifests as increased levels of PTH as a result of increased production from the parathyroid glands (four small glands in the neck). Patients with end stage renal disease who require maintenance dialysis often have substantial elevations of PTH that are commonly associated with abnormal calcium and phosphorus levels and an increased risk of significant clinical consequences.
About Etelcalcetide (AMG 416)Etelcalcetide is a novel calcimimetic agent in clinical development for the treatment of SHPT in CKD patients on hemodialysis that is administered intravenously at the end of the dialysis session. Etelcalcetide binds to and activates the calcium-sensing receptor on the parathyroid gland, thereby decreasing PTH levels.
About Sensipar® (cinacalcet)Sensipar® (cinacalcet) is the first oral calcimimetic agent approved by the FDA for the treatment of SHPT in adult patients with CKD on dialysis. Sensipar is not indicated for use in adult patients with CKD who are not on dialysis because of an increased risk of hypocalcemia. The therapy is also approved in the U.S. for treatment of hypercalcemia in adult patients with parathyroid carcinoma and hypercalcemia in adult patients with primary HPT for whom parathyroidectomy would be indicated on the basis of serum calcium levels, but who are unable to undergo parathyroidectomy. Sensipar binds to the calcium-sensing receptor, resulting in a drop in PTH levels by inhibiting PTH synthesis and secretion. In addition, the reductions in PTH lower serum calcium and phosphorus levels.
Milestones
  • 25 Aug 2015 Preregistration for Secondary hyperparathyroidism in USA (IV)
  • 29 May 2015 Pooled analysis efficacy and adverse events data from two phase III trials in secondary hyperparathyroidism released by Amgen
  • 21 Apr 2015 Amgen plans to submit Biological License Application to USFDA and Marketing Authorisation Application to EMA for Secondary hyperparathyroidism

PATENT

WO2011014707

http://www.google.com/patents/WO2011014707A2?cl=en

 

 

PATENT

WO 2015154031

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2015154031&recNum=1&maxRec=&office=&prevFilter=&sortOption=&queryString=&tab=PCTDescription

The hydrochloride salt of AMG 416 has the chemical structure:

H-L-Cys-OH

I

s— s

I

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2 · x(HCl)

(SEQ ID NO:l)

The main chain has 7 amino acids, all in the D-configuration. The side-chain cysteine residue is in the L-configuration. The molecular formula of AMG 416 (free base) is C38H73N21O10S2, and has a calculated average molecular mass of 1048.3 Da.

AMG 416 and a method for its preparation are described in International Pat. Publication No. WO 2011/014707, which is incorporated herein by reference for any purpose. As described in International Pat. Publication No. WO 2011/014707, AMG 416 may be assembled by solid-phase synthesis from the corresponding Fmoc-protected D-amino acids. After cleavage from the resin, the material may be treated with Boc-L-Cys(NPyS)-OH to form the disulfide bond. The Boc group may then be removed with trifluoroacetate (TFA) and the resulting product purified by reverse-phase high pressure liquid chromatography (HPLC) and isolated as the TFA salt form by lyophilization. The TFA salt can be converted to a pharmaceutically acceptable salt by carrying out a subsequent salt exchange procedure. Such procedures are well known in the art and include, e.g., an ion exchange technique, optionally followed by purification of the resultant product (for example by reverse phase liquid chromatography or reverse osmosis).

There is a need for an efficient method of producing AMG 416, or a pharmaceutically acceptable salt thereof (e.g., AMG 416 HC1), and particularly one appropriate for commercial scale manufacturing.

In a first aspect, provided is a method for preparing AMG 416, the method comprising: providing a resin-bound peptide having a structure selected from the group consisting of Fmoc-D-Cys(Trt)-D-Ala-D- Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-[Resin] (SEQ ID NO:2) and Ac-D-Cys(Trt)-D-Ala-D- Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-[Resin] (SEQ ID NO:3); cleaving the peptide from the solid support; and activating the side chain of the D-Cys residue of the cleaved peptide.

In a second aspect, provided is a method for preparing AMG 416, the method comprising: providing a peptide having a structure of Ac-D-Cys(SPy)-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2 (SEQ ID NO:4); and contacting the peptide with L-Cys to produce a conjugated product.

In yet a third aspect provided is a method for preparing AMG 416, the method comprising: providing a resin-bound peptide having a structure selected from the group consisting of Fmoc-D-Cys(Trt)-D-Ala-D-Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-[Resin] (SEQ ID NO:2) and Ac-D-Cys(Trt)-D-Ala-D-Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-[Resin] (SEQ ID NO:3); cleaving the peptide from the solid support, i.e., to provide an unsupported peptide, and activating the side chain of the D-Cys residue of the unsupported peptide to generate an AMG 416 SPy intermediate (where SPy is 2-pyridinesulfenyl or S-Pyr), dissolving the AMG 416 SPy intermediate in an aqueous 0.1% TFA (trifluoroacetic acid solution), and purifying the AMG 416 SPy derivative by HPLC.

The term “AMG 416”, also known as etelcalcetide, formerly known as velcalcetide or KAI-4169, refers to a compound having the chemical name: N-acetyl-D-cysteinyl-D-alanyl-D-arginyl-D-arginyl-D-arginyl-D-alanyl-D-arginamide disulfide with L-cysteine, which has the following structural formula:

H-L-Cys-OH

I

s— s

I

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2

Reference to AMG 416, or to any compound or AMG 416 fragment, intermediate, or precursor as described herein, is intended to encompass neutral, uncharged forms thereof, as well as pharmaceutically acceptable salts, hydrates and solvates thereof.

The terms “AMG 416 hydrochloride” and “AMG 416 HC1” are interchangeable and refer to a hydrochloride salt form of AMG 416 having the following structural formula:

H-L-Cys-OH

I

s— s

I

Ac-D-Cys-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2 · xHCl

BRIEF DESCRIPTION OF THE DRAWINGS

 FIG. 1 shows the chemical structure of AMG 416 (Ac-D-Cys(L-Cys-OH)-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2) (SEQ ID NO: l).

WP_000398

 

 FIG. 2 shows the chemical structure of Rink Amide AM resin and Ac-D-Cys(Trt)- D-Ala-D-Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-Resin (SEQ ID NO:3).

FIG. 3 shows a reaction scheme in which the SPy intermediate product (Ac-D-Cys(SPy)-D-Ala-D-Arg-D-Arg-D-Arg-D-Ala-D-Arg-NH2) (SEQ ID NO:4) is formed from the peptidyl-resin (Ac-D-Cys(Trt)-D-Ala-D-Arg(Pbf)-D-Arg(Pbf)-D-Arg(Pbf)-D-Ala-D-Arg(Pbf)-NH-Resin) (SEQ ID NO:3).

FIG. 4 shows a reaction scheme in which a TFA salt of AMG 416 is formed from the SPy intermediate (AA1_7(SPy)).

FIG. 5 shows a reaction scheme in which the HC1 salt of AMG 416 is formed from the TFA salt of AMG 416.

FIG. 6 shows a reaction scheme in which Boc-D-Arg(Pbf)-OH is formed from Boc-D-Arg-OH.

FIG. 7 shows a reaction scheme in which D-Arg(Pbf)-OH is formed from Boc-D-Arg(Pbf)-OH.

EXAMPLE 5

Purification of the SPy Intermediate and Production of AMG 416 HC1

An alternative method for preparation of AMG 416 HC1 salt is described here. As described in Example 2 above, the SPy intermediate product was dried at 20°C under full vacuum after cleavage from the resin, precipitation and filtration. The precipitate was then dissolved in a 0.1% TFA aqueous solution and loaded onto a C-18 column for HPLC purification. The column was run at <60 bar and the solution temperature was 15-25 °C throughout. The eluents were 0.1% TFA in acetonitrile and 0.1% TFA in water. The fractions were stored at 5°C, they were sampled and then fractions were pooled. The combined pools from two runs were diluted and a concentration/purification run was performed using the same HPLC column to decrease the total volume and remove additional impurities. The fractions were stored at 5°C.

The fractions containing the AMG 416 SPy intermediate were subjected to azeotropic distillation to change the solvent from the 0.1% TFA to a 15% water in IPA solution, charging with IPA as needed. To the resultant AMG 416 SPy intermediate in IPA solution was then added L-Cysteine 1.15 eq and the reaction was allowed to proceed at room temperature for conjugation to occur and to form the AMG 416 TFA salt as described above in Example 4. The AMG 416 TFA solution was added to a solution of 12M aqueous HC1, 0.27 L/kg and IPA 49.4 L/kg over 3 hours via subsurface addition, resulting in direct precipitation of the AMG 416 4.5 HC1 salt. The batch was aged for 3 hours and sampled for analysis.

The material was filtered and slurry washed with 96 wt% IPA, 10 L/kg. The cake was then re-slurried for 4 hours in 10 L/kg of 96% wt% IPA. The material was filtered and further slurry washed with 96% IPA, 10 L/kg and then IPA 10 L/kg. The material was dried under full vacuum at 25°C. The dry cake was dissolved in water 8 L/kg and the batch was concentrated via distillation to remove residual IPA and achieve the desired concentration. The solution temperature was kept below 25 °C throughout the distillation.

 

 

 

PATENT

WO2014210489

SEE

https://patentscope.wipo.int/search/en/detail.jsf;jsessionid=2A32CFD9CE075079399E9DD298899C9D.wapp2nC?docId=WO2014210489&recNum=1&maxRec=&office=&prevFilter=&sortOption=&queryString=&tab=PCTDescription

EXAMPLE 1

Solubility of AMG 416 in Succinate Buffered Saline

In this study, the solubility of AMG 416 in succinate buffered-saline was investigated. AMG 416 HC1 (103 mg powder, 80 mg peptide) was dissolved in 200 iL of sodium succinate buffered saline (25 mM succinate, 0.9% saline, pH 4.5). After briefly vortexing, a clear solution was obtained with a nominal concentration of 400 mg/mL. Because expansion of the solution volume was not determined, the solubility of AMG 416 can be conservatively stated as at least 200 mg/mL. Although the maximal solubility was not determined in this experiment, AMG 416 is soluble in pH 4.5 succinate buffered saline to concentrations of at least 200 mg/mL.

REFERENCES

  1. “Amgen Submits New Drug Application For Novel Intravenous Calcimimetic Etelcalcetide (AMG 416)”
  2. “Velcalcetide (AMG 416), a novel peptide agonist of the calcium-sensing receptor, reduces serum parathyroid hormone and FGF23 levels in healthy male subjects
  3. “Evidence for Chronic Kidney Disease-Mineral and Bone Disorder Associated With Metabolic Pathway Changes”

KAI-4169, a novel calcium sensing receptor agonist, decreases serum iPTH, FGF-23 and improves serum bone markers in a phase 2 study in hemodialysis subjects with chronic kidney disease-mineral and bone disorder
49th Congr Eur Renal Assoc – Eur Dialysis Transpl Assoc (May 24-27, Paris) 2012, Abst SAO054

KAI-4169, a novel peptide agonist of the calcium sensing receptor, attenuates PTH and soft tissue calcification and restores parathyroid gland VDR levels in uremic rats
49th Congr Eur Renal Assoc – Eur Dialysis Transpl Assoc (May 24-27, Paris) 2012, Abst SAO014
Long term safety and efficacy of velcalcetide (AMG 416), a calcium-sensing receptor (CaSR) agonist, for the treatment of secondary hyperparathyroidism (SHPT) in hemodialysis (HD) patients
Kidney Week (November 5-10, Atlanta, GA) 2013, Abst SA-PO575
Preclinical PK and PD relationship for KAI-4169, a novel calcimimetic
93rd Annu Meet Endo Soc (June 4-7, Boston) 2011, Abst P1-198
KAI-4169, a novel calcimimetic for the treatment of secondary hyperparathyroidism
93rd Annu Meet Endo Soc (June 4-7, Boston) 2011, Abst P2-98
Characterization of KAI-4169, a novel peptide for the treatment of chronic kidney disease – Mineral and bone disorder, in a phase I study in healthy males
44th Annu Meet Am Soc Nephrol (ASN) (November 8-13, Philadelphia) 2011, Abst FR-PO1238
WO2011014707A2 Jul 29, 2010 Feb 3, 2011 Kai Pharmaceuticals, Inc. Therapeutic agents for reducing parathyroid hormone levels

 

//////////////Etelcalcetide,  AMG 416, KAI-4169, velcalcetide, peptide drugs

Ravidasvir, PPI-668, BI 238630


CAS # 1303533-81-4, Ravidasvir dihydrochloride

Ravidasvir dihydrochloride

C42H50N8O6.2(HCl), 835.83

CAS 1303533-81-4

Phase II/IIIHepatitis C

Ravidasvir
PPI-668 free base; BI 238630;
CAS:1242087-93-9

C42H50N8O6, 762.38
Chemical Name:methyl N-[(1S)-1-({(2S)-2-[5-(6-{2-[(2S)-1-{(2S)-2-[(methoxycarbonyl)amino]- 3- methylbutanoyl}pyrrolidin-2-yl]-1H-imidazol-4-yl}naphthalen-2-yl) -1H- benzimidazol- 2-yl]pyrrolidin-1-yl}carbonyl)-2-methylpropyl]carbamate
Mechanism of Action:NS5A Inhibitor
Indication: hepatitis C
Development Stage: Phase II
Developer:Presidio Pharmaceuticals, Inc

  • OriginatorXTL Biopharmaceuticals
  • Developer Pharco Corporation; Presidio Pharmaceuticals
  • Class Antivirals; Benzimidazoles; Carbamates; Naphthalenes; Pyrrolidines; Small molecules
  • Mechanism of Action Hepatitis C virus NS 5 protein inhibitors; Hepatitis C virus replication inhibitors
  • 31 Aug 2015 Ascletis plans to initiate the phase II EVEREST trial for Hepatitis C (Combination therapy; Treatment-naive) in Taiwan
  • 31 Aug 2015 Taiwan Food and Drug Administration approves Clinical Trial Application to initiate a phase II trial for interferon free regimen comprising danoprevir and ravidasvir in Hepatitis C
  • 24 Jun 2015 Efficacy data from a phase IIa trial in Hepatitis C released by Ascletis

r12

Ravidasvir [Methyl N-[(1S)-1-({(2S)-2-[5-(6-{2-[(2S)-1-{(2S)-2-[(methoxycarbonyl)amino]- 3- methylbutanoyl}pyrrolidin-2-yl]-1H-imidazol-4-yl}naphthalen-2-yl) -1H- benzimidazol- 2-yl]pyrrolidin-1-yl}carbonyl)-2-methylpropyl]carbamate] is an Nonstructural protein 5A (NS5A) inhibitor. It is an antiviral agent that is being developed as a potential treatment for hepatitis C virus infection.

PPI-668, a non-structural 5A (NS5A) protein of hepatitis C virus (HCV) inhibitor, is in phase II clinical studies at Presidio Pharmaceuticals for the treatment of chronic genotype 1 hepatitis C virus infection.

Ravidasvir has 50% inhibitory concentrations (EC50s) values of 0.02-1.3 nM in replicon assays for HCV genotypes 1-7 (gt1-gt7).

Ravidasvir was developed by Presidio Pharmaceuticals Inc, later Ascletis licensed it. Ravidasvir is in Phase II clinical trials proving interferon (IFN)-free regimen to treat chronic hepatitis C (CHC). Ascletis is now the first Chinese company to file clinical trial applications in China for an IFN-free regimen.
In 2014, Ascletis acquired rights for development and commercialization in Greater China and Pharco in Egypt for the treatment of hepatitis C.

Hepatitis C virus infection is a major health problem worldwide and no vaccine has yet been developed against this virus. The standard therapy of pegylated-interferon and ribavirin induces serious side effects and provides viral eradication in less than 50% of patients. Combination therapy of HCV including ribavirin and interferon are currently is the approved therapy for HCV. Unfortunately, such combination therapy also produces side effects and is often poorly tolerated, resulting in major clinical challenges in a significant proportion of patients. The combination of direct acting agents can also result in drug-drug interactions. To date, no HCV therapy has been approved which is interferon free. There is therefore a need for new combination therapies which have reduced side effects, and interferon free, have a reduced emergence of resistance, reduced treatment periods and/or and enhanced cure rates.

Nonstructural protein 5A (NS5A) is a zinc-binding and proline-rich hydrophilic phosphoprotein that plays a key role in Hepatitis C virus RNA replication.

A number of direct-acting antiviral agents (DAAs) are under development for the treatment of chronic HCV infection. These agents block viral production by directly inhibiting one of several steps of the HCV lifecycle. several viral proteins involved in the HCV lifecycle, such as the non-structural (NS)3/4A serine protease, the NS5B RNA-dependent RNA polymerase (RdRp), and the NS5A protein, have been targeted for drug development. Two NS3/4A protease inhibitors already approved for clinical use, numerous other protease inhibitors are being developed as well as inhibitors of viral replication, including nucleoside/nucleotide analogue inhibitors of HCV RdRp, non-nucleoside inhibitors of RdRp, cyclophilin inhibitors, and NS5A inhibitors.

Inhibition of NS5A at picomolar concentrations has been associated with significant reductions in HCV RNA levels in cell culture-based models, which makes these agents among the most potent antiviral molecules yet developed.


Activity:

This NS5A inhibitor has been shown to possess high efficacy against HCV genotype 1, with up to 3.7 log10 mean HCV RNA reductions, in a Phase Ib clinical trial. Activity was demonstrated against variants harbouring the L31M substitution. In an added genotype-2/3 cohort, the first 2 patients achieved mean 3.0 log10 RNA level reductions [1].

Results from the Phase IIa study involving a combination therapy with Faldaprevir and Deleobuvir plus Ravidasvir came with positive news where the said combination cured 92 percent of those with genotype 1a of hepatitis C virus (HCV) when given with ribavirin.  The results presented at the 49th annual meeting of the European Association for the Study of the Liver (EASL) in London [2, 3].

The 36 study participants were randomly dived into three even cohorts of 12 each: The first received 600 mg of Deleobuvir twice a day as well as once-daily doses of Faldaprevir (120 mg), Ravidasvir and Ribavirin. The second group received the same regimen except the Faldaprevir dose was 400 mg. The third group took the regimen with the higher dose of Faldaprevir, but without Ribavirin. All participants were treated for 12 weeks with follow up for next 24 weeks.

Ninety-two percent of the first and second cohorts (11 out of 12 in both cases) achieved a sustained virologic response 12 weeks after completing therapy (SVR12, considered a cure). In the end, 14 participants were required for the third cohort, because one was incarcerated early on during treatment and another experienced viral rebound at week eight as a result of not adhering to the treatment regimen. Of the other 12 participants, eight, or two-thirds, have achieved an SVR12, while one more participant stopped taking the therapy at week eight but has since achieved an SVR8.

PATENT

WO 2011054834

http://www.google.co.in/patents/WO2011054834A1?cl=en

Scheme 1

Figure imgf000018_0001

GOING TO PRODUCT USING STRUCTURES FROM PATENT

Figure imgf000031_0002 IIa

Figure imgf000032_0001  IIIa   one of side chain

DO NOT MISS OUT synthesis of XIIIa or XIII’a, this is needed in one of side chain

Figure imgf000034_0004L-boc-prolinol

Figure imgf000035_0001Z-boc-prolinal

Figure imgf000035_0002XXIV

Figure imgf000036_0001XIIIa

or

Figure imgf000036_0002

Figure imgf000038_0002XVIb

Figure imgf000043_0001

Figure imgf000045_0001

MY CONSTRUCTION of 3

R1

Figure imgf000052_0001

Compound 3 was prepared following the procedure reported for the synthesis of compound 1 using intermediate XVIIIb instead of intermediate XVIIIa. see my construction below

R1

Compound 3. BASE

1H NMR (400 MHz, DMSO-d6) δ ppm 8.34 (2 H, s), 8.21 (1 H, s), 8.19

(1 H, d, J=8.69 Hz), 8.06 – 8.11 (2 H, m), 8.00 (1 H, dd, J=8.88, 1.61 Hz), 7.88 – 7.96

(2 H, m), 7.86 (1 H, d, J=8.48 Hz), 7.32 (1 H, d, J=8.48 Hz), 7.34 (1 H, d, J=8.53 Hz), 5.27 (1 H, dd, J=8.17, 5.33 Hz), 5.17 (1 H, t, J=7.00 Hz), 4.15 (2 H, t, J=7.95 Hz), 3.84

– 3.96 (4 H, m), 3.56 (6 H, s), 2.38 – 2.47 (2 H, m), 1.95 – 2.30 (8 H, m), 0.86 (3 H, d,

J=6.70 Hz), 0.85 (3 H, d, J=6.70 Hz), 0.81 (6 H, d, J=6.63 Hz).

[a] 2°= -148.98 0 (c 0.3336 w/v %, MeOH)

Alternative preparation of compound 3 and the corresponding HC1 salt

Figure imgf000052_0001

N-methoxycarbonyl-L- Valine (3.09 g, 17.7 mmol, 2.1 equiv) was dissolved in dichloro- methane (300 mL). Triethylamine (11.7 mL, 84.1 mmol, 10 equiv) and (l-cyano-2- ethoxy-2-oxoethylidenaminooxy)dimethylamino-morpholino-carbenium hexafluoro- phosphate were added (7.57 g, 17.7 mmol, 2.1 eq). The reaction mixture was stirred at room temperature for 5 minutes, after which XVIIIb was added (5 g, 8.41 mmol in case x.HCl equals 4 HC1). Stirring was continued for 30 minutes. HC1 in iPrOH (6N) was added to the mixture (until pH = 2), and the resulting mixture was stirred for 5 minutes. The solution was then washed with saturated aqueous sodium carbonate (2 x 200 mL) and once with brine (200 mL). The organic layer was separated, dried on magnesium sulphate and filtrated. After removal of the solvent in vacuum, the obtained residue was further dried in vacuum to afford an orange powder (6.84 g)

The powder was purified by silica gel column chromatography using gradient elution with 0 to 10 % MeOH (7N NH3) in dichloromethane, resulting in compound 3 (2.81 g) as a foam.

Compound 3 was dissolved in iPrOH (40 mL) and HC1 (6N in iPrOH, 10 mL) was added. The volatiles were removed in vacuum. Then, iPrOH (30 mL) was added and the mixture was heated at reflux. The solution was cooled to room temperature and stirred at room temperature for 4 days. tBuOMe (100 mL) was added to the solution, resulting in white precipitation, which was filtered, washed immediately with tBuOMe (3 x 10 mL) under nitrogen atmosphere and dried under vacuum at 40°C. The residue was mixed with acetonitrile and evaporated to dryness (2x). The residue was stirred in acetonitrile (150 mL) and the mixture was sonicated for 10 minutes. The precipitate was filtered under nitrogen atmosphere, washed twice with acetonitrile (50 mL) and dried in vacuum at 40°C, resulting in a slightly yellow powder (4 g).

HCL salt of compound 3:

[a] *° = -110.02 ° (589 nm, 20 °C, c 0.429 w/v%, MeOH)

1H NMR (600 MHz, DIMETHYLFORMAMIDE- y, 280K) δ ppm 0.86 (d, J=6.6 Hz, 6 H), 0.95 (d, J=7.0 Hz, 6 H), 2.03 – 2.20 (m, 2 H), 2.26 – 2.37 (m, 3 H), 2.39 – 2.61 (m, 5 H), 3.61 – 3.63 (m, 6 H), 3.93 – 4.01 (m, 2 H), 4.23 – 4.32 (m, 2 H), 4.32 – 4.39 (m, 2 H), 5.49 (t, J=7.5 Hz, 1 H), 5.52 (dd, J=8.3, 5.3 Hz, 1 H), 7.22 (d, J=8.8 Hz, 1 H), 7.27 (d, J=8.8 Hz, 1 H), 7.98 (d, J=8.6 Hz, 1 H), 8.01 (dd, J=8.6, 1.1 Hz, 1 H), 8.03 (dd, J=8.8, 1.8 Hz, 1 H), 8.09 (d, J=8.8 Hz, 1 H), 8.19 (d, J=8.8 Hz, 1 H), 8.22 (dd, J=8.4, 1.8 Hz, 1 H), 8.25 (s, 1 H), 8.32 (s, 1 H), 8.41 (s, 1 H), 8.88 (s, 1 H).

Anal. Calcd for C42H5oN806 . 2 HCl . 4 H20: C 55.56, H 6.66 , N 12.34. Found: C 55.00, H 6.60, N 12.30

Going reverse…………………..

Intermediate XVIIIb

2.8 preparation of intermediate XVIIIb (A=

Figure imgf000044_0002

To a solution of XVIIb (960 mg, 1.48 mmol) in CH2C12 (25mL) was added HCI (5-6 M in isopropanol, 5 mL). The mixture was stirred at room temperature overnight. The solvent was evaporated, the obtained solid was dried in vacuum and used as such in the next step. 2.8a Alternative preparation of intermediate XVIIIb (A=

Figure imgf000045_0001

XVIIb (19.52 g, 30.1 mmol, 1.00 equiv.) was dissolved in dichloromethane (200 mL) and HCI in isopropanol (5-6 N, 300 mL) was added. The reaction mixture was stirred for 1 hour at room temperature. tBuOMe (1000 mL) was added to the suspension and the slurry was stirred at roomtemperature for 30 minutes. The filtered solid was rinced with tBuOMe (2x 100 mL) and dried under vacuum overnight to afford XVIIIb as a powder (15.2 g). 1H NMR (400 MHz, MeOD-d4) δ ppm 2.15 – 2.37 (m, 2 H), 2.37 – 2.52 (m, 2 H), 2.52 – 2.69 (m, 2 H), 2.69 – 2.88 (m, 2 H), 3.56 – 3.71 (m, 4 H), 5.19 – 5.41 (m, 2 H), 7.90 – 8.02 (m, 3 H), 8.05 (dd, J= 8.6, 1.6 Hz, 1 H), 8.10 – 8.25 (m, 4 H), 8.30 (d, J=1.4 Hz, 1 H), 8.47 (d, J=1.2 Hz, 1 H)

INTERMEDIATE XVIIb

2.7 reparation of intermediate XVIIb (A= PG= Boc)

Figure imgf000043_0001

To boronic ester XVIb (1.22 g, 2.26 mmol), bromide Xllla (1072 mg, 3.39 mmol), sodium bicarbonate (380 mg, 4.52 mmol), Pd(dppf)Cl2 (166 mg, 0.226 mmol) in toluene (50 mL), was added water (1 mL). The resulting mixture was heated at reflux overnight. The reaction mixture was filtered, evaporated to dryness and purified by column chromatography by gradient elution with heptane to ethyl acetate. The collected fractions containing the product were pooled and the volatiles were removed under reduced pressure. The residue (960 mg, 65 %) was used as such in the next reaction.

2.7a Alternative preparation of intermediate XVIIb (A= . PG= Boc)

Figure imgf000043_0002

XVIb (10 g, 18.5 mmol), Xlll’a (8.76 g, 24 mmol), NaHC03 (9.32 g, 111 mmol) and Pd(dppf)Cl2 (lg) were stirred in dioxane/water (140 mL, 6/1) under argon. The mixture was heated to 85 °C for 15 hours. Brine (100 mL ) was added and the mixture was extracted with CH2CI2, after drying on MgSC^, filtration and evaporation of the solvent, the residue was purified by column chromotography by gradient elution with CH2CI2 to EtOAc to afford XVIIb (7 g, 58 %).

Figure imgf000044_0001

To a stirred, deoxygenated solution of Vlllb (20.0 g, 45.2 mmol, 1.00 equiv.), Ilia (20.6 g, 49.7 mmol, 1.1 equiv.) and sodium bicarbonate (11.4 g, 136 mmol, 3.0 equiv.) in 1 ,4-dioxane/water (500 mL, 5: 1) under nitrogen, was added l.,.r-Bis(diphenyi~ phosphmo)ferrocene-paiIadium(]I)dichloride dichJoromethane complex (2.50 g, 4.52 mmol, 0.1 equiv.). The mixture was heated at 80°C under argon for 15 hours and cooled to room temperature. The reaction mixture was diluted with dichloromethane (500 mL) and washed with brine (2 x 150 mL) dried on magnesium sulphate; filtered and evaporated to dryness to afford a dark brown foam (43 g). The foam was purified using silicagel column chromatography (gradient elution with 0-6% MeOH in CH2CI2) to afford XVIIb (19.52 g, 65%) as an off-white powder.

INTERMEDIATE XVIb

Figure imgf000038_0001

Bromide XVb (1890 mg, 3.83 mmol), 4,4,4\4\5,5,5\5*-octamethyl-2,2′-bis(l,3,2- dioxaborolane) (2437 mg, 9.59 mmol), KF (390 mg; 6.71 mmol) and (dppf)PdCl2 (281 mg, 0.384 mmol) were dissolved in toluene (50 mL) and heated 3 days at reflux.

The solids were removed by filtration over dicalite and the filtrate was evaporated to dryness on silica. The residue was purified by column chromatography using a heptane to ethylacetate gradient. The fractions containing the product were pooled and the solvent was removed under reduced pressure. The residue (1.22 g, 59 %) was used as such in the next reaction

Figure imgf000038_0002

Under nitrogen, Ilia (25 g, 60.5 mmol), 6-bromonaphthalen-2-yl trifluoromethane- sulfonate (20 g, 56.7 mmol), K3P04 (36.65 g, 173 mmol) and (PPh3)4Pd (717 mg, 0.62 mmol) were stirred in THF (60 mL) and water (15 mL) with the heating mantle at 85 °C (reflux) for 2 hours. CH2CI2 (50 mL) was added and the water layer was separated. The organic layer was dried on MgS04 and after filtration, the filtrate was concentrated resulting in a sticky solid. The residue was purified by column

chromatography (petroleum ether/Ethyl acetate 15/1 to 1/1) to afford XVb (20 g;

40.6 mmol). Compound XVb (1 g, 2.0 mmol), potassium acetate (0.5 g, 5.0 mmol), 4,4,4′,4′,5,5,5′,5′-octamethyl-2,2′-bis(l,3,2-dioxaborolane) (1.29 g, 5.0 mmol), and Pd(dppf)Cl2 (0. lg) were stirred in DMF (15 mL) under argon. The mixture was heated at 60°C for 5 hours. After cooling, CH2CI2 (50 mL) was added and the mixture was washed with saturated NaHC03. The water layer was separated and extracted with CH2CI2. The organic layers were combined and dried on MgSC^. After filtration the solvent was removed and the product was purified by column chromatography (gradient elution with petroleum ether/ethyl acetate 10/1 to 1/1) to give of XVIb (0.7 g,1.3 mmol, 65 %) as light yellow solid.

INTERMEDIATE XVb

Figure imgf000037_0001

2,6-Dibromonaphthalene (6.92 g, 24.2 mmol), boronic ester Ilia (2 g, 4.84 mmol), NaHC03 (813 mg, 9.68 mmol), (dppf)PdCl2(710 mg, 0.968 mmol) were dissolved in toluene (75 mL). Water (1 mL) was added and the mixture was heated for 7 hours at reflux. The solids were removed by filtration over dicalite and the filtrate was evaporated to dryness on silica. The residue was purified by column chromatography by gradient elution with heptane to ethylacetate. The appropriate fractions were pooled and the solvent was removed under reduced pressure. The residue (1.89 g, 79 %) was used as such in the next step.

1.2 Preparation of intermediate IIIa (PG= Boc)

Figure imgf000032_0001 IIIa

To a mixture of Ila (200 g, 546 mmol), potassium acetate (160.8 g, 1.64 mol) and 4,4,4*,4*,5,5,5*,5*-octamethyl-2,2,-bis(l,3,2-dioxaborolane) (416 g, 1.64 mol) in DMF (3L) was added Pd(dppf)Cl2 (20 g) under nitrogen gas. The reaction mixture was stirred at 85°C for 15 hours. The mixture was diluted with ethyl acetate, washed with water and brine, dried over magnesium sulfate, the solids removed by filtration, and the solvents of the filtrate were removed under reduced pressure. The residue was purified by silica column chromatography (petroleum ether : ethyl acetate 10: 1 to 2: 1) to afford 125 g of Ilia as a white solid (contains 15% of boronic acid).

INT IIa

1.1 preparation of intermediate Ila (PG= Boc; X= Br)

Figure imgf000031_0002

Ma

To a solution of Boc-Z-Proline (2669 mg, 12.4 mmol) in pyridine/DMF (30 mL, 1/1) was added di(lH-imidazol-l-yl)ketone (2205 mg, 13.6 mmol). The mixture was stirred at 45°C for 2 hours. 4-bromobenzene-l,2-diamine (2319 mg, 12.4 mmol) was added and the mixture was stirred at ambient temperature overnight. The solvent was removed and the residue heated in acetic acid (15 mL) at 100°C for 30 minutes. After

concentration of the residue, the mixture was partitioned between ethyl acetate and a saturated sodium bicarbonate solution. The organic phase was separated and washed with water, after drying over Na2SC”4, the mixture was filtrated and the filtrate was concentrated in vacuum. The obtained residue was purified by flash chromatography using CH2Cl2/EtOAc 90/10 to 50/50, resulting in compound Ila (3.146 g, 69 %).

DO NOT MISS OUT synthesis of XIIIa or XIII’a, this is needed in one of side chain

2.1 preparation of L-boc-prolinol

Figure imgf000034_0004

Borane-methyl sulfide complex (180 mL, 1.80 mol) was added dropwise to a solution of N-Boc- L-Proline (300 g, 1.39 mol) in anhydrous THF (3.0 L) which was cooled to 0°C. When gas evolution ceased, the ice bath was removed and the solution was stirred at 10°C for 18 hours. Thin layer chromatography (TLC) showed that no starting material remained and that the desired product was formed. The solution was cooled to 0°C and methanol (2.4 L) was slowly added. The solvents were removed under reduced pressure. The residue was reconstituted in dichloromethane (1 L), washed with

NaHC03 (500 mL, saturated, aqueous) and brine (500 mL), dried over MgS04, the solids were removed via filtration, and the solvents of the filtrate were removed under reduced pressure to afford a white solid, 260 g (93%), used in the next step without further purification.

2.2 preparation of Z-boc-prolinal

Figure imgf000035_0001

To a solution of Z-boc-prolinol (100 g, 500 mmol) in CH2CI2 (1.5 L) at 0°C were added successively, under vigorous stirring, 2,2,6,6-tetramethylpiperidine-l-oxyl (TEMPO; 1.56 g, 10 mmol) and NaBr (5.14 g, 50 mmol). To the resulting mixture was added dropwise a solution of NaHC03 (6.3 g, 75 mmol) and 6% NaCIO in active chlorine (750 mL, 750 mmol) at 0°C over a period of 1 hour. TLC showed no starting material remained and that the desired product was formed. The mixture was rapidly extracted with dichloromethane (2 x 1.5 L). The organic layers were combined, washed with NaHS04 (10%, 1 L) and KI (4%, 200 mL), then with Na2S203 (10%, 1 L) and brine (1.5 L), dried over MgS04, the solids were removed via filtration, and the solvents evaporated to afford a yellow oil, Z-boc-prolinal, (89 g, 92%>), used in the next step without further purification.

2.3 preparation of intermediate XXIV

Figure imgf000035_0002

ammonia

XXIV

Aqueous ammonia (25~28%>, 200 mL) was added dropwise to a solution of L-boc- prolinal (89 g, 0.44 mol) and glyoxal (183 mL of 40% in water) in methanol (1 L). The reaction mixture was sealed and reacted at 10°C. After 16 hours, additional glyoxal (20 mL) and aqueous ammonia (20 mL) were added and reacted for an additional 6 hours. The solvents were removed under reduced pressure, and the crude was reconstituted in ethyl acetate (1.0 L), washed with water and brine, dried over MgSC^, the solids were removed via filtration and the solvents were removed under reduced pressure. The crude was purified by column chromatography (silica gel, dichloromethane to methanol/dichloromethane 1 :70) to obtain 73 g (70%) intermediate XXIV as a white solid.

1H NMR: (CD3OD 400 MHz) δ 6.95 (s, 2H), 4.82-4.94 (m, 1H), 3.60-3.70 (m, 1H), 3.41-3.50 (m, 1H), 2.20-2.39 (m, 1H), 1.91-2.03 (m, 3H), 1.47 (s, 3H), 1.25 (s, 6H)

2.4 preparation of intermediate XHIa (PG= Boc)

Figure imgf000036_0001

XXIV Xllla

N-Bromosuccinimide (47.2 g, 0.26 mol) was added portion wise over 1 hour to a cooled (ice-ethanol bath, -10 °C) solution of XXIV (63.0 g, 0.26 mol) in CH2C12 (1.5 L) and stirred at similar temperature for 2 hours. The reaction mixture was concentrated in vacuum and the residue was purification by preparatory HPLC to provide 25.3 g (30%) of Xllla as a pale yellow solid.

1H NMR: CD3OD 400Mhz

δ 6.99-7.03 (s,lH), 4.77-4.90 (m, 1H), 3.61-3.68 (m, 1H), 3.42-3.50 (m, 1H), 2.20-2.39 (m, 1H), 1.89-2.05 (m, 3H), 1.47 (s, 3H), 1.27 (s, 6H).

2.4a preparation of intermediate XHI’a (PG= Boc)

Figure imgf000036_0002

To a solution of iodine (43.3 g, 170.5 mmol, 2 eq) in chloroform (210 mL) in a round bottomed flask (1L) a suspension of XXIV (20 g, 84.3 mmol) in an aqueous NaOH solution (2M, 210 mL) was added. The mixture was stirred at room temperature for 15 hours. To the resulting reaction mixture was added a saturated aqueous Na2S2C”3 solution (100 mL) and the organic layer was separated. The aqueous layer was extracted with chloroform (4x 150 mL). The organic layers were combined, washed with water and dried on magnesium sulphate. The solids were filtered and the solution was evaporated to dryness to afford diiodide (38.61 g, 89 %).

The above obtained intermediate diiodide (2.24 g, 4.58 mmol) and sodium sulfite (4.82 g, 38 mmol) were placed in a round bottomed flask (100 mL) and suspended in 30% EtOH/water (80 mL). The resulting mixture was refluxed for 40 hours. The solvent was removed and after addition of H20 (20 mL), the mixture was stirred at room temperature overnight. The solids were filtered, washed with water and dried in a vacuum oven to afford compound XHI’a (1.024 g, 61 %).

1H NMR (400 MHz, DMSO-d6) δ ppm 1.16 and 1.38 (2x br. s., 9 H), 1.68 – 2.02 (m, 3 H), 2.02 – 2.27 (m, 1 H), 3.18 – 3.38 (m, 1 H), 3.38 – 3.59 (m, 1 H), 4.53 – 4.88 (m, 1 H), 6.81 (m, -0.1 H), 7.05 – 7.28 (m, -0.9 H), 11.90 – 12.20 (m, -0.9 H), 12.22 – 12.40 (m, -0.1 H)

PATENT

WO 2011149856

http://www.google.co.in/patents/WO2011149856A1?cl=en

1st scheme

Figure imgf000107_0001

IN ABOVE SCHEME CONVERSION OF f to g N-methoxycarbonyl-L-Val-OH is used,

USE R =H IN LAST STEP TO GET RAVIDASVIR

EXAMPLE 1 – Synthesis of compounds of Formula lie

Scheme 1-1 describes preparation of target molecules and their analogs with symmetrical and non-symmetrical functionalized ends.

[0341] Step a. To a solution of 2-bromonaphthane a (62.0 g, 300 mmol) in DCM (1 L) was added A1C13 (44.0 g, 330 mmol) and 2-chloroacetyl chloride (34.0 g, 330 mmol) at 0 °C. The reaction mixture was stirred at 0 °C for 1 h and then H20 added (500 mL) and extracted. The organic layer was washed with H20, dried over anhydrous Na2S04, evaporated under reduced pressure to give 80 g crude product, which was purified by re-crystallization from 10% EtOAc- hexane (v/v) to yield b (28 g, 36% yield) as a white solid: JH NMR (500 MHz, CDC13) δ 8.44 (s, 1H), 8.07 (s, 1H), 8.04 (d, J= 11.0 Hz, 1H), 7.84 (d, J= 8.5 Hz, 2H), 7.66 (d, J= 8.5 Hz, 1H), 4.81 (s, 2H) ppm; LCMS (ESI) m/z 282.9 (M + H)+.

Step b. To a solution of b (28.0 g, 100 mmol) in DCM (500 mL) was added N-Boc- L-Pro-OH (24.7 g, 115 mmol) and Et3N (70.0 mL, 500 mmol) and the mixture was stirred at rt for 2 h. The mixture was concentrated under reduced pressure to afford crude c which was used for the next step without further purification. LC-MS (ESI) m/z 462.1 (M + H)+.

Step c. To a solution of c (46.0 g, 100 mmol) in toluene (500 mL) was added

NH4OAc (77 g, 1.0 mol) and the mixture was stirred at 110 °C overnight, and concentrated under reduced pressure. The resulting residue was purified by silica gel column chromatography (petroleum ether/EtOAc l :l(v/v)) to afford d (30 g, 68% yield) as a yellow solid: LC-MS (ESI) m/z 442 A (M + H)+.

Step d. To a solution of d (10.0 g, 23.0 mmol) in anhydrous DME (200 mL) and equal molar of boronate e was added PPh3 (1.2 g, 4.6 mmol), Pd(PPh3)4 (1.6 g, 2.3 mmol), and 2.0 M Na2C03 solution. The mixture was refluxed under argon overnight. The organic solvent was removed under reduced pressure and the residue was treated with H20, extracted with EtOAc (2 x 200 mL). The combined organic phase was dried, filtered, and concentrated in vacuo to give a residue, which was purified by silica gel column chromatography (petroleum

ether/EtOAc 3: l(v/v)) to afford f (10 g, 96% yield) as a yellow solid. LC-MS (ESI): m/z 709.3 (M+H)+.

Step e. To a stirred solution of f (150 mg, 0.29 mmol) in dioxane (3 mL) was added 4.0 N HCl in dioxane (3 mL) dropwise. The mixture was stirred at rt for 4 h, and then

concentrated to yield a yellowish solid (134 mg), which was used directly for the next step. The residue (134 mg, 0.290 mmol) was suspended in THF (5 mL) and DIPEA (0.32 mL) was added and followed by addition of N-methoxycarbonyl-L-Val-OH (151 mg, 0.860 mmol). After stirring for 15 min, HATU (328 mg, 0.860 mmol) was added and the mixture was stirred at rt for another 2 h and then concentrated. The residue was purified by prep-HPLC to obtain g (40 mg, 19% yield).

2nd scheme

Figure imgf000110_0001

SCHEME SIMILAR UPTO PENULTIMATE STEP

Note 9 is not final product pl ignore it

Step a. Referring to Scheme 1-2, to a solution of compound 3 (2.0 g, 4.5 mmol) in dioxane (25 mL) was added 4.0 N HCl in dioxane (25 mL). After stirring at rt for 4 h, the reaction mixture was concentrated and the residue was dried in vacuo to give a yellowish solid (2.1 g), which was used directly for the next step without further purification.

[0347] Step b. To the residue of step a (4.5mmol) was added DMF (25 mL), followed by adding HATU (2.1 g, 5.4 mmol), DIPEA (3.7 mL, 22.5 mmol) and N-methyl carbamate-L-valine (945 mg, 5.4 mmol). After stirring at rt for 15 min, the reaction mixture was added slowly to H20 (400 mL). A white solid precipitated was filtered and dried to give compound 6 (2.2 g, 98% yield). LC-MS (ESI): m/z 499.1 (M+H)+.

[0348] Step c. To a mixture of compound 6 (800 mg, 1.6 mmol), compound 7 (718 mg, 1.6 mmol), and NaHC03 (480 mg, 5.7 mmol) in 1 ,2-dimethoxyethane (15mL) and H20 (5mL) was added Pd(dppf)Cl2 (59 mg, 0.08 mmol). After stirring at 80°C overnight under an atmosphere of N2, the reaction mixture was concentrated. The residue was partitioned between 20%

methanol/CHCl3 (100 mL) and H20 (100 mL). The organic phase was separated and the aqueous phase was extracted with 20% methanol/CHCl3 (100 mL) again. The combined organic phase was consequently washed with brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (Petroleum

ether/EtOAc=15: l(v/v)) to give compound 8 (1.0 g, 85% yield) as a yellow solid. LC-MS (ESI): m/z 732.4 (M+H)+.

Step d. To a solution of compound 8 (200 mg, 0.27 mmol) in dioxane (3.0 mL) was added 4 N HCl in dioxane (3.0 mL). After stirring at rt for 2 h, the reaction mixture was concentrated and the residue was dried in vacuo to give an HCl salt in quantitative yield, which was used directly for the next step without further purification…………..CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

CAUTION SIMILAR BUT NOT SAME……..Step e. To a solution of the salt (0.27 mmol) in DMF (5.0 mL) was added DIPEA (0.47mL, 2.7 mmol), followed by adding N,N-dimethyl-D-phenyl glycine (59 mg, 0.33 mmol) and HATU (125 mg, 0.33 mmol). After stirring at rt for lh, the reaction mixture was partitioned between H20 and DCM. The organic phase was washed successively with H20 and brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by prep-HPLC to give compound 9……..CAUTION SIMILAR BUT NOT SAME. LC-MS (ESI): m/z 793.4 (M+H)+.

3rd scheme

Figure imgf000112_0001

SCHEME SIMILAR UPTO PENULTIMATE STEP

15 NOT THE COMPD PL IGNORE IT IF YOU NEED RAVIDASVIR

Step a. To a mixture of compound 3 (3.2 g, 7.2 mmol), bis(pinacolato)diboron (3.86 g, 15.2 mmol), and KOAc (1.85g, 18.8mmol) in 1,4-dioxane (100 mL) was added Pd(dppf)Cl2 (440 mg, 0.6 mmol). After stirring at 80 °C for 3 h under an atmosphere of N2, the reaction mixture was concentrated. The residue was purified with silica gel column chromatography (Petroleum ether/EtOAc=2/l(v/v)) to give compound 11 (2.8 g, 80% yield) as a white solid. LC- MS (ESI): m/z 490.3 (M+H)+.

[0352] Step b. To a mixture of compound 11 (626 mg, 1.27 mmol), compound 12 (570 mg, 1.27 mmol), and NaHC03 (420 mg, 4.99 mmol) in 1, 2-dimethoxyethane (30 mL) and H20 (10 mL) was added Pd(dppf)Cl2 (139 mg, 0.19 mmol). After stirring at 80°C overnight under an atmosphere of N2, the reaction mixture was concentrated. The residue was partitioned between 20% methanol/CHCl3 (100 mL) and H20 (100 mL). The aqueous phase was extracted with 20% methanol/CHCl3 (100 mL) again. The combined organic phase was consequently washed with brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (Petroleum ether/EtOAc=2/l(v/v)) to give compound 13 (635 mg, 68% yield) as a yellow solid. LC-MS (ESI): m/z 732.4 (M+H)+.

Step c. To a solution of compound 13 (200 mg, 0.27 mmol) in dioxane (3.0 mL) was added 4 N HC1 in dioxane (3.0 mL). After stirring at rt for 2 h, the reaction mixture was concentrated and the residue was dried in vacuo to yield the HC1 salt of compound 14 in quantitative yield, which was used directly for the next step without further purification…..CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

CAUTION SIMILAR BUT NOT SAME………Step d. To a solution of the salt (0.27 mmol) in DMF (5.0 mL) was added DIPEA (0.47 mL, 2.7 mmol), followed by adding N,N-dimethyl-D-phenyl glycine (59 mg, 0.33 mmol) and HATU (125 mg, 0.33 mmol). After stirring at rt for lh, the reaction mixture was partitioned between H20 and DCM. The organic phase was consequently washed with H20 and brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by prep-HPLC to give compound 15..CAUTION SIMILAR BUT NOT SAME. LC-MS (ESI): m/z 793.4 (M+H)+.

4 th scheme

Figure imgf000114_0001

SCHEME SIMILAR UPTO PENULTIMATE STEP

5 NOT THE COMPD,  PL IGNORE IT IF YOU NEED RAVIDASVIR

4 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

scheme ……..CAUTION SIMILAR BUT NOT SAME

EXAMPLE 2 – Synthesis of compounds of Formula Hie

Step a. Referring to Scheme 2-1, to a mixture of compound 1 (5.05 g, 13.8 mmol), bis(pinacolato)diboron (7.1 g, 27.9 mmol), and KOAc (3.2 g, 32.5 mmol) in 1,4-dioxane (100 mL) was added Pd(dppf)Cl2 (400 mg, 0.5 mmol). After stirring at 80 °C for 3 h under an atmosphere of N2, the reaction mixture was concentrated. The residue was purified by silica gel column chromatography (Petroleum ether/EtOAc=2/l(v/v)) to give compound 2 (3.0 g, 53% yield) as a gray solid. LC-MS (ESI): m/z 414.2 (M+H)+.

Step b. To a mixture of compound 2 (522 mg, 1.26 mmol), compound 3 (500 mg, 1.13 mmol), and NaHC03 (333 mg, 3.96 mmol) in 1, 2-dimethoxyethane (30 mL) and H20 (10 mL) was added Pd(dppf)Cl2 (74 mg, 0.1 mmol). After stirring at 80°C overnight under an atmosphere of N2, the reaction mixture was concentrated. The residue was partitioned between 20% methanol/CHCl3 (100 mL) and H20 (100 mL). The organic phase was separated and the aqueous phase was extracted with 20% methanol/CHCl3 (100 mL) again. The combined organic phase was consequently washed with brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (DCM/MeOH=50:l (v/v)) to give compound 4 (450 mg, 55% yield) as a yellow solid. LC-MS (ESI): m/z 649.3 (M+H)+.

Step c. To a stirred solution of compound 4 (160 mg, 0.25 mmol) in dioxane (2.0 mL) was added 4N HCl in dioxane (2.0 mL). After stirring at rt for 3h, the reaction mixture was concentrated and the residue was dried in vacuo to give an HCl salt in quantitative yield, which was used directly for the next step without further purification.4 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

SCHEME SIMILAR UPTO PENULTIMATE STEP

5 NOT THE COMPD,  PL IGNORE IT IF YOU NEED RAVIDASVIR

scheme ……..CAUTION SIMILAR BUT NOT SAME

5 th scheme

Figure imgf000116_0001

SCHEME SIMILAR UPTO PENULTIMATE STEP

18NOT THE COMPD,  PL IGNORE IT IF YOU NEED RAVIDASVIR

17 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

scheme ……..CAUTION SIMILAR BUT NOT SAME

Step a. Referring to Scheme 2-2, to a mixture of compound 2 (1.16 g, 2.32 mmol), compound 6 (1.40 g, 3.39 mmol), and NaHC03 (823 mg, 9.8 mmol) in 1, 2-dimethoxyethane (30 mL) and H20 (10 mL) was added Pd(dppf)Cl2 (103 mg, 0.14 mmol). After stirring at 80 °C over night under an atmosphere of N2, the reaction mixture was concentrated. The residue was partitioned between 20% methanol/CHCl3 (150 mL) and H20 (150 mL). The aqueous phase was extracted with 20% methanol/CHCl3 (150 mL) again. The combined organic phase was consequently washed with brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (Petroleum ether/acetone=1.5/l (v/v)) to give compound 16 (1.32g, 80% yield) as a yellow solid. LC-MS (ESI): m/z 706.4 (M + H)+.

tep b. To a solution of compound 16 (200 mg, 0.28 mmol) in dioxane (3.0 mL) was added 4 N HC1 in dioxane (3.0 mL). After stirring at rt for 2 h, the reaction mixture was concentrated and the residue was dried in vacuo to give the HC1 salt of compound 17 in quantitative yield, which was used directly for the next step…….17 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

6 th scheme

 

Figure imgf000118_0001scheme 2-3

SCHEME SIMILAR UPTO PENULTIMATE STEP

22NOT THE COMPD,  PL IGNORE IT IF YOU NEED RAVIDASVIR

21 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

scheme ……..CAUTION SIMILAR BUT NOT SAME

Scheme 2-3

Step a. Referring to Scheme 2-3, to a solution of compound 1 (4.0 g, 10.9 mmol) in dioxane (40 mL) was added 4 N HC1 in dioxane (40 mL). After stirring at rt overnight, the reaction mixture was concentrated. The residue was washed with DCM, filtered, and dried in vacuo to afford a hydrochloride salt in quantitative yield, which was used for the next step without further purification.

Step b. To a solution of the salt (10.9 mmol) in DMF (30 mL) was added DIPEA (5.8 mL, 33.0 mmol), followed by adding N-methoxycarbonyl-L-valine (2.1 g, 12.1 mmol) and HATU (4.6 g, 12.1 mmol). After stirring at rt for lh, the reaction mixture was partitioned between H20 and DCM. The organic phase was consequently washed with H20 and brine, dried with anhydrous Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (DCM/Petroleum ether=4/l (v/v)) to give compound 19 (3.0 g, 65% yield). LC- MS (ESI): m/z 423.1 (M+H)+.

Step c. To a mixture of compound 11 (800 mg, 1.9 mmol), compound 19 (700 mg, 1.7 mmol), and NaHC03 (561 mg, 6.6 mmol) in 1, 2-dimethoxyethane (60 mL) and H20 (20 mL) was added Pd(dppf)Cl2 (183 mg, 0.25 mmol). After stirring at 80 °C overnight under an atmosphere of N2, the reaction mixture was concentrated. The residue was then partitioned between 20% methanol/CHCl3 (100 mL) and H20 (100 mL). The aqueous phase was extracted with 20% methanol/CHCl3(100 mL) again. The combined organic phase was consequently washed with brine, dried with Na2S04, filtered, and concentrated. The residue was purified by silica gel column chromatography (Petroleum ether/EtOAc=2/l(v/v)) to give compound 20 (600 mg, 52% yield) as a yellow solid. LC-MS (ESI): m/z 706.4 (M+H)+.

Step d. To a solution of compound 20 (200 mg, 0.28 mmol) in dioxane (3.0 mL) was added 4N HC1 in dioxane (3.0 mL). After stirring at rt for 2h, the reaction mixture was concentrated and the residue was dried in vacuo to yield the HC1 salt of compound 21 in quantitative yield, which was used directly for the next step without further purification.

21 CAN BE USED AS PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

7 th scheme

 

Figure imgf000148_0001

Scheme 6-2

SCHEME SIMILAR UPTO n-2 STEP in above scheme

84, 85 NOT THE COMPD,  PL IGNORE IT IF YOU NEED RAVIDASVIR

83 CAN BE USED AS early PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

scheme ……..CAUTION SIMILAR BUT NOT SAME

Step a. Referring to Scheme 6-2, a solution of compound 78 (50.0 g, 0.30 mol) in THF (500 mL) and H20 (500 mL) was added K2C03 (83 g, 0.60 mol) and (Boc)20 (73. Og, 0.330 mol). After stirring at rt overnight, the reaction mixture was concentrated and the residue was extracted with EtOAc (250 mL x 3). The extracts were combined, washed with brine, and dried with anhydrous Na2S04. The solvent was removed and the residue was dried in vacuo to give crude compound 78 (62 g), which was used for the next step without further purification. LC-MS (ESI) m/z 230.1 (M + H)+.

[0453] Step b. To a solution of compound 78 (60.0 g, 260 mmol) in EtOH (1 L) was slowly added NaBH4 (50.0 g, 1.30 mol) at rt. After stirring at rt overnight, the reaction was quenched by adding acetone (10 mL). The resulting mixture was concentrated and the residue was diluted with EtOAc (500 mL). The mixture was washed with brined and dried in vacuo. The solvent was removed and the residue was purified by silica gel column chromatography (Petroleum ether/EtOAc = 1/1 (v/v)) to give compound 79 (42.0 g, 80% yield) as a white solid. LC-MS (ESI) m/z 202 A (M + H)+.

[0454] Step c. To a solution of compound 79 (30.0 g, 150 mmol) and DMSO (35.0 g, 450 mmol) in DCM (1 L) was added oxalyl chloride (28.0 g, 220 mmol) at -78 °C. After stirring at – 78 °C for 4 h, the reaction mixture was added Et3N (60.0 g, 600 mol) and the resulting mixture was stirred for another 1 h at -78 °C. Subsequently, the reaction was quenched by adding H20. The organic layer was separated and the aqueous layer was extracted with DCM (200mL x 2). The extracts were combined, washed with brine, and dried with Na2S04. The solvent was removed and the residue was dried in vacuo to give crude compound 80 (22.0 g) as a colorless oil, which was used immediately without further purification. LC-MS (ESI) m/z 200.1 (M + H)+.

[0455] Step d. A mixture of compound 80 (7.7 g, 38.5 mmol), 6-bromopyridine-2,3-diamine (8.0 g, 42.8 mmol) (PCT Intl. Appl. WO 2008021851) , and iodine (1.08 g, 4.28 mmol) in AcOH (30 mL) was stirred at rt overnight. The reaction mixture was neutralized by adding saturated aqueous NaHC03. The resulting mixture was extracted with EtOAc (200 mL x 3). The extracts were combined, washed with brine, and dried with anhydrous Na2S04. The solvent was removed and the residue was purified by silica gel column chromatography (DCM/MeOH = 80/1 (v/v)) to give compound 81 (7.8 g, 55% yield). LC-MS (ESI) m/z 367.1 (M + H)+.

[0456] Step e. A mixture of compound 82 (10.0 g, 20.1 mmol), bis(pinacolato)diboron (7.65 g, 30.1 mmol), potassium acetate (6.89 g, 70.3 mmol), and Pd(dppf)Cl2-CH2Cl2 (886 mg, 1.0 mmol) in 1,4-dioxane (200 mL) was stirred at 80 °C for 3 h under an atmosphere of N2. The reaction mixture was filtered through CELITE™ 545 and the filtered cake was washed with EtOAc (200 mL x 3). The filtrate was washed with brine and dried with anhydrous Na2S04. The solvent was removed and the residue was purified by silica gel column chromatography

(DCM/MeOH = 50/1 (v/v)) to give compound 83 (9.8 g, 89% yield) as a white solid: LC-MS (ESI) m/z 547.3 (M + H)+.83 CAN BE USED AS early PRECURSOR FOR RAVIDASVIR UPTO THIS POINT

PATENT

CN 102796084

http://www.google.com/patents/CN102796084A?cl=en

Step One: Formula (2) compounds strokes trichloride catalyst (AlCl3), chloroacetyl chloride (2-chloroacetylchloride) at room temperature to obtain a compound of formula (3),

Figure CN102796084AD00072

(3);

  wherein the reaction temperature is room temperature, the solvent is methylene chloride. Material I (i.e., formula (2) compound) and chloroacetyl chloride (2-chloroacetyl chloride) was slowly added, higher yields can be obtained. (3) The compound was recrystallized from ether to obtain.

  In the present embodiment, the 20.5 g of formula (2) compound (0. Imol) and 26.2 g AlCl3 (0.2mol) was added to 200ml of dichloromethane, cooled to room temperature, stirring speed slowly was added 13.4 g of chloroacetyl chloride (I. 2mol), within three hours after the addition and then mixed by stirring maintained at room temperature for 3 hours. Was slowly added 50 ml of ice water, the precipitate was collected by filtration. The filter cake was washed with 10 ml of water and 10 ml petroleum ether (twice). The filtrate and the organic layer together with 50 ml of dichloromethane and extracted twice with 50 ml brine and then paint extraction solution, the extract was dried over magnesium sulfate, the solution was removed, the solid with 100 ml of diethyl ether and recrystallized to afford 20g (71% yield compounds) of formula (3).

Step II: Formula (3) with a compound of formula (4) compound under acidic conditions and chloroform (CCl3H) heating the reaction, and the reaction system reached reflux to give a compound of formula (5),

Figure CN102796084AD00073

(5);

[0042] wherein, the formula (3) with a compound of formula (4) compound in acetonitrile (chloroform (CCl3H), the reaction system must be reached reflux, and must be reacted under acidic conditions to give the compound of formula (5). [0043] In this embodiment, the compound (3) (0. Imol) 28. 2 克 formula and the compound (4) (0. Imol) 21. 5 克 style with 3 g of trifluoroacetic acid was added to 200 ml of chloroform, in was stirred at reflux under nitrogen for 17 hours. After cooling to room temperature, spin-dry, to give 46. I g of a yellow solid of formula (5) compound (99% yield).

  Step three: (5) the compound obtained in toluene (toluene) and ammonium acetate (NH4OAc) reflux (6) of

Thereof,

Figure CN102796084AD00081

Compound  of formula (5) is ammonium acetate with toluene under reflux conditions for ring closure.

In the present embodiment, the compound (0. Imol) and 10 g of ammonium acetate (NH4OAc) was added 46. I g of formula (5) to IJ 200ml of toluene, heated under reflux for 3 hours with stirring. Was slowly added 50 ml of ice water, filtered, washed with 100 ml of toluene and extracted twice with 50 ml brine and then paint extraction solution, the extract was dried over magnesium sulfate, the solution was removed, the solid with 100 ml of diethyl ether and recrystallized to afford 40g (89% compound yield) of the formula (6).

Step Four: (6) compound in the catalyst and the associated button pinacolato ester (Bis (pinacolato) diboron) reacting a compound of formula (7),

Figure CN102796084AD00082

  wherein, Pd (dppf) 2Cl2 can be replaced by another of a palladium catalyst, a palladium catalyst with the other, the same effect.

  In the present embodiment, 44 g of the compound of formula (6) (0. Imol) and 3 g Pd (dppf) 2C12,25. 4 克 United pinacolato ester (0. Imol) and 8.4 g of sodium bicarbonate (0. Imol) was added to a 200 ml I. 4- dioxane, stirred at reflux for 24 hours. Diatomaceous earth filtration, spin dry. Spin-dry 100 ml of ethyl acetate dissolved. Anhydrous magnesium sulfate and spin dry. Recrystallization from ether to yield 40 g (82% yield) of a yellow solid of formula (7) compound.

Step Five: formula (7) under palladium catalyst compound and the compound (8) obtained by reacting the compound of formula (9),

Figure CN102796084AD00083

  wherein, Pd (dppf) 2Cl2 can be replaced by another of a palladium catalyst, a palladium catalyst with the other, the same effect.

  In the present embodiment, 48.9 g of the compound of formula (7) (0. Imol) and 3 g Pd compound (8) (0. Imol) (dppf) 2C12,41. 3 and 8 克 style. 4 g of sodium hydrogen carbonate (0. Imol) was added to a 200 ml I. 4- dioxane, stirred at reflux for 24 hours. Diatomaceous earth filtration, spin dry. Spin-dry 100 ml of ethyl acetate dissolved. Anhydrous magnesium sulfate and spin dry. Recrystallized from ether to give compound 55 g (85% yield) of a yellow solid of formula (9).

[0056] Step Six: formula (9) compound deprotected under acidic conditions to give a compound of formula (10),

[0057]

Figure CN102796084AD00091

  In the present embodiment, the 64.8 grams of formula (9) compound (0. Imol) was added to 100 ml I. 4_ dioxane was stirred, 100 ml of 5M / L of I under nitrogen 4- dioxane solution of hydrochloric acid. Spin-dry for 24 hours later, get 52. I g of pale yellow solid formula (10) compound (99% yield).

Step 7: Formula (10) with a compound (11) in a condensing agent is 2- (7-azo BTA) -N, N, N ‘, N’- tetramethyluronium hexafluorophosphate phosphate (HATU) under condensation reaction conditions to give the final product compound C0S-101, i.e. the compound of formula (I):

Figure CN102796084AD00092

In the present embodiment, the compound of formula 52. I g of (10) (0. Imol) was added to a 200 ml N, N- dimethylformamide (DMF) cooled to 0 ° with stirring, in a nitrogen atmosphere was added 20.2 g of triethylamine (0. 2mol) 0 After 10 minutes of stirring, was added 19 g of formula (11) compound (0. Ilmol) was added followed by 26 g HATU (0. 2mol), stirred at room temperature for 32 hours . Was slowly added 50 ml of ice water, the precipitate was collected by filtration. The filter cake was washed with 10 ml of water and 50 ml dichloromethane twice. Together with the filtrate and the organic layer was extracted 2 times 50 ml of dichloromethane, and then washed with 50 ml brine solution, the extract was dried over magnesium sulfate, the solution was removed, solid was recrystallized from 100 ml of ethanol, to give 50g (66% yield) The pale yellow compound C0S-101.

  In summary this compound on C0S-101 non-structural protein 5A inhibitor, or a pharmaceutically acceptable salt thereof, the treatment of hepatitis C active substance. A compound of formula (3) Friedel-Crafts reaction occurs directly from 2-bromo-naphthalene chloride and chlorine. A compound of formula (3) with a compound of formula (4) condensing a compound of formula (5). The compound of formula (5) self-condensation of a compound of formula (6). Of formula (6) is reacted with boronic acid pinacol ester linking reaction of the compound of formula (7). A compound of formula (7) with a compound of formula (8) coupling reaction of a compound of formula (9). Off compound under acidic conditions (9) protect the compound of formula (10) and formula (10) compound condensation of the final product C0S-101, method of operation of the invention is simple, mild conditions, process maturity, yield and high purity suitable for industrial production.

PATENT

WO 2013123092

http://www.google.com/patents/WO2013123092A1?cl=en

Figure imgf000003_0001

Scheme 3

Figure imgf000025_0001

3-3 2HCI salt

Step 1. Referring to Scheme 3, compounds l-5a (1.3 kg , 1.0 eq.), 2-2a (975.0 g, 1.0 eq.), NaHCOs (860.0 g, 3.80 eq.), Pd(dppf)Cl2 (121.7 g, 0.05 eq.), purified water (5.2 L, 4.0 volume) and 1 ,2-dimethoxy ethane (DME) (24.7 L, 19.0 volume) were charged into a 50.0 L 4-necked round bottom flask under argon atmosphere. After being degassed using argon for a period of 30 min, the reaction mass was slowly heated to ~ 80 °C and stirred at this temperature for 12 – 14 hrs. HPLC analysis indicated that > 97% of compound 2-2a was consumed. Next, the reaction mass was concentrated to completely remove DME under vacuum (600 mmHg) at 40 – 45 °C and the residue was diluted with 20% (v/v) MeOH in DCM (13.0 L , 10 volume) and purified water (13.0 L, 10.0 volume) with stirring. The organic layer was separated and the aqueous layer was extracted with 20% (v/v) MeOH in DCM (6.5 L x 2, 10.0 volume). The combined organic extracts were washed twice with water (6.5 L x 2, 10.0 volume) and once with saturated brine (6.5 L, 5.0 volume) and dried over anhydrous Na2S04. The solvent was removed under vacuum (600 mmHg) and the residue was purified by flash column chromatography using silica gel with hexanes/EtOAc as eluent to give compound 3-1 (1.0 kg, 63% yield) as off white solid with a purity of > 98.0%> determined by HPLC analysis. LC-MS (ESI): m/z 649.3 [M + H]+. 1H NMR (400 MHz, d6– DMSO): δ 12.26 – 12.36 (m, 1H), 11.88 – 11.95 (m, 1H), 8.23 (s, 1H), 8.11 (s, 1H), 7.91 (m, 3H), 7.85 – 7.87 (m, 2H), 7.51 – 7.81 (m, 3H), 4.78 -4.99 (m, 2H), 3.55 – 3.59 (m, 2H), 3.35 – 3.44 (m, 2H), 2.30 – 2.47 (m, 2H), 1.85 – 2.01 (m, 6H), 1.39, 1.14, 1.04 (s, s, s, 18H) ppm. Alternatively, compound 3-1 can be obtained following the same procedure and using compounds l-4a and 2-3a instead of compounds l-5a and 2-2a as the Suzuki coupling components.

Step 2. Compound 3-1 (1.0 kg, 1.0 eq.) and IPA (7.0 L, 7.0 volume) were charged into a 20.0 L four-necked RB flask under nitrogen atm. The reaction mass was cooled to 18 – 20°C and 3.0 N HC1 in isopropyl alcohol (7.0 L, 7.0 volume) was added over a period of 90 – 120 min under nitrogen atmosphere. After stirring at 25 – 30 °C for 10 – 12 hrs under nitrogen atmosphere, HPLC analysis indicated that > 98%> compound 3-1 was consumed. Next, the reaction mass was concentrated to remove IPA under vacuum at 40 – 45 °C. The semi solid obtained was added to acetone (2.0 L, 2.0 volume) with stirring and the resulting suspension was filtered under nitrogen atmosphere. The solid was washed with acetone (2.0 L, 2.0 volume) and dried in a vacuum tray drier at 40 – 45 °C for 10 hrs to give compound 3- 2 (860 g, 94%o yield) as pale yellow solid with a purity of > 98.0%> determined by HPLC analysis. LC-MS (ESI): m/z 449.2 [M + H]+. 1H NMR (400 MHz, -DMSO): δ 10.49 – 10.59 (m, 2H), 10.10 and 9.75 (m, m, 2H), 8.60 (s, 1H), 8.31 (s, 2H), 8.15 (m, 1H), 8.13 – 8.15 (m, 2H), 7.96 – 8.09 (m, 2H), 7.82 (s, 2H), 5.08 (m, 2H), 3.39 – 3.53 (m, 4H), 2.47 – 2.54 (m, 3H), 2.37 (m, 1H), 2.14 – 2.21 (m, 2H), 2.08 (m, 2H) ppm.

Step 3. Compound 3-2 (2.2 kg, 1.0 eq.) was added to a four necked round bottom flask charged with DMF (4.4 L, 20.0 volume) under a nitrogen atmosphere. After stirring for 15 min, the mixture was added N-Moc-L-Valine (226.2 g, 3.52 eq.) in one lot at 25 – 30 °C. Next, the mixture was cooled to -20 to -15 °C, followed by adding HATU (372.9 g, 2.0 eq.) portion wise over 30 min. After stirring for 10 min, a solution of DIPEA (238.9 g, 5.0 eq.) in DMF (1.1 L, 5.0 volume) was added over 45 min. Subsequently, the reaction mass was warmed to 25 – 30 °C with stirring. After stirring for 1 hr, HPLC analysis indicated that > 99%) of compound 3-2 was consumed. The reaction mixture was poured into water (38.0 L) and the mixture was extracted with DCM (10.0 L x 3, 45.0 volume). The combined organic extracts were washed with water (10.0 L x 3, 45.0 volume) and saturated brine (10 L, 45.0 volume) and dried over anhydrous Na2S04. The solvent was removed at 40 – 45 °C under vacuum (600 mmHg) and the residue was purified by column chromatography on silica gel using DCM and MeOH as the eluent to give compound 3-3 (1.52 kg, 47% yield) as off white solid with a purity of > 97.0% determined by HPLC analysis. LC-MS (ESI): m/z 763.4 [M + H]+. 1H NMR (400 MHz, -DMSO): δ 8.60 (s, 1H), 8.29 (s, 1H), 8.20 (s, 1H), 8.09 – 8.14 (m, 2H), 7.99 – 8.05 (m, 2H), 7.86 – 7.95 (m, 3H), 7.20-7.21 (m, 2H), 5.24 – 5.33 (m, 2H), 4.06 – 4.18 (m, 4H), 3.83 (m, 2H), 3.53 (m, 6H), 2.26 – 2.55 (m, 10H), 0.85 (m, 6H), 0.78 (m, 6H) ppm. The transformation of 3-2 to 3-3 (Compound I) can be achieved via a range of conditions. One of these conditions is described below.

A reactor was charged with N-Moc-V aline (37.15 g, 0.211 mol), acetonitrile (750 mL) and DIPEA (22.5 g). The reaction mixture was agitated for 10 min and HOBT (35.3 g 0.361 mole) and EDCI (42.4 g, 0.221 mole) were added while keeping temperature < 2 °C. The reaction mixture was agitated for 30 min and DIPEA (22.5 g) and compound 3-2 (48.0 g, 0.092 mole) was added slowly to reactor over 30 min to keep temperature < 3 °C. The reaction mixture was agitated 4 hrs at 20 – 25 °C, and sample was submitted for reaction completion analysis by HPLC (IPC specification: < 1.0% area 3-2 remaining). At the completion of reaction as indicated by HPLC analysis, isopropyl acetate (750 mL) was added to the reactor and stirred for 10 min. The organic layer (product layer) was washed with brine (300 mL x 2) and 2% NaOH (200 mL). The organic solution was filtered through a silica gel pad to remove insoluble material. The silica gel pad was washed with isopropyl acetate and concentrated under vacuum (400 mm/Hg) to a minimum volume. The crude product was purified by column chromatography on silica gel using ethyl acetate and methanol as eluent to give compound 3-3 (38.0 g, 65%> yield) with purity of > 95 %>. LC-MS (ESI): m/z 763.4 [M + H]+.

Step 4. Compound 3-3 (132.0 g, 1.0 eq.) and ethanol (324.0 mL, 2.0 volume) were charged into a 10 L four-necked round bottom flask under nitrogen atmosphere. After stirring for 15 min, the suspension was cooled to 5 – 10 °C, to it was added 2.0 N HC1 in ethanol (190 mL, 1.5 volume) over 30 min. The resulting solution was allowed to warm to 25 – 30 °C. Acetone (3.96 L, 30.0 volume) was added over 90 min in to cause the slow precipitation. Next, the suspension was warmed to 60 °C and another batch of acetone (3.96 L, 30.0 volume) was added over 90 min. The temperature was maintained at 55 – 60 °C for 1 hr, and then allowed to cool to 25 – 30 °C. After stirring at 25 – 30 °C for 8 – 10 hrs, the mixture was filtered. The solid was washed with acetone (660.0 mL, 5.0 volume) and dried in a vacuum tray drier at 50 – 55 °C for 16 hrs to give the di-HCl salt of compound 3-3

(compound I) (101 g, 71% yield) as pale yellow solid with a purity of > 96.6% determined by HPLC analysis.

Preparation of N-Moc-L-Valine

N-Moc-L-Valine is available for purchase but can also be made. Moc-L-Valine was prepared by dissolving 1.0 eq of L-valine hydrochloride in 2-methyltetrahydrofuran (2- MeTHF) /water containing sodium hydroxide and sodium carbonate, and then treating with 1.0 eq of methyl chloroformate at 0 – 5°C for 6 hr. The reaction mixture was diluted with 2- MeTHF, acidified with HC1, and the organic layer was washed with water. The 2-MeTHF solution is concentrated and the compound is precipitated with n-heptane. The solid was rinsed with 2-MeTHF/ n-heptane and dried in vacuo to give N-Moc-L-Valine in 68% yield. Crystallization of Compound I to Yield Form A

Compound I Salt Formation and Crystallization, Example 1

Ethanol (3.19 L, 1.0 volume, 200 proof) was charged to the 230-L glass lined reactor under nitrogen atmosphere. Free base form of compound 3-3 (3.19 kg, 4.18 mol) was added to the flask with stirring, stir continued for an additional 20 to 30 min. To the thick solution of 3-3 in ethanol was added slowly 2.6 N HC1 in ethanol (3.19 L, 1.0 volume) to the above mass at 20 – 25 °C under nitrogen atmosphere. The entire mass was stirred for 20 min at rt, and then heated to 45 – 50 °C. Acetone (128.0 L, 40.0 volume) was added to the above reaction mass at 45 – 50 °C over a period of 3-4 hrs before it was cooled to ~25 °C and stirred for ~15 hrs. The precipitated solid was collected by filtration and washed with acetone (6.4 L x 2, 4.0 volume), suck dried for 1 hr and further dried in vacuum tray drier at 40 – 45 °C for 12 hrs. Yield: 2.5 kg (71.0% yield), purity by HPLC: 97.70%, XRPD: amorphous.

Isopropyl alcohol (7.5 L, 3.0 volume) was charged to a 50.0 L glass reactor protected under a nitrogen atmosphere. The amorphous di-HCl salt of 3-3 (2.5 kg) was added to the above reactor with stirring. The entire mass was heated to 60 – 65 °C to give a clear solution. Stir continued at 65 ± 2 °C for ~15 hrs, solid formation started during this time. The heating temperature was lowered to ~50 °C over a period of 3 hrs, methyl tertiary butyl ether (12.5 L, 5.0 volume) was added to the above mass slowly over a period of ~3 hrs with gentle agitation. The above reaction mass was further cooled to 25 – 30 °C over 2 – 3 hrs. The solid was collected by filtration, washed with 10.0% isopropyl alcohol in methyl tertiary butyl ether (6.25 L, 2.5 volume), suck dried for 1 hr and further dried in a tray drier at 45 – 50 °C under vacuum (600 mm/Hg) for 70 – 80 hrs. Yield: 2.13 kg (85.0% recovery, 61.0% yield based on the input of compound free base 3-3), purity by HPLC: 97.9%.

FIG. 1 : 1H NMR (500 MHz, -DMSO): δ 15.6 (bs, 2H), 14.7 (bs, 2H), 8.58 (s, 1H), 8.35 (s, 1H), 8.25 (s, 1H), 8.18 (d, J= 8.7 Hz, 1H), 8.13 (s, 1H), 8.06 (d, J= 8.6 Hz, 1H), 8.04 (s, 1H), 8.00 (s, 1H), 7.98 (d, J= 8.7 Hz, 1H), 7.91 (d, J= 8.6 Hz, 1H), 7.36 (d, J = 8.6 Hz, 1H), 7.33 (d, J= 8.6 Hz, 2H), 5.31 (m, 1H), 5.26 (m, 1H), 4.16 (d, J= 7.7 Hz, 1H), 4.04 (m, 2H), 3.87 (m, 2H), 3.55 (s, 6H), 2.42 (m, 2H), 2.22-2.26 (m, 4H), 2.07-2.14 (m, 4H), 0.86 (d, J= 2.6 Hz, 3H), 0.84 (d, J= 2.6 Hz, 3H), 0.78 (d, J= 2.2 Hz, 3H), 0.77 (d, J= 2.2 Hz, 3H), 3.06 (s, OMe of MTBE), 1.09 (s, t-Bu of MTBE), 1.03 (d, 2Me of IP A) ppm.

FIG. 2: 13C NMR (500 MHz, /-DMSO): δ 171.6, 171.5, 157.4, 156.1, 150.0, 138.2, 138.0, 133.5, 132.5, 131.3, 129.8, 129.4, 128.0, 127.0, 126.4, 125.6, 125.3, 124.4, 124.2, 115.8, 115.0, 112.5, 58.37, 58.26, 54.03, 53.34, 52.00 (2 carbons), 47.71 (2 carbons), 31.52, 31.47, 29.42 (2 carbons), 25.94, 25.44, 20.13, 20.07, 18.37, 18.36 ppm.

FIG. 3: FT-IR (KBr pellet): 3379.0, 2963.4, 2602.1, 1728.4, 1600.0, 1523.4, 1439.7, 1420.6, 1233.2, 1193.4, 1100.9, 1027.3 cm“1.

Elemental Analysis: Anal. Calcd for C42H52C12N806: C, 60.35; H, 6.27; N, 13.41; CI, 8.48. Found C, 58.63; H, 6.42; N, 12.65, CI, 8.2.

FIG. 1 is a representative 1H NMR spectrum of Compound I Form A.

FIG. 2 is a representative 13C NMR spectrum of Compound I Form A.

FIG. 3 is a representative FT-IR spectrum of Compound I Form A.

References:
1. Lalezari, J. P.; et. al. PPI-668, a potent new pan-genotypic HCV NS5A inhibitor: phase 1 efficacy and safety. Hepatology 2012, 56, 1065A-1066A.

  1. ClinicalTrials.govA Study of the Efficacy and Safety of PPI-668 (NS5A Inhibitor) Plus Sofosbuvir, With or Without Ribavirin, in Patients With Chronic Hepatitis C Genotype-4. NCT02371408(retrieved on 24-03-2015)
    3. ClinicalTrials.gov Study of PPI-668, BI 207127 and Faldaprevir, With and Without Ribavirin, in the Treatment of Chronic Hepatitis C. NCT01859962 (retrieved on 15-09-2015)
    4. Lalezari, J.; et. al. High rate of sustained virologic response in patients with hcv genotype-1a infection: a phase 2 trial of faldaprevir, deleobuvir and ppi-668, with and without ribavirin. EASL-The International Liver Congress 2014– 49th Annual Meeting of the European  Association for the Study of the Liver London, United Kingdom  April 9-13 (article here)
US20070185175 * 27 Jul 2006 9 Aug 2007 Bristol-Myers Squibb Company Benzothiazole and azabenzothiazole compounds useful as kinase inhibitors
US20080050336 * 8 Aug 2007 28 Feb 2008 Bristol-Myers Squibb Company Hepatitis C Virus Inhibitors
WO2012087976A2 * 19 Dec 2011 28 Jun 2012 Intermune, Inc. Novel inhibitors of hepatitis c virus replication
WO2013123092A1 * 13 Feb 2013 22 Aug 2013 Presidio Pharmaceuticals, Inc. Solid forms comprising inhibitors of hcv ns5a, compositions thereof, and uses therewith
WO2013158776A1 * 17 Apr 2013 24 Oct 2013 Gilead Sciences, Inc. Compounds and methods for antiviral treatment
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////////////Phase III, Hepatitis C, RAVIDASVIR, PPI-668,  BI 238630

BEXAGLIFLOZIN


Figure imgf000045_0001

Bexagliflozin
THR1442; THR-1442, EGT 0001442; EGT1442
CAS :1118567-05-7
(2S,3R,4R,5S,6R)-2-[4-chloro-3-({4-[2- (cyclopropyloxy) ethoxy] phenyl} methyl)phenyl]-6-(hydroxymethyl)tetrahydro-2H- pyran-3,4,5-triol

D-Glucitol, 1,5-anhydro-1-C-(4-chloro-3-((4-(2-(cyclopropyloxy)ethoxy)phenyl)methyl)phenyl)-, (1S)-

(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6- (hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol

1-[4-Chloro-3-[4-[2-(cyclopropyloxy)ethoxy]benzyl]phenyl]-1-deoxy-beta-D-glucopyranose
1,5-Anhydro-1(S)-[4-chloro-3-[4-[2-(cyclopropyloxy)ethoxy]benzyl]phenyl]-D-glucitol

(1S)-1,5-anhydro-1-C-[4-chloro-3-({4-[2- (cyclopropyloxy)ethoxy]phenyl}methyl)phenyl]-D-glucitol

Chemical Formula: C24H29ClO7
Exact Mass: 464.16018

Mechanism of Action:SGLT2 inhibitor, Sodium-glucose transporter 2 inhibitors
Indication:Type 2 diabetes

FDA APPROVED

Brenzavvy

To improve glycemic control in adults with type 2 diabetes mellitus as an adjunct to diet and exercise
Drug Trials Snapshot
Phase II
Developer:Theracos, Inc.

Conditions Phases Recruitment Interventions Sponsor/Collaborators
Diabetes Mellitus Type 2 Phase 2 Completed Drug: EGT0001442|Drug: Placebo capsules to match EGT0001442 Theracos
Diabetes Mellitus Phase 2 Completed Drug: EGT0001442|Drug: Placebo Theracos
Type 2 Diabetes Mellitus Phase 3 Not yet recruiting Drug: Bexagliflozin|Drug: Placebo Theracos
Diabetes Mellitus, Type 2 Phase 2|Phase 3 Recruiting Drug: Bexagliflozin tablets Theracos

Figure US20130267694A1-20131010-C00062DIPROLINE COMPLEX

 

Bexagliflozin diproline
RN: 1118567-48-8, C24-H29-Cl-O7.2C5-H9-N-O2
Molecular Weight, 695.2013

L-Proline, compd. with (1S)-1,5-anhydro-1-C-(4-chloro-3-((4-(2-(cyclopropyloxy)ethoxy)phenyl)methyl)phenyl)-D-glucitol (2:1)

im1

Bexagliflozin [(2S,3R,4R,5S,6R)-2-[4-chloro-3-({4-[2-(cyclopropyloxy) ethoxy] phenyl} methyl)phenyl]-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol] is an orally administered drug for the treatment of Type 2 Diabetes Mellitus (T2DM) and is classified as a Sodium Glucose co-Transporter 2 (SGLT2) Inhibitor. It is in Phase 2b study to evaluate the effect of bexagliflozin tablets in subjects with type 2 diabetes mellitus.

2D chemical structure of 1118567-05-7

Bexagliflozin, also known as EGT1442, is a potent and selective SGLT2 inhibitor, attenuates blood glucose and HbA(1c) levels in db/db mice and prolongs the survival of stroke-prone rats. The IC(50) values for EGT1442 against human SGLT1 and SGLT2 are 5.6μM and 2nM, respectively. In normal rats and dogs a saturable urinary glucose excretion was produced with an ED(50) of 0.38 and 0.09mg/kg, respectively. EGT1442 showed favorable properties both in vitro and in vivo and could be beneficial to the management of type 2 diabetic patients.

One promising target for therapeutic intervention in diabetes and related disorders is the glucose transport system of the kidneys. Cellular glucose transport is conducted by either facilitative (“passive”) glucose transporters (GLUTs) or sodium-dependent (“active”) glucose cotransporters (SGLTs). SGLTl is found predominantly in the intestinal brush border, while SGLT2 is localized in the renal proximal tubule and is reportedly responsible for the majority of glucose reuptake by the kidneys.

Recent studies suggest that inhibition of renal SGLT may be a useful approach to treating hyperglycemia by increasing the amount of glucose excreted in the urine (Arakawa K, et al., Br J Pharmacol 132:578-86, 2001; Oku A, et al., Diabetes 48:1794-1800, 1999).

The potential of this therapeutic approach is further supported by recent findings that mutations in the SGL T2 gene occur in cases of familial renal glucosuria, an apparently benign syndrome characterized by urinary glucose excretion in the presence of normal serum glucose levels and the absence of general renal dysfunction or other disease (Santer R, et al., J Am Soc Nephrol 14:2873-82, 2003). Therefore, compounds which inhibit SGLT, particularly SGL T2, are promising candidates for use as antidiabetic drugs.

Compounds previously described as useful for inhibiting SGLT include C-glycoside derivatives (such as those described in US6414126, US20040138439, US20050209166, US20050233988, WO2005085237, US7094763, US20060009400, US20060019948, US20060035841, US20060122126, US20060234953, WO2006108842, US20070049537 and WO2007136116), O-glycoside derivatives (such as those described in US6683056, US20050187168, US20060166899, US20060234954, US20060247179 and US20070185197), spiroketal-glycoside derivatives (described in WO2006080421), cyclohexane derivatives (such as those described in WO2006011469), and thio- glucopyranoside derivatives (such as those described in US20050209309 and WO2006073197).

PATENT

WO 2009026537……………PRODUCT PATENT

http://www.google.co.in/patents/WO2009026537A1?cl=en

Example 19

[0289] The synthesis of compound BQ within the invention is given below.

[0290] Preparation of 2-cyclopropoxyethanol (Intermediate BO)

Figure imgf000073_0002

To a suspension of Mg powder (0.87 g, 36.1 mmol) and iodine (catalytic) in THF (4 mL) was added slowly BrCH2CH2Br (4.6 g, 24.5 mmol) in THF (8 mL). The exothermic reaction was cooled in an ice-bath. After complete addition OfBrCH2CH2Br, a solution of 2- (2-bromoethyl)-l,3-dioxolane (1 g, 5.6 mmol) was added dropwise. The reaction mixture was then kept at reflux for 24 h, quenched by addition of aqueous NH4Cl, and extracted with DCM. The combined organic layers were washed with brine, dried over Na2SO4, and concentrated to give crude intermediate BO (400 mg) as yellow oil. [0292] Preparation of 2-cyclopropoxyethyl 4-methylbenzenesulfonate (Intermediate BP)

Ts0^°V

To a solution of 2-cyclopropoxyethanol (400 mg, 3.92 mmol) in DCM (10 niL) were added TsCl (821 mg, 4.31 mmol) and Et3N (0.6 mL, 4.31 mmol). The reaction was stirred at room temperature overnight. Then, IN HCl was added, and the reaction was extracted with DCM. The combined organic layers were washed with brine, dried over Na2SO4, and concentrated to give a yellow oil. The oil was purified by preparative TLC to obtain intermediate BP (50 mg) as a yellow oil.

Preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2- cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (Compound BQ)

Figure imgf000074_0001

To a solution of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-hydroxybenzyl)phenyl)-6- (hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (intermediate Dl) (30 mg, 0.08 mmol) in anhydrous DMF (1 mL) were added 2-cyclopropoxyethyl 4-methylbenzenesulfonate (intermediate BP) (20 mg, 0.08 mmol) and Cs2CO3 (52 mg, 0.16 mmol). The mixture was stirred at room temperature for 12 h. Then the reaction mixture was poured into water, extracted with EA, washed with brine, dried with anhydrous Na2SO4 and concentrated to an oil. The oil was purified by preparative HPLC to obtain compound BQ (11 mg) as a colorless oil. 1H NMR (CD3OD): δ 7.30 (m, 3H), 7.11 (d, J= 8.8 Hz, 2H), 6.82 (d, J= 8.8 Hz, 2H), 4.13 (m, 5H), 3.85 (m, 3H), 3.81 (m, IH), 3.40 (m, 4H), 3.30 (m, IH), 0.52 (m, 4H); MS ESI (m/z) 465 (M+H)+, calc. 464.

Example 33

The synthesis of complex DM within the invention is outlined in FIG. 30, with the details given below.

Preparation of 2-cyclopropoxyethanol (Intermediate BO)

Figure US08802637-20140812-C00109

To a suspension of Mg powder (86.7 g, 3.6 mol) and I2 (catalytic) in anhydrous THF (0.7 L) was added slowly 1,2-dibromoethane (460 g, 2.4 mol) in anhydrous THF (2 L) at a rate that maintained the reaction temperature between 40-55° C. A solution of 2-(2-bromoethyl)-1,3-dioxolane (100 g, 0.56 mol) in anhydrous THF (750 mL) was added dropwise, and the reaction mixture was kept at 40-55° C. for 16 h. The reaction was quenched by addition of an aqueous solution of ammonium chloride. The mixture was extracted with methylene chloride. The organic layer was dried over sodium sulfate, and concentrated to give intermediate BO (27 g) as yellow oil, which was used in the next step without further purification.

Preparation of 2-cyclopropoxyethyl 4-methylbenzenesulfonate (Intermediate BP)

Figure US08802637-20140812-C00110

To a stirred solution of sodium hydroxide (32 g, 0.8 mol) in water (180 mL) and THF (180 mL) was added crude 2-cyclopropoxyethanol from the previous step (27 g, 0.26 mol) at −5 to 0° C. A solution of p-toluenesulfonyl chloride (52 g, 0.27 mol) in THF (360 mL) was added dropwise, and the reaction mixture was kept at −5 to 0° C. for 16 h. The reaction mixture was then incubated at room temperature for 30 min, the organic layer was separated and the aqueous layer was extracted with ethyl acetate (2×1.0 L). The combined organic layers were washed with brine, dried over Na2SO4 and concentrated to get the crude intermediate BP as a yellow oil (53.3 g), which was used for the preparation of intermediate DK below without further purification.

Preparation of 4-(5-bromo-2-chlorobenzyl)phenol (Intermediate H)

Figure US08802637-20140812-C00111

To a stirred solution of 4-bromo-1-chloro-2-(4-ethoxybenzyl)benzene (intermediate B) (747 g, 2.31 mol) in dichloromethane was added slowly boron tribromide (1.15 kg, 4.62 mol) at −78° C. The reaction mixture was allowed to warm to room temperature. When the reaction was complete as measured by TLC, the reaction was quenched with water. The mixture was extracted with dichloromethane. The organic layer was washed with an aqueous solution of saturated sodium bicarbonate, then with water, and then with brine, and dried over Na2SO4. The residue was concentrated and then recrystallized in petroleum ether to obtain intermediate H as a white solid (460 g, yield 68%). 1H NMR (CDCl3, 400 MHz): δ 7.23˜7.29 (m, 3H), 7.08 (d, J=8.8 Hz, 2H), 6.79 (d, J=8.8 Hz, 2H), 5.01 (s, 1H), 4.00 (s, 2H).

Preparation of 4-bromo-1-chloro-2-(4-(2-cyclopropoxyethoxy)benzyl)benzene (Intermediate DK)

Figure US08802637-20140812-C00112

A mixture of 4-(5-bromo-2-chlorobenzyl)phenol (56.7 g, 210 mmol) and Cs2CO3 (135 g, 420 mmol) in DMF (350 mL) was stirred at room temperature for 30 min, and then 2-cyclopropoxyethyl 4-methylbenzenesulfonate (crude intermediate BP from the second preceeding step above) (53.3 g, 210 mmol) was added. The reaction mixture was stirred at room temperature overnight, and then diluted with water (3 L) and extracted with EtOAc. The organic layer was washed with water, then with brine, and dried over Na2SO4. The residue was concentrated and then purified by flash column chromatography on silica gel (eluent PE:EA=10:1) to give intermediate DK as a liquid (51 g, yield 64%). 1H NMR (CDCl3, 400 MHz): δ 7.22˜7.29 (m, 3H), 7.08 (d, J=8.8 Hz, 2H), 6.88 (d, J=8.8 Hz, 2H), 4.10 (t, J=4.8 Hz, 2H), 3.86 (t, J=4.8 Hz, 2H), 3.38-3.32 (m, 1H), 0.62-0.66 (m, 2H), 0.49-0.52 (m, 2H).

Preparation of (2S,3R,4S,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)-2-methoxytetrahydro-2H-pyran-3,4,5-triol (Intermediate DL)

Figure US08802637-20140812-C00113

To a stirred solution of 4-bromo-1-chloro-2-(4-(2-cyclopropoxyethoxy)benzyl)benzene (213 g) in anhydrous THF/toluene (1:2 v/v, 1.7 L) under argon was added n-BuLi (2.5 M in hexane, 245.9 mL) dropwise at −60±5° C. The mixture was stirred for 30 min, and then transferred to a stirred solution of (3R,4S,5R,6R)-3,4,5-tris(trimethylsilyloxy)-6-((trimethylsilyloxy)methyl)tetrahydro-2H-pyran-2-one (310.5 g) in toluene (1.6 L) at −60±5° C. The reaction mixture was continuously stirred at −60±5° C. for 1 before quenching with an aqueous solution of saturated ammonium chloride (1.5 L). The mixture was allowed to warm to room temperature and stirred for 1 h. The organic layer was separated and the water layer was extracted with ethyl acetate (3×500 mL). The combined organic layers were washed with brine (1 L), dried over Na2SO4, and concentrated. The residue was dissolved in methanol (450 mL), and methanesulfonic acid (9.2 mL) was added at 0° C. The solution was allowed to warm to room temperature and stirred for 2.0 h. The reaction was quenched with an aqueous solution of sodium bicarbonate (50 g) in water (500 mL) and then additional water (900 mL) was added. The mixture was extracted with ethyl acetate (3×1.0 L). The combined organic layers were washed with brine, dried over Na2SO4, and concentrated. The crude product was used in the next step without further purification.

Preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol, bis(L-proline) complex (Complex DM)

Figure US08802637-20140812-C00114

To a stirred solution of crude (2S,3R,4S,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)-2-methoxytetrahydro-2H-pyran-3,4,5-triol from the previous step in CH2Cl2/CH3CN (1:1, 1.3 L) at −5° C. was added triethylsilane (28.2 mL, 563 mmol), followed by BF3.Et2O (52.3 mL, 418.9 mmol). The reaction was stirred for 16 h while the temperature was allowed to warm gradually to room temperature. The reaction was quenched by addition of an aqueous solution of saturated sodium bicarbonate to pH 8.0. The organic volatiles were removed under vacuum. The residue was partitioned between ethyl acetate (2.25 L) and water (2.25 L). The organic layer was separated, washed with brine, dried over Na2SO4 and concentrated to give the crude product (230 g, purity 82.3%). To the crude product was added L-proline (113.7 g) in EtOH/H2O (15:1 v/v, 2.09 L), and the mixture was stirred at 80° C. for 1 h until it became a clear solution. Hexane (3.0 L) was added dropwise over 50 min, while the temperature was maintained at about 60° C. The reaction mixture was stirred overnight at room temperature. The solid was filtered and washed with EtOH/H2O (15:1 v/v, 2×300 mL), hexane (2×900 mL), and dried at 45° C. under vacuum for 10 h to give pure complex DM as a white solid (209 g; HPLC purity 99.2% (UV)). 1H NMR (CD3OD, 400 MHz): δ 7.25˜7.34 (m, 3H), 7.11 (d, J=8.8 Hz, 2H), 6.84 (d, J=8.8 Hz, 2H), 4.03-4.11 (m, 5H), 3.96-4.00 (m, 2H), 3.83-3.90 (m, 3H), 3.68-3.72 (m, 1H), 3.36-3.46 (m, 6H), 3.21-3.30 (m, 3H), 2.26-2.34 (m, 2H), 2.08-2.17 (m, 2H), 1.94-2.02 (m, 4H), 0.56-0.57 (m, 2H), 0.52-0.53 (m, 2H).

Crystalline complex DM was analyzed by X-ray powder diffraction using CuKα1 radiation. The diffraction pattern is shown inFIG. 31 and summarized in Table 1 (only peaks up to 30° in 2θ are listed). The melting point of complex DM was determined by differential scanning calorimetry (DSC) as 151±1° C. (evaluated as onset-temperature; heating from 50° C. to 200° C. at 10° C./min). The DSC spectrum is shown in FIG. 32.

Preparation of (3R,4R,5S,6R)-2-(4-chloro-3-(4-hydroxybenzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (Intermediate D)

Figure US08802637-20140812-C00007

To a stirred solution of (3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (Intermediate C) (2 g, 5.9 mmol) in dichloromethane was added BBr3 (14.6 mL, 1 M) dropwise at −78° C. After the addition was complete, the mixture was allowed to warm to 0° C. and held at this temperature for 2 h. When LC-MS showed that no starting material remained, the mixture was cooled to −78° C. again, and quenched with water. When the temperature was stable, saturated NaHCO3 solution was added. The mixture was evaporated under reduced pressure, and the residue was extracted with EtOAc. The organic layer was washed with NaHCO3 and brine, dried over Na2SO4, evaporated and purified to obtain intermediate D (0.7 g).

In addition, for use in the synthesis of certain compounds of the invention, the 2S isomer (intermediate D1) and the 2R isomer (intermediate D2) of intermediate D were separated by preparative LC-MS. Intermediate D1: 1H NMR (CD3OD): δ 7.30 (m, 3H), 6.97 (d, 2H, J=6.8 Hz), 6.68 (d, 2H, J=6.8 Hz), 4.56 (s, 1H), 4.16 (s, 1H), 3.91˜4.02 (m, 5H), 3.79 (m, 1H), 3.64 (m, 1H). Intermediate D2: 1H NMR (CD3OD): δ 7.29˜7.33 (m, 3H), 7.00 (d, 2H, J=6.8 Hz), 6.70 (d, 2H, J=6.8 Hz), 4.58 (d, 1H, J=4.0 Hz), 3.96˜4.02 (m, 4H), 3.93˜3.95 (m, 1H), 3.81˜3.85 (m, 1H), 3.64˜3.69 (m, 1H).

PATENT

http://www.google.com/patents/US20130267694

Example 14 Preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol crystals

This example describes preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol by crystallization of ((2S,3R,4R,5S,6R)-2-(4-chloro-3-(442-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol bis(L-proline) complex in methanol/water solvent mixture.

Figure US20130267694A1-20131010-C00066

(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (1.3 kg) was added to a propylene drum (25 L) and methanol (3.6 kg) and water (1.3 kg) and the mixture was stirred until the solids dissolved. The solution was filtered through filter membrane (Millipore, 0.45 μm) into a clean glass reactor (50 L). The mixture was refluxed for 30 min and water (7.2 kg) was added over 1.0 h while maintaining the temperature between 50 and 65° C. The mixture was slowly cooled to ˜42° C. over 2 h. A suspension of seed crystal (26 g) in cold (−5° C.) mixture of methanol/water (78 mL, 2.8/6.5 (w/w)) and the slow cooling was continued to −5° C. over 12 h. The suspension was stirred for another 5 h and was filtered. The solid was slurried with cold water and filtered (0 to 5° C., 3×2.6 kg). The filter cake was dried under reduced pressure for 24 h until the loss on drying was no more than 0.5% to give a white solid (825 g, 92% yield, 99.3% pure by \HPLC-0001).

Example 15 Preparation of 4-(2-Chloro-5-Iodobenzyl)Phenol

This example describes preparation of 4-(2-chloro-5-iodobenzyl)phenol using gaseous hydrobromic acid.

Figure US20130267694A1-20131010-C00067

Preparation of (2-chloro-5-iodophenyl)methan-1-ol

Figure US20130267694A1-20131010-C00068

A 250 mL of 4-necked flask equipped with thermometer and mechanical stirring was charged with NaBH4 (4.16 g, 0.11 mol) and THF (60 mL) under argon. After cooling to 0˜5° C. with stirring, a solution of iodine in THF (12.7 g I2 in 25 mL THF) was added slowly dropwise over 30 min and the reaction temperature was maintained below 10° C. After the addition was completed, a solution of 2-chloro-5-iodobenzoic acid (15.0 g, 50 mmol) in THF (20 mL) was added dropwise over 30 min and kept the reaction temperature below 10° C. After stirring for another 3 h at 20˜25° C., the reaction mixture was heated to reflux for additional 16 h and monitored by TLC (PE/EA=1:1, Rf=0.2). The mixture was cooled to 20˜25° C. and poured into ice water (100 mL), extracted with ethyl acetate (2×100 mL), washed with water (2×100 mL), brine (100 mL), concentrated and the residue was purified by flash chromatography (PE:EA=20:1 as eluant, 200 mL) to give an off-white solid. Yield: 10.0 g (70%) MS ESI (m/z): 269 [M+1]+.

Preparation of 4-(2-Chloro-5-Iodobenzyl)Phenol

Figure US20130267694A1-20131010-C00069

A 100 mL of 4-necked flask equipped with thermometer and mechanical stirrer was charged with (2-chloro-5-iodophenyl)methanol (268.5 mg, 1 mmol), anhydrous ZnCl2 (136.3 mg, 1 mmol), dichloromethane (5.0 mL) and n-hexane (29 mL) under argon. After stirring for 10 min at 20 to 25° C., HBr (gas) was bubbled into the mixture for 10 min and a solution of phenol (197.6 mg, 2.1 mmol) in dry dichloromethane (3.0 mL) was added dropwise over 30 min. After bubbling HBr for additional 2 h, the mixture was refluxed for 3 days. The conversion was about 65%. The mixture was quenched with ice water (50 mL), extracted with ethyl acetate (2×30 mL), washed with water (2×30 mL), brine (30 mL), concentrated and the residue was purified by flash chromatography (PE:EA=25:1 as eluant, 200 mL) to give an off-white solid. Yield: 180 mg (52%). 1H NMR (CDCl3, 400 MHz): δ 7.44 (d, J=8.4 Hz, 2H), 7.03˜7.09 (m, 3H), 6.77 (d, J=8.4 Hz, 2H), 4.76 (s, 1H), 3.95 (s, 2H), 3.82 (s, 2H). MS ESI (m/z): 345 [M+1]+. 13C NMR (CDCl3, 100 MHz): δ 154.1, 141.4, 139.5, 136.6, 134.2, 131.2, 130.9, 130.1, 115.5, 91.67, 38.07.

Example 16 Preparation of 2-(4-(2-Cyclopropoxyethoxy)Benzyl)-1-Chloro-4-Iodobenzene

This example describes the preparation of 2-(4-(2-cyclopropoxyethoxy)benzyl)-1-chloro-4-iodobenzene via coupling of the 4-(2-chloro-5-iodobenzyl)phenol with 2-cyclopropoxyethyl 4-methylbenzenesulfonate.

Figure US20130267694A1-20131010-C00070

Under nitrogen a 500 L glass-lined reactor was charged with acetone (123 kg) with stirring (120 RPM), 4-(2-chloro-5-iodobenzyl)phenol (19.37 kg, 0.056 kmol), 2-cyclopropoxyethyl 4-methylbenzenesulfonate (15.85 kg, 0.062 kmol), cesium carbonate (18.31 kg, 0.0562 kmol) powder, potassium carbonate (23.3 kg, 0.169 kmol) powder and TBAI (4.15 kg, 0.011 kmol). After stirring for 4045 h at 40° C., TLC (PE:EA=4:1, Rf=0.3) showed that starting material was consumed. The mixture was cooled to 20˜25° C.

The reaction mixture was filtered over diatomite (28 kg) and the filter cake was washed with acetone (2×31 kg). The combined filtrates were transferred to a 500 L glass-lined reactor and concentrated. The residue was dissolved in ethyl acetate (175 kg, washed with water (2×97 kg) and concentrated until the volume was about 100 L and was transferred to a 200 L glass-lined reactor and continued to concentrate to get about 22.5 kg of crude material.

The crude material was dissolved in methanol/n-hexane (10:1, 110 kg) under refluxing for 30 min with stirring (100 RPM) until it was a clear solution. The mixture was cooled to 5 to 10° C. and some crystal seeds (20 g) were added. The suspension was stirred for another 5 h at 5 to 10° C. The mixture was filtered at 0 to 5° C. and the filter cake was washed with pre-cooled methanol/n-hexane (10:1, 5° C., 2×11 kg). The filter cake was dried under at 15 to 20° C. for 15 h to give off-white to white solid. Yield: 18.1 kg, 75%. Melting Point: 31° C. (DSC onset). 1H NMR (CDCl3, 400 MHz): δ 7.45˜7.50 (m, 2H), 7.09˜7.12 (m, 3H), 6.88 (d, J=8.8 Hz, 2H), 4.11 (t, J=5.2 Hz, 2H), 3.99 (s, 2H), 3.88 (t, J=5.2 Hz, 2H), 3.40˜3.44 (m, 1H), 0.63˜0.67 (m, 2H), 0.49˜0.54 (m, 1H). MS ESI (m/z): 429 [M+1]+. 13C NMR (CDCl3, 100 MHz): δ 157.5, 141.5, 139.5, 136.6, 134.2, 131.2, 130.8, 129.9, 114.9, 91.66, 69.00, 67.13, 53.72, 38.08, 5.63.

Example 9 Preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol, bis(L-proline) complex

This example describes preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol, bis(L-proline) complex by co-crystallization of ((2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol with L-proline in ethanol/water/n-heptane solvent mixture.

Figure US20130267694A1-20131010-C00062

The crude (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol (2.5 kg) was added to a glass reactor containing ethanol (95%, 16 kg) and L-proline (1.24 kg) and the mixture was refluxed for 1 h. While keeping the temperature above 60° C., n-heptane (8.5 kg) was added over 40 min. The mixture was slowly cooled to 25 to 20° C. and stirred at this temperature for 10 h. The mixture was filtered and the solids were washed with cold (−5° C.) ethanol (95%, 2×2.5 L) and n-heptane (2×5 L) and the solids were dried under reduced pressure at 55 to 65° C. for 20 h to give a white solid (3.03 kg, 81% yield, 99.4% pure by HPLC-0001).

Example 7 Preparation of ((2S,3R,4R,5S,6R)-2-(4-Chloro-3-(4-(2-Cyclopropoxyethoxy)Benzyl)Phenyl)-6-(Hydroxymethyl)Tetrahydro-2H-Pyran-3,4,5-triol

This example describes preparation of (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol by removal of the anomeric OH or OMe.

Figure US20130267694A1-20131010-C00061

(2S,3R,4S,5S,6R)-2-(4-Chloro-3-(4-(2-Cyclopropoxyethoxy)Benzyl)Phenyl)-6-(Hydroxymethyl)-2-Methoxytetrahydro-2H-Pyran-3,4,5-Triol Solution

A 30 L glass reactor equipped with a thermometer was charged with crude (2S,3R,4S,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)-2-methoxytetrahydro-2H-pyran-3,4,5-triol (1.15 kg), DCM (2.3 kg) and acetonitrile (1.4 kg), and the mixture was magnetically stirred until all the solids dissolved under nitrogen sparging. The solution was cooled to ˜−15° C.

Triethylsilane Solution:

BF3.Et2O (1.2 kg) was added to a cold (−20 to −15° C.) solution of triethysilane (1.08 kg) dichloromethane (2.3 kg) and acetonitrile (1.4 kg) with nitrogen sparging.

The cold (2S,3R,4S,5S,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy)benzyl)phenyl)-6-(hydroxymethyl)-2-methoxytetrahydro-2H-pyran-3,4,5-triol solution was added to the cold triethylsilane solution at such a rate to maintain the temperature between −20 and −15° C. (˜2 to 3 h).

The reaction mixture was stirred for another 2 to 3 h and then quenched by addition of an aqueous solution of sodium bicarbonate (7.4% w/w, 7.8 kg) and the reaction mixture was stirred for about 15 min. The solvents were removed under reduced pressure (2 h, temperature below 40° C.). The residue was partitioned between ethyl acetate (6.9 kg) and water (3.9 kg). The layers were separated and the aqueous layer was extracted with ethyl acetate (2×3.5 kg). The combined organic layers were washed with brine (2×3.8 kg) and the solvents were removed under reduced pressure. Anhydrous ethanol (2.3 kg) was added and concentrated to give the crude product of the title compound (1 kg, 90% yield, 90% HPLC-0001) as yellow solid.

PATENT

WO 2011153953

https://www.google.com/patents/WO2011153953A1?cl=en

Example 1. Preparation of (2S.iR. R.5S.6R)-2-(4-chloro-3-(4-(2-cvclopropoxyethoxy) benzyl)phenyl)-6-(hvdroxymethyl)tetrahvdro-2H-pyran-3,4,5-triol, bis(X-proline) complex

Figure imgf000032_0001
Figure imgf000032_0002

Example 1A

Preparation of 2-cyclopropoxyethanol (1)

Figure imgf000032_0003

To a suspension of Mg powder (86.7 g, 3.6 mol) and iodine (cat) in anhydrous THF (0.7 L) was added slowly 1,2-dibromoethane (460 g, 2.4 mol) in anhydrous THF (2 L) slowly at a rate as to keep the internal temperature between 40-55 °C. After the addition, a solution of 2-(2-bromoethyl)-l,3-dioxolane (lOOg, 0.56 mol) in anhydrous THF (750 mL) was added dropwise. The reaction mixture was kept at 40-55 °C for 16h and was quenched by addition of aqueous solution of ammonium chloride. The mixture was extracted with methylene chloride. The organic layer was dried over sodium sulfate, and concentrated to give the title product (27 g) as yellow oil, which was directly used without further purification.

Example IB

Preparation of 2-cyclopropoxyethyl 4-methylbenzenesulfonate (2)

Figure imgf000033_0001

To a stirred solution of sodium hydroxide (32 g, 0.8 mol) in water (180 mL) and THF (180 mL) was added Example 1A (27 g, 0.26 mol) at -5 to 0 °C. Afterwards, a solution of ji?-toluenesulfonyl chloride (52 g, 0.27 mol) in THF (360 mL) was added dropwise. The reaction mixture was kept at -5 to 0 °C for 16 h. The reaction mixture was then kept at room temperature for 30 min. The organic layer was separated and the aqueous layer was extracted with ethyl acetate (2×1.0 L). The combined organic layers were washed with brine, dried over Na2S04 and concentrated to get the crude product as yellow oil (53.3 g). It was used directly without further purification.

Example 1C

Preparation of 4-(5-bromo-2-chlorobenzyl)phenol (3)

Figure imgf000033_0002

To a stirred solution of 4-bromo-l-chloro-2-(4-ethoxybenzyl)benzene (747 g, 2.31 mol) in dichloromethane was added boron tribromide (1.15 kg, 4.62 mol) slowly at -78 °C. The reaction mixture was allowed to rise to room temperature. When the reaction was complete as measure by TLC, the reaction was quenched with water. The mixture was extracted with dichloromethane. The organic layer was washed with aqueous solution of saturated sodium bicarbonate, water, brine, dried over Na2S04, and concentrated. The residue was recrystallized in petroleum ether to give the title compound as a white solid (460 g, yield 68%). 1H NMR (CDC13, 400MHz): δ 7.23-7.29 (m, 3H), 7.08 (d, J=8.8 Hz, 2H), 6.79 (d, J=8.8 Hz, 2H), 5.01 (s, 1H), 4.00 (s, 2H).

Example ID

Preparation of 4-bro -l-chloro-2-(4-(2-cyclopropoxyethoxy)benzyl)benzene (4)

Figure imgf000034_0001

A mixture of Example 1C (56.7 g, 210 mmol) and Cs2C03 (135 g, 420 mmol) in DMF (350 mL) was stirred at room temperature for 0.5 h. Example IB (53.3 g, 210 mmol) was added. The reaction mixture was stirred at room temperature overnight. It was diluted with water (3 L) and extracted with EtOAc. The organic layer was washed with water, brine, dried over Na2S04, and concentrated. The residue was purified by flash column

chromatography on silica gel eluting with petroleum ether:ethyl acetate (10:1) to give the title compound as liquid (51 g, yield 64%). 1H NMR (CDC13, 400MHz): δ 7.22-7.29 (m, 3H), 7.08 (d, J=8.8 Hz, 2H), 6.88 (d, J=8.8 Hz, 2H), 4.10 (t, J=4.8 Hz, 2H), 3.86 (t, J=4.8 Hz, 2H), 3.38-3.32 (m, 1H), 0.62-0.66 (m, 2H), 0.49-0.52(m, 2H).

Example IE

Preparation of (25,5R, S,55,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy) benzyl)phenyl)-6-(hydroxymethyl)-2-metlioxytetraliydro-2H-pyran-3,4,5-triol (5)

Figure imgf000034_0002

To a stirred solution of Example ID (213 g) in anhydrous THF/toluene (1 :2 (v/v), 1.7 L) under argon was added n-BuLi (2.5 M hexane, 245.9 mL) drop wise at -60 ± 5 °C. The mixture was stirred for 30 min. before transferred to a stirred solution of 2,3,4,6-tetra-O- trimethylsilyl-P-Z -glucolactone (310.5 g) in toluene (1.6 L) at -60 ± 5 °C. The reaction mixture was continuously stirred at -60 ± 5 °C for 1 h before quenching with aqueous solution of saturated ammonium chloride (1.5 L). Then mixture was allowed to warm to room temperature and stirred for 1 h. The organic layer was separated and the water layer was extracted with ethyl acetate (3×500 niL). The combined organic layers were washed with brine (1 L), dried over Na2S04, and concentrated. The residue was dissolved in methanol (450 mL) and methanesulfonic acid (9.2 mL) was added at 0 °C. The solution was allowed to warm to room temperature and stirred for 20 h. It was quenched with aqueous solution of sodium bicarbonate (50 g) in water (500 mL) and additional water (900 mL) was added. The mixture was extracted with ethyl acetate (3×1.0 L). The combined organic layers were washed with brine, dried over Na2S04, concentrated and used directly in the next step without further purification.

Example IF

Preparation of (25,5R, R,55,6R)-2-(4-chloro-3-(4-(2-cyclopropoxyethoxy) benzyl)phenyl)-6- (hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol, bis(Z-proline) complex (7)

Figure imgf000035_0001

To stirred solution of Example IE in CH2C12/CH3CN (650 mL:650 mL) at -5 °C was added triethylsilane (28.2 mL, 563 mmol), and followed by BF3-Et20 (52.3 mL, 418.9 mmol). The reaction was stirred for 16 h while the temperature was allowed to warm to room temperature gradually. The reaction was quenched with aqueous solution of saturated sodium bicarbonate to pH 8.0. The organic volatiles were removed under vacuum. The residue was partitioned between ethyl acetate (2.25 L) and water (2.25 L). The organic layer was separated, washed with brine, dried over Na2S04 and concentrated to give the crude product 6 (230 g, purity 82.3%). This product and L-proline (113.7 g) in EtOH/H20 (15:1 v/v, 2.09 L) was stirred at 80 °C for 1 h when it became a clear solution. Hexane (3.0 L) was added dropwise into the above hot solution over 50 min, with the temperature being kept at about 60 °C. The reaction mixture was stirred overnight at room temperature. The solid was filtered and washed with EtOH/ H20 (15:1 (v/v), 2×300 mL), hexane (2×900 mL), and dried at 45 °C under vacuum for 10 h to give the pure title compound 7 as a white solid (209 g).

Purity (HPLC) 99.2% (UV). 1H NMR (CD3OD, 400 MHz): δ 7.25—7.34 (m, 3H), 7.11 (d, J = 8.8 Hz, 2H), 6.84 (d, J= 8.8 Hz, 2H), 4.03-4.11 (m, 5H), 3.96-4.00 (m, 2H), 3.83-3.90 (m, 3H), 3.68-3.72 (m, 1H), 3.36-3.46 (m, 6H), 3.21-3.30 (m, 3H), 2.26-2.34 (m, 2H), 2.08-2.17 (m, 2H), 1.94-2.02 (m, 4H), 0.56-0.57 (m, 2H), 0.52-0.53(m, 2H).

Example 2. Direct Preparation of Crystalline Compound 8 from Complex 7

This example illustrates the preparation of a crystalline form of (2S, 3R, 4R, 5S, 6R)-2- (4-chloro-3-(4-(2-cyclopropoxyethoxy) benzyl)phenyl)-6- (hydroxymethyl)tetrahydro-2H- pyran-3,4,5-triol.

Figure imgf000036_0001

To a 5.0 L 4-necked flask equipped with a mechanical stirrer was added the starting co-crystal (150.0 g) and methanol (300 mL). The mixture was stirred at room temperature with mechanical stirring (anchor agitator, 2-blades 9 cm) until a cloudy solution/suspension formed, to which distilled water (1500 mL) was added dropwise at a rate of -12.5 mL/min. As the mixture warmed from the exotherm of adding water to methanol, the mixture became clear after adding about 1/5 to 1/3 of the water. After the addition was completed the reaction was stirred continuously at 80 rpm for another 5 h. The reaction mixture was filtered over medium-speed filter paper and the filter cake was washed with distilled water (450 mL and then 300 mL) and dried under vacuum using an oil pump (~6 mm Hg) at 45 °C for 48 hours to give the target product as a white crystalline solid (94.2 g, 93.9% yield, purity (HPLC): 99.3%).

Example 5. Indirect Preparation of Crystalline Compound 8 from Complex 7

Figure imgf000038_0001

[0113] To a 200 L glass lined reactor equipped with a double-tier paddle agitator and a glass condenser was added sequentially complex 7 (7.33 kg), ethyl acetate (67.5 kg) and pure water (74.0 kg). The mixture was heated to reflux and stirred at reflux for 30 min. The reaction mixture was cooled to approximately 50 °C and the organic layer was separated and the aqueous layer was extracted with ethyl acetate (34.0 kg). The combined organic layers were washed with pure water (3×74.0 kg) (IPC test showed that the IPC criteria for L-proline residue was met after three water washes). The mixture was concentrated at 40 °C under vacuum (-15 mmHg) for 3 h until the liquid level dropped below the lower-tier agitator paddle. The mixture (18 kg) was discharged and transferred to a 20L rotary evaporator. The mixture was concentrated under vacuum (40 °C, ~5 mmHg) to a minimum volume. The remaining trace amount of ethyl acetate was removed azeotropically at 40 °C under vacuum with methanol (10 kg). The residue was dried under vacuum of an oil pump (~6 mmHg) at 40 °C for 10 h to give 8 as a white amorphous solid (4.67 kg, purity (HPLC): 99.2%) which was used in the next step without further purification.

The recrystallization was accomplished by the following steps. To a 100 L glass line reactor equipped with a double-tier paddle agitator and a glass condenser was added the above amorphous 8 (4.67 kg) and methanol (18.0 kg). The mixture was refluxed at 70 °C for 30 min until a clear solution formed, to which pure water (45.0 kg) was added over 2 hours. After the addition was completed (the reaction temperature was 41 °C), the reaction mixture was cooled to room temperature and stirred at room temperature for 15 hours. The reaction mixture was filtered and the wet cake was washed with pure water (2×15 kg) and dried under vacuum at 55-60 °C for 12 hours to give the target product as an off-white crystalline solid (3.93 kg, yield: 84% in two steps; purity (HPLC): 99.7%).

Example 6. Direct Preparation of Crystalline Compound 8 from Amorphous 8

Figure imgf000039_0001

A 5 L 4-neck flask was charged with 8 (amorphous), 116 g, and methanol (580 mL). The reaction mixture was heated to 60 C with mechanical stirring and the solution became clear. Water (2320 mL) was added dropwise to the reaction solution at 40 mL/min at 50 °C. The reaction mixture was stirred overnight at room temperature. The reaction mixture was filtered and the filter cake was washed with water (2×200 mL), dried under vacuum at 55 °C for 12 hours, to afford white crystalline 8. Yield is 112.8 g (97.2%).

References:
1. Clinical Trial, A Dose Range Finding Study to Evaluate the Effect of Bexagliflozin Tablets in Subjects With Type 2 Diabetes Mellitus. NCT02390050 (retrieved on 26-03-2015).

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////////BEXAGLIFLOZIN, APPROVALS 2023, FDA 2023

c1cc(ccc1Cc2cc(ccc2Cl)[C@H]3[C@@H]([C@H]([C@@H]([C@H](O3)CO)O)O)O)OCCOC4CC4

SYN

https://doi.org/10.1021/acs.jmedchem.4c02079J.Med.Chem.2025,68,2147−2182

Bexagliflozin (Brenzavvy). Bexagliflozin (3) was discoveredanddevelopedbyTheracosBioforthetreatmentof
type2diabetesmellitus.28Bexagliflozinisasodium-dependent glucose cotransporter 2 (SGLT2) inhibitor. Inhibition of SGLT2 reduces blood sugar without stimulating insulin release.29 Bexagliflozin shows >2000-fold selectivity forSGLT2 over SGLT1 and demonstrated improvement inglycemiccontrolwithaoncedaily,20mgdose.28Since 2011, there have been 11 therapeutics targeting
SGLT2.30Thesedrugsexhibit commonstructural features(abiarylmethaneandglycoside)andlikelyfacesimilarsynthetic challenges.31 The medicinal chemistry efforts to identifybexagliflozinweredisclosedintheprimaryliterature.32Apatent fromTheracos, Inc. in2013describedasyntheticapproachto bexagliflozinonmultikilogramscale.33Slightvariations inthe
reactionconditions,yieldandisolationstrategyofintermediates wereincludedinthepatent.Theimplementationoftelescoping intheprocessislikelyduetopoorcrystallinityofintermediates,
whichmaybeacommonchallengetootherSGLT2inhibitors.31
Anotherpatent disclosedbyPiramal Enterprises suggesteda
similarbondformationstrategybut includedanacetylationof bexagliflozinprior tothefinal isolation inorder toprovidea crystallinesolid.34
Bexagliflozinwas assembled by cryogenicmetal halogen exchangeof aryl iodide3.1with turboGrignard(i-PrMgCl·LiCl)andsubsequentadditiontoprotectedgluconolactone3.2
whichwaspreparedbytreatmentofD-(+)-glucono-1,4-lactonewithTMSClandNMMinTHFin94%yield(Scheme4).WhentheGrignardadditionwascomplete,thereactionwasquenchedand a solution of the product inEtOAcwas treatedwith
activated carbon, filtered, concentrated, and diluted with methanol.ThissolutionwastreatedwithconcentratedHCl to remove thesilyl protectinggroupsandprovidecrudemethyl ketal3.3inyields rangingfrom79to95%.Themethyl ketal
functionalitywasreducedusingtriethylsilaneandBF3·Et2Oin DCMandMeCNatcryogenictemperaturestoprovidecrude bexagliflozin (3) as a solid after concentrating the reaction mixture. Alternatively, a larger-scale demonstration of this processinthepatenttelescopedasolutionofcrudebexagliflozin toformabis-L-prolinecomplexinethanol,water,andheptane,
whichwasisolatedasacrystallinesolidin81%yield.Thiswas convertedto the free formin82%yieldbycrystallization in methanolandwater.Arecrystallizationofbexagliflozin(3)was
reported in 92% yield. Details on stereoselectivity of this
approachwerenotdisclosed.
Amilligram-togram-scaleconstructionofthearyliodide3.1 wasalsodisclosedintheTheracospatent from2013(Scheme 5).33First,carboxylicacid3.5wasreducedtoprimaryalcohol
3.6using sodiumborohydride and iodine. Next, the diaryl methanecorewas assembledbyFriedel−Crafts alkylationof phenol with3.6 after activationwithHBr andZnCl2. This reactionwasdemonstratedonmilligramscaleandachieved65% conversion, with 52% isolated yield after chromatographic purification.Analternativeapproachtoabromovariantofaryl iodide3.7waspresentedina2009patentfromTheracos,where Friedel−Craftsacylationprovidedtheanalogousbenzophenone intermediatewhichwas thensubsequentlyreduced.35Finally,alkylationofthephenolwasconductedusingthetosylatedether
3.8toprovidearyl iodide3.1in75%yieldonkilogramscale.A syntheticapproachtothetosylatedetherwasprovidedinthe earlyTheracospatent,35wherecyclopropylether formationin 3.10wasgeneratedviaGrignardformationandrearrangement of 2-(2-bromoethyl)-1,3-dioxolane 3.9 (Scheme 6). The primary alcohol 3.10was protectedas the tosylate3.8and employedinthealkylationstepwithoutpurification.Noyields wereprovided.

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453.
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glucose co-transporter-2 inhibitors for the treatment of diabetes
mellitus. Curr. Opin. Endocrinol. Diabetes Obes. 2017, 24, 73−79.
(30) Guo, Y.-Y.; Zhang, J.-Y.; Sun, J.-F.; Gao, H. A comprehensive
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(31) Aguillón, A. R.; Mascarello, A.; Segretti, N. D.; de Azevedo, H. F.
Z.; Guimaraes, C. R. W.; Miranda, L. S. M.; de Souza, R. O. M. A.
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(32) Xu, B.; Feng, Y.; Cheng, H.; Song, Y.; Lv, B.; Wu, Y.; Wang, C.;
Li, S.; Xu, M.; Du, J.; et al. C-aryl glucosides substituted at the 4′
position as potent and selective renal sodium-dependent glucose co
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.

European Journal of Medicinal Chemistry

Volume 265, 5 February 2024, 116124

https://doi.org/10.1016/j.ejmech.2024.116124

Bexagliflozin (Brenzavvy)
On January 20, 2023, the FDA granted approval to Bexagliflozin, a medication developed by Theracos Inc, for the treatment of type 2 diabetes mellitus (T2DM) [104–106]. The SGLT2 inhibitor Bexagliflozin
can increase energy expenditure, reduce fluid retention, and increase urinary glucose excretion by inhibiting SGLT2 in renal tubular epithelial cells [106]. SGLT2 inhibitors have significant advantages compared to other drugs: (1) they can lower both pre-meal and post-meal blood sugar levels (not all drugs can lower both); (2) they have a lower risk of hypoglycemia as they do not stimulate insulin secretion; (3) they have adiuretic effect due to their primary action on the renal tubules, which
lowers systolic blood pressure; (4) research has shown that SGLT2 in hibitors have therapeutic effects on diabetic kidney disease [107,108].
The process of synthesizing Bexagliflozin started by conducting theFriedel-Crafts acylation of ethoxybenzene (BEXA-002) with 5-bromo-2-chlorobenzoic acid (BEXA-001) (Scheme 29) [109]. This reaction produced ketone BEXA-003. Subsequently, the carbonyl reduction of BEXA-003 was carried out using trifluoromethanesulfonic acid (TfOH),triethylsilane, and TFA. This step yielded BEXA-004. Next, n-butyllithium (n-BuLi) and pyrone BEXA-005 were combined with BEXA-004 at78◦C. This reaction produced an intermediate, which was thenreacted with triethylsilane and BF◦3⋅Et2O at 0C. The final product obtained from this reaction was BEXA-006, which contained a sugar ring.
BEXA-006 underwent dealkylation upon treatment with boron tribromide, resulting in the formation of BEXA-007, which was a phenol.
Subsequently, BEXA-007 was alkylated using 2-cyclopropoxyethyl4-methylbenzenesulfonate (BEXA-008) to yield Bexagliflozin.

[104] S.M. Hoy, Bexagliflozin: first approval, Drugs 83 (2023) 447–453.
[105] W. Zhang, A. Welihinda, J. Mechanic, H. Ding, L. Zhu, Y. Lu, Z. Deng, Z. Sheng,
B. Lv, Y. Chen, J.Y. Roberge, B. Seed, Y.X. Wang, EGT1442, a potent and selectiveSGLT2 inhibitor, attenuates blood glucose and HbA(1c) levels in db/db mice and
prolongs the survival of stroke-prone rats, Pharmacol. Res. 63 (2011) 284–293.
[106] O. Azzam, R. Carnagarin, L.M. Lugo-Gavidia, J. Nolde, V.B. Matthews, M.
P. Schlaich, Bexagliflozin for type 2 diabetes: an overview of the data, Expet Opin.
Pharmacother. 22 (2021) 2095–2103.
[107] B.F. Palmer, D.J. Clegg, Kidney-protective effects of SGLT2 inhibitors, Clin. J. Am.
Soc. Nephrol. 18 (2023) 279–289.
[108] M. Singh, A. Kumar, Risks associated with SGLT2 inhibitors: an overview, Curr.
Drug Saf. 13 (2018) 84–91.
[109] Y. Song, Y. Chen, H. Cheng, S. Li, Y. Wu, Y. Feng, B. Lv, B. Xu, B. Seed, M.J. Hadd,
J. Du, C. Wang, J.Y. Roberge, Preparation of Benzylbenzene Glycoside Derivatives
as Antidiabetic Agents, 2009. WO2009026537A1.

.

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Chi-Med Says Fruquintinib Successful in Lung Cancer Trial


Fruquintinib

Phase 3…cancer

Hutchison Medipharma Enterprises Limited

Hutchison MediPharma for the treatment of locally advanced or metastatic colorectal cancer

 C21H19N3O5
Exact Mass: 393.1325

cas 1194506-26-7, 6 ((6,7-dimethoxyquinazolin-4-yl) oxy) – N, 2-dimethylbenzofuran-3-carboxamide,

3-​Benzofurancarboxamid​e, 6-​[(6,​7-​dimethoxy-​4-​quinazolinyl)​oxy]​-​N,​2-​dimethyl-

Synonym: Fruquintinib; HMPL-013; HMPL 013; HMPL013.

HPLC.http://www.medkoo.com/Product-Data/Fruquintinib/QC-Fruquintinib-CRB50706web.pdf

Fruquintinib, also known as HMPL-013, is an orally available, small molecule inhibitor of vascular endothelial growth factor receptors (VEGFRs), with potential anti-angiogenic and antineoplastic activities.

HMPL-013, a novel small molecule compound that selectively inhibits vascular endothelial growth factor receptor (VEGFR), is in phase III clinical studies at Hutchison MediPharma for the treatment of locally advanced or metastatic colorectal cancer. Phase II clinical trials are also ongoing for the treatment of non-squamous non-small cell lung cancer.

Early clinical development is under way at the company for the treatment of gastric cancer in combination with paclitaxel.

Fruquintinib’s mechanism of action is the inhibition of all three forms of VEGF receptors (VEGFR-1, 2, 3). Competitive advantages over currently marketed therapies are the compound’s unique kinase profile, a highly potent efficacy and excellent kinase selectivity, large safety margin, a broad spectrum antitumor activity and a low cost of goods.
Upon oral administration, fruquintinib inhibits VEGF-induced phosphorylation of VEGFRs 1, 2, and 3 which may result in the inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death. Expression of VEGFRs may be upregulated in a variety of tumor cell types.

In 2013, the company entered into a licensing, co-development, and commercialization agreement in China with Eli Lilly.

Angiogenesis is a physiological process of growing new blood vessels from pre-existing vessels. It takes place in a healthy subject to heal wounds, i.e., restoring blood flow to tissues after injury or insult.

Excessive angiogenesis may be triggered by certain pathological conditions such as cancer, age-related macular degeneration, and chronic inflammatory disease. As a result, new blood vessels feed diseased tissues and destroy normal tissues. In cancer, new blood vessels also allow tumor cells to escape into the circulation and lodge in other organs.

Vascular endothelial growth factor (VEGF), a homodimeric glycoprotein, and its receptors, e.g., kinase insert domain receptor (KDR), constitute an important angiogenic pathway. Studies have shown that inhibition of KDR resulted in endothelial cell apoptosis and, thus, suppression of angiogenesis. See Rubin M. Tuder, Chest, 2000; 117: 281. KDR inhibitors are therefore potential candidates for treating an angiogenesis-related disorder.

Chi-Med Says Fruquintinib Successful in Lung Cancer Trial

Written by Richard Daverman, PhD, Executive Editor, Greg B. Scott.

Hutchison MediPharma, a division of Chi-Med reported that fruquintinib met its primary endpoint in a second proof-of-concept China trial, this time as a treatment for advanced non-squamous non-small cell lung cancer. The company said fruquintinib “clearly” met its primary endpoint of  progression-free survival, though specific data are being held for a scientific meeting. In 2013, Hutchison out-licensed China rights for the drug to Lilly. In May, the first proof-of-concept trial triggered two payments from Lilly to HMP totaling $18 million. More details…. http://www.chinabiotoday.com/articles/20150904

………….

Patent

US 20090281130

https://www.google.com.ar/patents/US20090281130

EXAMPLE 1 Synthesis of 6-(6,7-dimethoxyquinazolin-4-yloxy)-N,2-dimethylbenzofuran-3-carboxamide:

Figure US20090281130A1-20091112-C00009

To a solution of 4-chloro-6,7-dimethoxyquinazoline (1 equiv.) in 2 ml CH3CN were added 6-hydroxy-N,2-dimethylbenzofuran-3-carboxamide (1 equiv.) and K2CO3 (1.5 equiv.). The mixture was refluxed under stirring for 10 hr. After the solvent was evaporated, the residue was washed with water, dried over MgSO4, filtered, concentrated, and purified by column chromatography to give the title compound in a yield of 85%.

1H NMR (DMSO-d6, 400 MHz) δ: 2.49 (s, 3H), 2.81 (d, J=8.4 Hz, 3H,10), 3.97 (s, 3H), 3.98 (s, 3H), 7.24 (dd, J=2.0, 8.4 Hz, 1H), 7.38 (s, 1H), 7.58 (s, 1H), 7.61 (d, J=2.0 Hz, 1H), 7.79 (d, J=8.4 Hz, 1H), 7.96 (m, 1H), 8.52 (s, 1H).

MS(m/e): 394.1 (M+1).

 

………………

WO 2009137797

https://www.google.com/patents/WO2009137797A2

……………….

CN 101575333

Example a: 6- (6,7-dimethoxy-quinazolin-4-oxo) -N, 2- dimethyl-benzofuran-3-carboxamide

[0048]

Figure CN101575333BD00111

[0049] 4-Chloro-6,7-dimethoxy-quinazoline (1 mmol) was dissolved in 2 ml of acetonitrile, followed by addition of 6-hydroxy -N, 2- dimethyl-benzofuran-3- amide (1 mmol) and potassium carbonate (1.5 mmol). The reaction mixture was heated at reflux for 10 hours, concentrated to dryness, washed with water, and purified to give the desired product, yield 85%.

[0050] 1H NMR (DMS0-d6,400MHz) δ ppm:. 2 49 (s, 3H); 2.81 (d, J = 8. 4Hz; 3H, 10); 3.97 (s; 3H); 3.98 (s, 3H);. 7 24 (dd, J = 2. 0,8 4Hz;. 1H);. 7 38 (s, lH);. 7 58 (s, lH); 7.61 (d, J = 2. OHz; 1H);. 7 79 (d, J = 8. 4Hz; 1H);. 7 96 (m, 1H);. 8 52 (s, 1H).

[0051] MS (m / e)::. 394 1 (M + l).

………..

 

EP1265874A2 * Jan 23, 2001 Dec 18, 2002 Gödecke Gmbh Method for the simplified production of (3-chloro-4-fluoro-phenyl)- 7-(3-morpholino-4-yl-propoxy)-6-nitro-quinazoline-4-yl]-amine or (3-chloro-4-fluoro-phenyl)- 7-(3-morpholino-4-yl-propoxy)-6-amino-quinazoline-4-yl]-amine
US20070208056 * Jan 23, 2007 Sep 6, 2007 Bristol-Myers Squibb Company Piperidinyl derivatives as modulators of chemokine receptor activity
US20080033000 * May 15, 2007 Feb 7, 2008 Senex Biotechnology, Inc. Identification of CDKI pathway inhibitors
2 See also references of EP2297115A2
Citing Patent Filing date Publication date Applicant Title
US8212033 * Sep 29, 2010 Jul 3, 2012 Hutchison Medipharma Enterprises Limited Use of substituted quinazoline compounds in treating angiogenesis-related diseases
US8497372 Jun 4, 2012 Jul 30, 2013 Hutchison Medipharma Enterprises Limited Use of substituted quinazoline compounds in treating age-related macular degeneration
US8575184 Sep 1, 2010 Nov 5, 2013 Bristol-Myers Squibb Company Quinazolines as potassium ion channel inhibitors

Hutchison Medipharma Enterprises Limited

 

Simon To, M.B.A.
Chairman

Simon To

Mr To has been a Director since 2000 and an Executive Director and Chairman since 2006. He is also Chairman of the Remuneration Committee and a member of the Technical Committee of the Company. He is managing director of Hutchison Whampoa (China) Limited (“Hutchison China”) and has been with Hutchison China for over thirty years, building its business from a small trading company to a billion dollar investment group. He has negotiated major transactions with multinationals such as Procter & Gamble, Lockheed, Pirelli, Beiersdorf, United Airlines and British Airways.

Mr To’s career in China spans more than thirty years and he is well known to many of the top Government leaders in China. Mr To is the original founder of Hutchison Whampoa Limited’s healthcare business and has been instrumental in the acquisitions made to date. He received a First Class Honours Bachelor’s Degree in Mechanical Engineering from Imperial College, London and an MBA from Stanford University’s Graduate School of Business.

Christian Hogg, M.B.A.
Chief Executive Officer, Hutchison China MediTech Limited and Director, Hutchison MediPharma Holdings Limited

Christian Hogg

Mr Hogg has been an Executive Director and Chief Executive Officer since 2006. He is also a member of the Technical Committee of the Company. He joined Hutchison Whampoa (China) Limited in 2000 and has since led all aspects of the creation, implementation and management of the Company’s strategy, business and listing. This includes the creation of the Company’s start-up businesses and the acquisition and operational integration of assets that led to the formation of the Company’s China joint ventures.

Prior to joining Hutchison China, Mr Hogg spent ten years with Procter & Gamble starting in the US in Finance and then Brand Management in the Laundry and Cleaning Products Division. Mr Hogg then moved to China to manage P&G’s detergent business followed by a move to Brussels to run P&G’s global bleach business. Mr Hogg received a Bachelor’s degree in Civil Engineering from the University of Edinburgh and an MBA from the University of Tennessee.

Weiguo Su, Ph.D.
Executive Vice President and Chief Scientific Officer

Weiguo Su

Dr. Su has headed all drug discovery and research since he joined, including creating our R&D strategy, the formation and growth of research platform, and the research and discovery of each and every small molecule drug candidate in the Company’s portfolio.

Prior to joining in 2005, Dr. Su spent 15 years with Pfizer’s US R&D organization. Dr. Su delivered several high quality new drug candidates during his time with Pfizer, most recently as a director in the Medicinal Chemistry Department.

He received his Ph.D. and post-doctoral fellowship in Chemistry from Harvard University under the guidance of Nobel Laureate Professor E. J. Corey, and his Bachelor’s degree in Chemistry from Fudan University in Shanghai, China.

Ba

R & D Center Address (A):
Building 4, 720 Cailun Road
Zhangjiang Hi-Tech Park
Pudong, Shanghai, China
Postal Code: 201203, China
Head Office Address (B):
Building 4, 917 Halei Road
Zhangjiang Hi-Tech Park
Pudong, Shanghai, China
Postal Code: 201203, China
Tel:     +86 21 2067 3000 Email: BD@hmplglobal.com

Addresses in Chinese:

R & D Center ( A): Chinese Cai Lun Road, Zhangjiang Hi-Tech Park in Pudong New Area, Shanghai, Lane 720 (intermediate哈雷路爱迪way out), Building 4

Head Office (B): Harley Road, Zhangjiang Hi-Tech Park, Pudong New Area, China, Shanghai, Lane 917, Building 4

HMP location

 


 

///////

Bococizumab


 

 

Bococizumab

PF-04950615, RN-316, RN316

PCSK9 (proprotein convertase subtilisin/kexin type 9, neural apoptosis-regulated convertase 1, NARC1, NARC-1, proproteine convertase 9, PC9) [Homo sapiens]

IgG2 – kappa

Hypercholesterolemia

Cardiovascular diseases

STRUCTURAL FORMULA
Heavy chain
QVQLVQSGAE VKKPGASVKV SCKASGYTFT SYYMHWVRQA PGQGLEWMGE 50
ISPFGGRTNY NEKFKSRVTM TRDTSTSTVY MELSSLRSED TAVYYCARER 100
PLYASDLWGQ GTTVTVSSAS TKGPSVFPLA PCSRSTSEST AALGCLVKDY 150
FPEPVTVSWN SGALTSGVHT FPAVLQSSGL YSLSSVVTVP SSNFGTQTYT 200
CNVDHKPSNT KVDKTVERKC CVECPPCPAP PVAGPSVFLF PPKPKDTLMI 250
SRTPEVTCVV VDVSHEDPEV QFNWYVDGVE VHNAKTKPRE EQFNSTFRVV 300
SVLTVVHQDW LNGKEYKCKV SNKGLPSSIE KTISKTKGQP REPQVYTLPP 350
SREEMTKNQV SLTCLVKGFY PSDIAVEWES NGQPENNYKT TPPMLDSDGS 400
FFLYSKLTVD KSRWQQGNVF SCSVMHEALH NHYTQKSLSL SPGK 444
Light chain
DIQMTQSPSS LSASVGDRVT ITCRASQGIS SALAWYQQKP GKAPKLLIYS 50′
ASYRYTGVPS RFSGSGSGTD FTFTISSLQP EDIATYYCQQ RYSLWRTFGQ 100′
GTKLEIKRTV AAPSVFIFPP SDEQLKSGTA SVVCLLNNFY PREAKVQWKV 150′
DNALQSGNSQ ESVTEQDSKD STYSLSSTLT LSKADYEKHK VYACEVTHQG 200′
LSSPVTKSFN RGEC 214′
Disulfide bridges location
22-96 22”-96” 23′-88′ 23”’-88”’ 132-214′ 132”-214”’
134′-194′ 134”’-194”’ 145-201 145”-201” 220-220” 221-221”
224-224” 227-227” 258-318 258”-318” 364-422 364”-422”

Bococizumab nonproprietary drug name

bococizumab

RN-316, PF-04950615

target-PC9

USAN (AB-55) BOCOCIZUMAB
PRONUNCIATION boe” koe siz’ ue mab
THERAPEUTIC CLAIM Treatment of dyslipidemia
CHEMICAL NAME
1. Immunoglobulin G2, anti-(human neural apoptosis-regulated proteinase
1)(human-Mus musculus monoclonal PF-04950615 heavy chain), disulfide
with human-Mus musculus monoclonal PF-04950615 light chain, dimer
2. Immunoglobulin G2-kappa, anti-[human proprotein convertase subtilisin/hexin type 9 (neural apoptosis-regulated convertase 1, PC9)], humanized mouse monoclonal antibody; gamma 2 heavy chain (1-444) [humanized VH (Homo sapiens IGHV1-46-1*03 (90.8%) -(IGHD)-IGHJ6*01) [8.8.11] (1-118)-Homo sapiens IGHG2*01 CH2A100>S(327),CH2P101>S(328) (119-444)] (132-214′)-
disulfide with kappa light chain (1′-214′) [humanized V-KAPPA (Homo sapiensIGKV1-39*01 (88.2%)-IGKJ2*01 [6.3.9] (1′-107′)-IGKC*01 (108′-214′)]; dimer
(220-220”:221-221”:224-224”:227-227”)-tetrakisdisulfide

MOLECULAR FORMULA C6414H9918N1722O2012S54
MOLECULAR WEIGHT 145.1 kDa
TRADEMARK None as yet
SPONSOR Pfizer, Inc.
CODE DESIGNATIONS RN316, PF-04950615
CAS REGISTRY NUMBER 1407495-02-6
WHO NUMBER 9840

Bococizumab[1] (RN316)[2] is a drug in development by Pfizer targeting PCSK9 to reduce LDL cholesterol.[3]

Description

Bococizumab is a monoclonal antibody that inhibits PCSK9, a protein that interferes with the removal of LDL. LDL levels are a major risk factor for cardiovascular disease.

Clinical trials

A phase 2b study of statin patients was presented at the 2014 American College of Cardiology. Monthly or bimonthly injections resulted in significantly reduced LDL-C at week 12.

The Phase 3 SPIRE trials plan to enroll 17,000 patients to measure cardiovascular risk. High risk and statin intolerant subjects will be included.

References

 

Bococizumab?
Monoclonal antibody
Type Whole antibody
Source Humanized (from mouse)
Target Proprotein convertase subtilisin/kexin type 9 (PCSK9)
Clinical data
Legal status
  • Investigational
Routes of
administration
Subcutaneous injection
Identifiers
CAS Registry Number 1407495-02-6
ATC code None
PubChem SID: 194168554
IUPHAR/BPS 7730
ChEMBL CHEMBL3137349
Chemical data
Formula C6414H9918N1722O2012S54
Molecular mass 145.1 kDa

//////

Lusutrombopag….Oral thrombopoietin (TPO) mimetic


 LUSUTROMBOPAG.pngChemSpider 2D Image | Lusutrombopag | C29H32Cl2N2O5S

Lusutrombopag

Update…..FDA approved july2018

(E)-3-[2,6-dichloro-4-[[4-[3-[(1S)-1-hexoxyethyl]-2-methoxyphenyl]-1,3-thiazol-2-yl]carbamoyl]phenyl]-2-methylprop-2-enoic acid

(S)-(-)-(E)-3-(2,6-dichloro-4-{4-[3-(1-hexyloxyethyl)-2-methyloxyphenyl]thiazol-2-ylcarbamoyl}phenyl)-2-methylacrylic acid

(2E)-3-{2,6-Dichloro-4-[(4-{3-[(1S)-1-(hexyloxy)ethyl]-2-methoxyphenyl}-1,3-thiazol-2-yl)carbamoyl]phenyl}-2-methylacrylic acid

UNII 6LL5JFU42F,  CAS 1110766-97-6,

D10476, MW591.546 , [US2010267783], MF C29H32Cl2N2O5S, S-888711

Shionogi & Co., Ltd., 塩野義製薬株式会社 INNOVATOR

Optically active compound (C-3B)  Melting point: 142-145°C…………….EP2184279B1

NMR (DMSO-d6) δ ppm: 12.97 (brs, 1H), 8.29 (s, 2H), 7.90 (dd, 1H, J = 1.8 Hz, 7.5 Hz), 7.72 (s, 1H), 7.35 – 7.40 (m, 2H), 7.26 (t, 1H, J = 7.5 Hz), 4.82 (q, 1H, J = 6.3 Hz), 3.62 (s, 3H), 3.16 – 3.37 (m, 2H), 1.69 (s, 3H), 1.18 – 1.51 (m, 11H), 0.82-0.87 (m, 3H) Optical rotation -4.5 degrees (DMSO, c = 1.001, 25°C)………….EP2184279B1

Optical rotation: -7.0 ± 0.5 degrees (CHCl3, c = 1.040, 21°C), NMR (CDCl3) δ ppm: 0.87 (3H, t, J = 6.8 Hz), 1.2 – 1.4 (6H, m), 1.48 (3H, d, J = 6.4 Hz), 1.52 – 1.64 (2H, m), 1.86 (3H, d, J = 1.4Hz)), 3.35 (2H, t, J = 6.7Hz), 3.55 (3H, s), 4.87 (1H, q, J = 6.3 Hz), 7.25 (1H, t, J = 7.7 Hz), 7.41 (1H, s), 7.49 (1H, dd, J = 7.9 Hz, J = 1.6 Hz), 7.51 (1H, dd, J = 7.5 Hz, J = 1.8 Hz), 7.65 (1H, d, J = 1.4 Hz), 8.33 (2H, s), 13.4 (2H, brs)………EP2184279B1

 

Thrombopoietin receptor agonist, Oral thrombopoietin (TPO) mimetic

  • 24 Mar 2015 Shionogi plans a phase III trial in Thrombocytopenia (in patients with chronic liver disease) in USA (NCT02389621)
  • 31 Dec 2014 Preregistration for Thrombocytopenia in Japan (PO)
  • 08 Nov 2013 Phase II development is ongoing in the US and the Europe

Process for preparing intermediates of an optically active 1,3-thiazole containing thrombopoietin receptor agonist  Also claims crystalline forms of lusutrombopag intermediates and a process for preparing lusutrombopag. Shionogi is developing lusutrombopag, a small-molecule thrombopoietin mimetic, as an oral tablet formulation for treating thrombocytopenia.

In December 2014, an NDA was submitted in Japan. In May 2015, the drug was listed as being in phase III development for thrombocytopenia in the US and Europe.

  

 

The lusutrombopag, a low molecular-human thrombopoietin receptor agonist, its chemical formula, “(E) -3- [2,6-Dichloro-4- [4- [3 – [(S) -1-hexyloxyethyl] – 2-methoxyphenyl] -thiazol- 2-ylcarbamoyl] -phenyl] is a -2-methylacrylic acid “. lusutrombopag is represented by the following chemical structural formula.

 

Figure JPOXMLDOC01-appb-C000001

 

Eltrombopag is represented by the following chemical structural formula.

Figure JPOXMLDOC01-appb-C000002

 

Avatrombopag is represented by the following chemical structural formula.

Figure JPOXMLDOC01-appb-C000003

 

 

Totrombopag choline is represented by the following chemical structural formula.

Figure JPOXMLDOC01-appb-C000004
C 3B IS THE COMPD OF ROT (-) AND S, E  FORM
Figure imgb0009
 Example 2
Synthesis of (R)-(E)-3-(2,6-dichloro-4-{4-[3-(1-hexyloxyethyl)-2-methyloxyphenyl]thiazol-2-ylcarbamoyl}phenyl)-2-methylacrylic acid (C-3A) (not included in the present invention) and (S)-(-)-(E)-3-(2,6-dichloro-4-{4-[3-(1-hexyloxyethyl)-2-methyloxyphenyl]thiazol-2-ylcarbamoyl}phenyl)-2-methylacrylic acid (C-3B)
According to the same method as in Example 1, an optically active compound (C-3A) and an opticallly active compound (C-3B) were synthesized from (RS)-(E)-3-(2,6-dichloro-4-{4-[3-(1-hexyloxyethyl)-2-methyloxyphenyl]thiazol-2-ylcarbamoyl}phenyl)-2-methylacrylic acid (B-3) obtained in Reference Example 3.Optically active compound (C-3A)Melting point: 139-141°C   UNDESIRED
NMR (DMSO-d6) δ ppm: 12.97 (brs, 1H), 8.29 (s, 2H), 7.90 (dd, 1H, J = 1.8 Hz, 7.5 Hz), 7.72 (s, 1H), 7.35 – 7.40 (m, 2H), 7.26 (t, 1H, J = 7.5 Hz), 4.82 (q, 1H, J = 6.3 Hz), 3.62 (s, 3H), 3.16 – 3.37 (m, 2H), 1.69 (s, 3H), 1.18 – 1.51 (m, 11H), 0.82 – 0.87 (m, 3H) Optical rotaion +4.5 degrees (DMSO, c = 1.001, 25°C)

Optically active compound (C-3B)Melting point: 142-145°C  DESIRED

NMR (DMSO-d6) δ ppm: 12.97 (brs, 1H), 8.29 (s, 2H), 7.90 (dd, 1H, J = 1.8 Hz, 7.5 Hz), 7.72 (s, 1H), 7.35 – 7.40 (m, 2H), 7.26 (t, 1H, J = 7.5 Hz), 4.82 (q, 1H, J = 6.3 Hz), 3.62 (s, 3H), 3.16 – 3.37 (m, 2H), 1.69 (s, 3H), 1.18 – 1.51 (m, 11H), 0.82-0.87 (m, 3H) Optical rotation -4.5 degrees (DMSO, c = 1.001, 25°C)

Example 4: Synthesis of (C-3B)

 

    • Figure imgb0021

First step: Synthesis of (S)-1-(3-bromo-2-methyloxyphenyl)ethane-1-ol (17)

Using the same method as that of the first step of Example 3, the compound (17) was obtained from the compound (16) at a yield 77%.

    • Optical rotation: -23.5 ± 0.6 degrees (CHCl3, c = 1.050, 21°C)
      NMR (CDCl3) θ ppm: 1.49 (3H, d, J = 6.6 Hz), 2.33 (1H, brs), 3.88 (3H, s), 5.19 (1H, q, J = 6.4 Hz), 7.01 (1H, t, J = 7.9 Hz), 7.40 (1H, dd, J = 7.7 Hz, J = 1.1 Hz), 7.46 (1H, dd, J = 8.0 Hz, J = 1.4 Hz)

Second step: Synthesis of (S)-1-bromo-3-(1-hexyloxyethyl)-2-methyloxybenzene (18)

    •  Using the same method as that of the second step of Example 3, the compound (18) was obtained from the compound (17) at a yield of 96%.
      Optical rotation: -29.8 ± 0.6 degrees (CHCl3, c = 1.055, 21°C)
      NMR (CDCl3) δ ppm: 0.87 (3H, t, J = 6.8 Hz), 1.2 – 1.4 (6H, m), 1.42 (3H, d, J = 6.5 Hz), 1.54 (2H, m), 3.29 (2H, m), 3.85 (3H, s), 4.78 (1H, q, J = 6.4 Hz), 7.02 (1H, t, J = 7.9 Hz), 7.39 (1H, dd, J = 7.8 Hz, J = 1.7 Hz), 7.45 (1H, dd, J = 7.9 Hz, J = 1.7 Hz)

Third step and fourth step: Synthesis of (S)-4-(3-(1-hexyloxyethyl)-2-methyloxyphenyl)thiazole-2-amine (20)

    • Using the same method as that of the fourth step of Example 3, the compound (19) was obtained from the compound (18), subsequently according to the same method as that of the fourth step, the compound (20) was obtained.

Compound (19)

    •  NMR (CDCl3) δ ppm: 0.87 (3H, t, J = 6.9 Hz), 1.2-1.4 (6H, m), 1.45 (3H, d, J = 6.6 Hz), 1.55 (2H, m), 3.29 (2H, m), 3.78 (3H, s), 4.73 (2H, m), 4.80 (1H, q, J = 6.4 Hz), 7.24 (1H, t, J = 7.8Hz), 7.52 (1H, dd, J = 7.7 Hz, J = 1.8 Hz), 7.65 (1H, dd, J = 7.7 Hz, J = 1.8 Hz)

Compound (20)

  •  Optical rotation: -4.2 ± 0.4 degrees (DMSO, c = 1.025, 21°C)
    NMR (CDCl3) δ ppm: 0.84 (3H, t, J = 7.0 Hz), 1.2 – 1.3 (6H, m), 1.35 (3H, d, J = 6.5 Hz), 1.48 (2H, m), 3.25 (2H, m), 3.61 (3H, s), 4.78 (1H, q, J = 6.4 Hz), 6.99 (2H, brs), 7.05 (1H, s), 7.16 (1H, t, J = 7.7 Hz), 7.27 (1H, dd, J = 7.5 Hz, J = 1.8 Hz), 7.81 (1H, dd, J = 7.6 Hz, J = 1.9 Hz)
  • Fifth step: Synthesis of ethyl (S)-(E)-3-(2,6-dichloro-4-(4-(3-(1-hexyloxyethyl)-2-metyloxyphenyl)thiazol-2-ylcarbamoyl)phenyl)-2-methylacrylate (21)
    •  Using the same method as that of the fifth step of Example 3, the compound (21) was obtained from the compound (20) at a yield of 94%.
      Optical rotation: +4.7 ± 0.4 degrees (CHCl3, c = 1.07, 21°C)
      NMR (CDCl3 ) δ ppm: 0.87 (3H, t, J = 6.9 Hz), 1.2 – 1.35 (6H, m), 1.38 (3H, t, J = 7.1
      Hz), 1.44 (3H, d, J = 6.4 Hz), 1.57 (2H, m), 1.77 (3H, d, J = 1.4 Hz), 3.30 (2H, m), 3.59 (3H, s), 4.31 (2H, q, J = 7.1 Hz), 4.83 (1H, q, J = 6.4 Hz), 7.17 (1H, t, J = 7.7 Hz), 7.42 (1H, d, J = 1.7 Hz), 7.42 (1H, dd, J = 7.7 Hz, J = 1.8 Hz), 7.51 (1H, s), 7.67 (1H, dd, J = 7.6 Hz, J = 1.7 Hz), 7.89 (2H, s), 10.30 (1H, brs)

Sixth step: Synthesis of (S)-(E)-3-(2,6-dichloro-4-(4-(3-(1-hexyloxyethyl)-2-metyloxyphenyl)thiazol-2-ylcarbamoyl)phenyl)-2-methylacrylic acid (C-3B)

  • Using the same method as that of the sixth step of Example 3, the compound (C-3B) was obtained from the compound (21) at a yield of 80%.
    Optical rotation: -7.0 ± 0.5 degrees (CHCl3, c = 1.040, 21°C)
    NMR (CDCl3) δ ppm: 0.87 (3H, t, J = 6.8 Hz), 1.2 – 1.4 (6H, m), 1.48 (3H, d, J = 6.4 Hz), 1.52 – 1.64 (2H, m), 1.86 (3H, d, J = 1.4Hz)), 3.35 (2H, t, J = 6.7Hz), 3.55 (3H, s), 4.87 (1H, q, J = 6.3 Hz), 7.25 (1H, t, J = 7.7 Hz), 7.41 (1H, s), 7.49 (1H, dd, J = 7.9 Hz, J = 1.6 Hz), 7.51 (1H, dd, J = 7.5 Hz, J = 1.8 Hz), 7.65 (1H, d, J = 1.4 Hz), 8.33 (2H, s), 13.4 (2H, brs)
  • Results of powder X-ray deffraction are shown in Fig. 5.
  • Diffraction angle of main peak: 2θ = 17.8, 21.1, 22.5, 23.3, 24.1, and 24.4 degrees

 

 

 

WO2005014561/EP1655291A1

 https://www.google.co.in/patents/EP1655291A1?cl=en

 

 

WO2014003155, claiming a composition comprising lusutrombopag, useful for treating thrombocytopenia.

https://www.google.co.in/patents/US20150148385?cl=en

 

 

 

.

WO  2015093586

Methods respectively for producing optically active compound having agonistic activity on thrombopoietin receptors and intermediate of said compound 

 

(Step 1) Synthesis of compound (VII ‘)  under a nitrogen atmosphere, it was dissolved compound 1 (2.00kg) in 1,2-dimethoxyethane (28.0kg). 25% LDA tetrahydrofuran – heptane – ethyl benzene solution (13.20kg) was added dropwise over 1 hour at -55 ℃, and stirred for 30 minutes. It was added dropwise over 40 minutes to 1,2-dimethoxyethane (3.0kg) solution of N- formyl morpholine (3.74kg) at -55 ℃, and stirred for 1 hour. 1,2-dimethoxyethane (3.0kg) solution of 2-phosphono-propanoic acid triethyl (3.74kg) was added dropwise over 45 minutes at 0 ℃, and stirred for 2 hours. 35% aqueous solution of sulfuric acid (15.8kg) was added dropwise over 40 minutes to the reaction solution. Water (16.0kg) was added and extracted. The resulting organic layer was washed with water (8.0kg), and the solvent was evaporated under reduced pressure. Acetonitrile (16.0kg) was added, and the mixture was stirred for 1 hour at 25 ℃, and the mixture was stirred and cooled to 0 ℃ 5 hours and 30 minutes. The precipitated crystals were collected by filtration, and washed with 5 ℃ acetonitrile (3.2kg). The resulting crystals it was dissolved in acetonitrile (16.0kg) at 75 ℃. It was cooled to 60 ℃, and the mixture was stirred for 30 minutes. Over 1 hour and then cooled to 30 ℃, and the mixture was stirred for 45 minutes. Over 40 minutes and then cooled to 5 ℃, and the mixture was stirred for 3 hours.The precipitated crystals were collected by filtration, and washed with 5 ℃ acetonitrile (3.2kg). The resulting crystals it was dissolved in acetonitrile (13.0kg) at 75 ℃. It was cooled to 60 ℃, and the mixture was stirred for 30 minutes. Furthermore, up to 30 ℃ over 1 hour and then cooled and stirred for 70 minutes. Over 30 minutes and then cooled to 5 ℃, and the mixture was stirred for 4 hours. I precipitated crystals were collected by filtration. Washed with 5 ℃ acetonitrile (3.2kg), and dried to give the compound (VII ‘) (1.63kg, 51.2% yield). NMR (CDCl 3 ) delta ppm: 8.07 (s, 2H), 7.47 (s, 1H), 4.32 (Q, 2H, J = 7.0 Hz), 1.79 (s, 3H), 1.38 (t, 3H, J = 7.0 Hz)  Results of powder X-ray diffraction and I shown in Figure 1 and Table 3. [Table 3]  In the powder X-ray diffraction spectrum, diffraction angle (2θ): 8.1 ± 0.2 °, 16.3 ± 0.2 °, 19.2 ± 0.2 °, 20.0 ± 0. 2 °, the peak was observed at 24.8 ± 0.2 °, and 39.0 ± 0.2 ° degrees.

 

(Synthesis of Compound (XI ‘))

(Step 2) Synthesis of Compound 4  under a nitrogen atmosphere over Compound 3 (3.00kg) and 1mol / L isopropylmagnesium chloride in tetrahydrofuran (11.40kg) 1 hour at 25 ℃ in The dropped, and stirred for 2 hours. 1mol / L isopropylmagnesium chloride in tetrahydrofuran solution (0.56kg) was added at 25 ℃, and stirred for 2 hours. To the reaction mixture N- methoxymethyl -N- methylacetamide the (1.45kg) was added dropwise over at 25 ℃ 40 minutes, and stirred for 80 minutes. 7% hydrochloric acid (9.7kg) was added to the reaction mixture, and the mixture was extracted with toluene (11.0kg). The resulting organic layer twice with water (each 7.5kg) washed, the solvent was evaporated under reduced pressure to give Compound 4 (2.63kg). NMR (CDCl 3 ) delta ppm: 7.69 (dd, 1H, J = 7.7 Hz, J = 1.5 Hz), 7.55 (dd, 1H, J = 7.7 Hz, J = 1.5 Hz), 7.05 (t, 1H, J = 7.7 Hz), 3.88 (s, 3H), 2.64 (s, 3H) ppm:

(Step 3) Synthesis of Compound 5  Under a nitrogen atmosphere, chloro [(1S Compound 4 (2.63kg), 2S) -N- ( p- toluenesulfonyl) -1,2-diphenyl-ethane diamine] (p- cymene) ruthenium (II) (28.6g), it was added to tetrahydrofuran (1.3kg) and triethylamine (880.0g). Formic acid (570.0g) was added dropwise over 6 hours at 40 ℃, and stirred for 1 hour. In addition 3.5% hydrochloric acid (14.4kg) to the reaction mixture, and the mixture was extracted with toluene (13.0kg).The organic layer was washed with 3.5% hydrochloric acid (14.4kg) and water (7.5kg), the solvent was concentrated under reduced pressure to obtain a toluene solution of Compound 5 (4.44kg).

(Step 4) Synthesis of Compound 6  under a nitrogen atmosphere, it was a potassium hydroxide (6.03kg) was dissolved in water (6.0kg). To the solution, it added tetrabutylammonium bromide (182.0g) and toluene solution of Compound 5 (4.44kg). 1-bromo-hexane (2.79kg) was added dropwise over 1 hour at 60 ℃, and the mixture was stirred for 4 hours. And extracted by adding water (4.4kg) to the reaction solution. The resulting organic layer was filtered through powdered cellulose and extracted with toluene (3.0kg) and water (7.6kg) to the filtrate. The solvent it was evaporated under reduced pressure from the organic layer. Toluene operation of evaporated under reduced pressure and the solvent by the addition of a (7.8kg) was repeated five times to obtain a toluene solution of Compound 6 (10.0kg).

(Step 5) Synthesis of Compound 7  under a nitrogen atmosphere, magnesium powder (301.0g), in tetrahydrofuran (1.3kg), the compound in toluene (6.4kg) and 1mol / L isopropylmagnesium chloride in tetrahydrofuran (432.0g) 6 In addition of the toluene solution (0.50kg) at 30 ℃, and the mixture was stirred for 2 hours. Toluene solution of Compound 6 (9.50kg) was added dropwise over 3 hours at 50 ℃, and stirred for 2 hours. 1-bromo-hexane (746.0g) was added at 50 ℃, and the mixture was stirred for 1 hour. It was added dropwise over 1 hour at 5 ℃ toluene (5.3kg) solution of 2-chloro -N- methoxy -N- methyl-acetamide (1.78kg), and stirred for 1 hour. 3.7% hydrochloric acid (16.7kg) was added to the reaction mixture, and the mixture was extracted. The obtained organic layer was washed with water (15.0kg), and concentrated under reduced pressure to give a toluene solution of Compound 7 (8.25kg).

 

(Step 6) Synthesis of Compound (II ‘)  under a nitrogen atmosphere, thiourea (1.03kg), in ethanol (1.2kg) and 65 ℃ toluene solution of compound 7 (8.25kg) in toluene (6.3kg) over 3 hours was added dropwise and stirred for 2 hours. The reaction solution was extracted by adding 0.7% hydrochloric acid (30.6kg), and washed twice with water (30.0kg). Ethanol in the organic layer (9.5kg), and extracted by addition of heptane (10.0kg) and 3.5% hydrochloric acid (5.9kg). The resulting aqueous layer with 4% hydrochloric acid (1.5kg) and ethanol (3.5kg) merged the aqueous layer was extracted from the organic layer, the ethanol was washed with heptane (10.0kg) (3.1kg) It was added. 8% aqueous sodium hydroxide (6.0kg) was added dropwise over at 5 ℃ 30 minutes, and stirred for 20 minutes. 8% aqueous sodium hydroxide (5.8kg) was added dropwise over a period at 5 ℃ 15 minutes.The precipitated crystals were collected by filtration, washed with 45% aqueous ethanol (10.9kg) and water (15.0kg) (crude crystals of Compound (II ‘)). The resulting crude crystals were dissolved in 50 ℃ in ethanol (8.1kg), over a period of 1 hour and then cooled to 10 ℃, and the mixture was stirred for 30 minutes. Water (10.0kg) over 2 hours was added dropwise and stirred for 30 minutes. The precipitated crystals were collected by filtration, washed with 50% aqueous ethanol (7.5kg) and water (10.0kg) (crystals of the compound after recrystallization from ethanol / water system (II ‘)). The resulting crystals were dissolved at 55 ℃ in toluene (1.6kg) and heptane (1.3kg), over 1 hour and cooled to 20 ℃, and stirred for 30 minutes. Heptane (6.3kg) over a period of 30 minutes was added dropwise and stirred for 15 minutes. The obtained crystals precipitated were collected by filtration, washed with a mixed solvent of toluene (0.3kg) and heptane (2.3kg), and dried to give compound (II ‘) (1.67kg, 44.5% yield) a (crystalline compound after recrystallization from toluene / heptane system (II ‘)).

NMR (CDCl 3 ) delta ppm: 0.84 (3H, t, J = 7.0 Hz), 1.2 – 1.3 (6H, M), 1.35 (3H, D, J = 6.5 Hz), 1.48 (2H, M), 3.25 ( 2H, m), 3.61 (3H, s), 4.78 (1H, q, J = 6.4 Hz), 6.99 (2H, brs), 7.05 (1H, s), 7.16 (1H, t, J = 7.7 Hz), 7.27 (1H, dd, J = 7.5 Hz, J = 1.8 Hz), 7.81 (1H, dd, J = 7.6 Hz, J = 1.9 Hz)  it is shown in Figure 2 and Table 4 the results of powder X-ray diffraction. [Table 4]  In the powder X-ray diffraction spectrum, diffraction angle (2θ): 12.5 ± 0.2 °, 13.0 ± 0.2 °, 13.6 ± 0.2 °, 16.4 ± 0. 2 °, 23.0 ± 0.2 °, a peak was observed at 24.3 ± 0.2 ° degrees.  Above, each of the compounds (II ‘) of the crude crystals, the ethanol / compound after recrystallization from water (II’) crystals and toluene / heptane compound after recrystallization from (II ‘) crystallographic purity of the results of the , Fig. 3, I 4 and 5 as well as Table 5. [Table 5](HPLC was measured by the above method A.)  As shown in the results of the above table, as compared to recrystallization from ethanol / water, recrystallized with toluene / heptane system, compounds having a high optical purity it is possible to manufacture a crystal of (II ‘).  Next, the above-mentioned compound (II ‘) of the crude crystals, the ethanol / compound after recrystallization from water (II’) crystals and toluene / heptane compound after recrystallization from (II ‘) results of crystals of HPLC of the respectively, Fig. 6, I 7 and 8 and Table 6. [Table 6] (units, .N.D shows the peak area of the (%). is, .HPLC to indicate not detected was measured by the above method B.)  As shown in the results of Table, with ethanol / water system Compared to recrystallization, recrystallization from toluene / heptane system is found to be efficiently remove organic impurities A and organic impurities B.

(Step 7) Compound ‘Synthesis of DMSO adduct of (VIII)  Under a nitrogen atmosphere, the compound (II ‘) (1.50kg) and compound (VII’) (1.43kg) in ethyl acetate (17.6kg) and triethylamine (1.09kg) were sequentially added, was dissolved.Diphenyl phosphorochloridate the (1.46kg) was added dropwise over 1 hour at 50 ℃, and the mixture was stirred for 3 hours. The reaction mixture was cooled to 25 ℃, after the addition of 2.6% hydrochloric acid (8.1kg), and extracted. The resulting organic layer to 6.3% aqueous solution of sodium hydroxide (3.2kg) and 14% aqueous sodium carbonate (5.2kg) was added and stirred for 20 minutes. Adjusted to pH7.5 with 8.3% hydrochloric acid and extracted. The organic layer it was washed with 4.8% sodium chloride aqueous solution (11.0kg). DMSO and (16.5kg) was added, and the mixture was concentrated under reduced pressure.DMSO and (5.8kg) was added, over a period at 40 ℃ 30 minutes was added dropwise water (0.9kg), and stirred for 1 hour. Over a period of 30 minutes, cooled to 25 ℃, and the mixture was stirred for 30 minutes. Over at 25 ℃ 30 minutes was added dropwise water (1.4kg), and the precipitated crystals were collected by filtration. After washing with 90% DMSO solution (10.0kg) and water (27.0kg), to obtain crystals of DMSO adduct and dried to Compound (VIII ‘) (2.98kg, 95.2% yield).

1H-NMR (CDCl 3 ) delta: 0.87 (t, J = 6.8 Hz, 3H), 1.20-1.34 (M, 6H), 1.37 (t, J = 7.1 Hz, 3H), 1.44 (D, J = 6.5 Hz , 3H), 1.52-1.59 (m, 2H), 1.77 (d, J = 1.3Hz, 3H), 2.62 (s, 6H), 3.28-3.34 (m, 2H), 3.59 (s, 3H), 4.31 ( q, J = 7.1Hz, 2H), 4.83 (q, J = 6.5Hz, 1H), 7.16 (t, J = 7.7Hz, 1H), 7.40-7.43 (m, 2H), 7.51 (s, 1H), 7.68 (dd, J = 7.7, 1.8Hz, 1H), 7.92 (d, J = 1.3Hz, 2H), 10.58 (s, 1H).  The results of the powder X-ray diffraction and I are shown in Figure 9 and Table 7. [Table 7]

In the powder X-ray diffraction spectrum, diffraction angle (2θ): 5.2 ° ± 0.2 °, 7.0 ° ± 0.2 °, 8.7 ° ± 0.2 °, 10.5 ° ± 0.2 °, 12.3 ° ± 0.2 °, 14.0 ° ± 0.2 °, 15.8 ° ± 0.2 °, 19.3 ° ± 0.2 °, 22.5 ° peak was observed to ± 0.2 ° and 24.1 ° ± 0.2 °.  TG / DTA analysis result it is shown in Figure 10.  Then, each result of HPLC of concentrated dry solid and the above DMSO adduct crystals described in the following Reference Examples 1, 11 and 12, 13 and 14, and I are shown in Table 8. [Table 8] (unit, .HPLC showing peak areas of (%) was measured by the above methods C.)  As shown in the results of the above Table, when compared with the extract, DMSO adduct of the compound (VIII ‘) The in the crystal, less residual organic impurities D, and it found to be about 56% removal.

(Step 8)  under nitrogen atmosphere, DMSO adduct of the compound (VIII ‘) and (2.50kg) it was dissolved in ethanol (15.8kg). 24% sodium hydroxide aqueous solution (1.97kg) was added dropwise over a period at 45 ℃ 30 minutes to the solution and stirred for 3 hours. The reaction mixture was cooled to 25 ℃, water was added (20.0kg) and ethanol (7.8kg). 18% hydrochloric acid (2.61kg) was added dropwise over at 25 ℃ 30 minutes, followed by addition of seed crystals prepared according to the method described in Patent Document 23. After stirring for 3 hours and allowed to stand overnight. Thereafter, the precipitated crystals were collected by filtration, to give after washing with 50% aqueous ethanol solution (14.2kg), and dried to a compound (XI ‘) (1.99kg, 93.9% yield).

NMR (CDCl 3 ) delta ppm: 0.87 (3H, t, J = 6.8 Hz), 1.2 – 1.4 (6H, M), 1.48 (3H, D, J = 6.4 Hz), 1.52 – 1.64 (2H, M), 1.86 (3H, d, J = 1.4Hz), 3.35 (2H, t, J = 6.7Hz), 3.55 (3H, s), 4.87 (1H, q, J = 6.3 Hz), 7.25 (1H, t, J = 7.7 Hz), 7.41 (1H, s), 7.49 (1H, dd, J = 7.9 Hz, J = 1.6 Hz), 7.51 (1H, dd, J = 7.5 Hz, J = 1.8 Hz), 7.65 (1H, d, J = 1.4 Hz), 8.33 (2H, s), 13.4 (2H, brs)  I is shown in Figure 15 the results of powder X-ray diffraction.

 

Patent Document 1: JP-A-10-72492 JP
Patent Document 2: WO 96/40750 pamphlet
Patent Document 3: JP-A-11-1477 JP
Patent Document 4: Japanese Unexamined Patent Publication No. 11-152276
Patent Document 5: International Publication No. 00/35446 pamphlet
Patent Document 6: JP-A-10-287634 JP
Patent Document 7: WO 01/07423 pamphlet
Patent Document 8: International Publication WO 01/53267 pamphlet
Patent Document 9: International Publication No. 02 / 059 099 pamphlet
Patent Document 10: International Publication No. 02/059100 pamphlet
Patent Document 11: International Publication No. 02/059100 pamphlet
Patent Document 12: International Publication No. 02/062775 pamphlet
Patent Document 13: International Publication No. 2003/062233 pamphlet
Patent Document 14: International Publication No. 2004/029049 pamphlet
Patent Document 15: International Publication No. 2005/007651 pamphlet
Patent Document 16: International Publication No. 2005/014561 pamphlet
Patent Document 17: JP 2005-47905 Japanese
patent Document 18: Japanese Patent Publication No. 2006-219480
Patent Document 19: Japanese Patent Publication No. 2006-219481
Patent Document 20: International Publication No. 2007/004038 pamphlet
Patent Document 21: International Publication No. 2007/036709 pamphlet
Patent Document 22: International Publication No. 2007/054783 pamphlet
Patent Document 23: International Publication No. 2009/017098 pamphlet

Non-Patent Document 1: Proceedings of the National Akademyi of Science of the United State of America (…. Proc Natl Acad Sci USA) 1992, Vol. 89, p 5640-5644.
Non-Patent Document 2: Journal of Organic (.. J. Org Chem) Chemistry 1984, Vol. 49, p 3856-3857.
Non-Patent Document 3: (.. J. Org Chem). Journal of Organic Chemistry, 1992, Vol. 57, p 6667-6669
Non-Patent Document 4:. Shinretto (Synlett) 2004 year Vol. 6, p 1092-1094

 

POSTER

101 Discovery and biological evaluation of Lusutrombopag (S-888711) as a novel nonpeptide drug candidate for thrombocytopenia
Masami Takayama, Hajime Yamada, Hiroshi Takemoto, Takeshi Shiota, Yoshikazu Tanaka, Noriko Yamane, Kouji Takahashi, Naoki Oyabu, Kenji Kuwabara, Itsuki Oshima, Kenzo Koizumi, Hiroshi Yoshida, Ayumu Nogami, Tomomi Yamada, Yutaka Yoshida, Takami Murashi, Shinichiro Hara.
101 – Discovery and biological evaluation of Lusutrombopag (S-888711) as a novel nonpeptide drug candidate for thrombocytopenia

Masami Takayama1, masami.takayama@shionogi.co.jp, Hajime Yamada3, Hiroshi Takemoto2, Takeshi Shiota2, Yoshikazu Tanaka2, Noriko Yamane2, Kouji Takahashi2, Naoki Oyabu3, Kenji Kuwabara3, Itsuki Oshima2, Kenzo Koizumi3, Hiroshi Yoshida3, Ayumu Nogami3, Tomomi Yamada3, Yutaka Yoshida3, Takami Murashi3, Shinichiro Hara2. (1) Department of Strategic Research Planning Offices, Shionogi & CO., LTD, Toyonaka, Osaka 561-0825, Japan, (2) Department of Innovative Drug Discovery Research Laboratories, Shionogi & CO.,LTD, Toyonaka, Osaka 561-0825, Japan, (3) Department of Medicinal Research Laboratories, Shionogi & CO., LTD, Toyonaka, Osaka 561-0825, Japan

As a drug candidate of thrombocytopenia, Lusutrombopag (S-888711) is in Phase III clinical trial stage right now. It is been proven that Lusutrombopag (S-888711) is excellent property in safety and efficacy by clinical trials. In this meeting, we will present in detail about the history of drug discovery of Lusutrombopag.Because Lusutrombopag (S-888711) acts specifically to human TPO receptor, we prepared TPOR-Ki/Shi mice expressing a mouse-human chimeric TPOR for evaluating the efficacy. This TPOR-Ki/Shi mice worked very well as an evaluation model of drug efficacy, so we were able to select Lusutrombopag from many candidate compounds. In this meeting, we will present the results of the efficacy in TPOR-Ki/Shi mice of Lusutrombopag and the similar drug (Eltrombopag).
Sunday, March 16, 2014 07:00 PM
General Poster Session (07:00 PM – 10:00 PM)
Location: Dallas Convention Center
Room: Hall E
Monday, March 17, 2014 08:00 PM
Sci-Mix (08:00 PM – 10:00 PM)
Location: Dallas Convention Center
Room: Hall F

http://acselb-529643017.us-west-2.elb.amazonaws.com/chem/247nm/program/divisionindex.php?nl=1&act=presentations&val=General+Poster+Session&ses=General+Poster+Session&prog=222964

 

update………..

FDA approves lusutrombopag for thrombocytopenia in adults with chronic liver disease

https://www.fda.gov/Drugs/InformationOnDrugs/ApprovedDrugs/ucm615348.htm

synthesis………..https://newdrugapprovals.org/2015/08/20/lusutrombopag-oral-thrombopoietin-tpo-mimetic/

On July 31, 2018, the Food and Drug Administration approved lusutrombopag (Mulpleta, Shionogi Inc.) for thrombocytopenia in adults with chronic liver disease who are scheduled to undergo a medical or dental procedure.

Approval was based on two randomized, double-blind, placebo-controlled trials (L-PLUS 1 and L-PLUS 2, NCT02389621) involving 312 patients with chronic liver disease and severe thrombocytopenia who were undergoing an invasive procedure and had a platelet count less than 50 x 109/L. Patients were randomized 1:1 to receive 3 mg of lusutrombopag or placebo once daily for up to 7 days.

In L-PLUS 1, 78% of patients (38/49) receiving lusutrombopag required no platelet transfusion prior to the primary invasive procedure, compared with 13% (6/48) who received placebo (95% CI for treatment difference: 49%, 79%; p<0.0001). In L-PLUS 2, 65% (70/108) of patients who received lusutrombopag required no platelet transfusion prior to the primary invasive procedure or rescue therapy for bleeding from randomization through 7 days after the procedure, compared with 29% (31/107) receiving placebo (95% CI for treatment difference: 25%, 49%; p<0.0001).

The most common adverse reaction in ≥ 3% of patients was headache.

The recommended lusutrombopag dosage is 3 mg orally once daily with or without food for 7 days.

View full prescribing information for Mulpleta.

FDA granted this application priority review and fast track designation. A description of FDA expedited programs is in the Guidance for Industry: Expedited Programs for Serious Conditions-Drugs and Biologics.

Healthcare professionals should report all serious adverse events suspected to be associated with the use of any medicine and device to FDA’s MedWatch Reporting System or by calling 1-800-FDA-1088.

Follow the Oncology Center of Excellence on Twitter @FDAOncology.

Check out recent approvals at the OCE’s podcast, Drug Information Soundcast in Clinical Oncology.

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//////

phase 3, shionogi, japan, lusutrombopag, S 888711

CCCCCCOC(C)C1=CC=CC(=C1OC)C2=CSC(=N2)NC(=O)C3=CC(=C(C(=C3)Cl)C=C(C)C(=O)O)Cl

Filgotinib


Filgotinib.png

Filgotinib

EU APPROVED 2020/9/24, JYSELECA

JAPAN APPROVED2020/9/25

  • C21H23N5O3S
  • MW425.504
  • Elemental Analysis: C, 59.28; H, 5.45; N, 16.46; O, 11.28; S, 7.54
1206161-97-8
Cyclopropanecarboxamide, N-[5-[4-[(1,1-dioxido-4-thiomorpholinyl)methyl]phenyl][1,2,4]triazolo[1,5-a]pyridin-2-yl]-
G146034
GLPG0634
N-(5-(4-((1,1-dioxidothiomorpholino)methyl)phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl)cyclopropanecarboxamide
Galapagos Nv INNOVATOR
PHASE 3,  Crohn’s disease, Rheumatoid arthritis, Ulcerative colitis
Filgotinib is an orally available inhibitor of JAK1/JAK2 and TYK2 in phase III clinical development at Galapagos and Gilead for the treatment of rheumatoid arthritis, moderate or severe Crohn’s disease and ulcerative colitis

IL-6 antagonist; Jak1 tyrosine kinase inhibitor; Tyk2 tyrosine kinase inhibitor; Jak3 tyrosine kinase inhibitor; Jak2 tyrosine kinase inhibitor

Autoimmune disease; Cancer; Colitis; Crohns disease; Inflammatory disease; Neoplasm; Rheumatoid arthritis; Transplant rejection

In 2017, orphan drug designation was assigned to the compound in the U.S. for the treatment of pediatric Crohn’s disease and pediatric ulcerative colitis.

GlaxoSmithKline had been developing filgotinib preclinically for the treatment of rheumatoid arthritis pursuant to a license; however, in 2010, the compound was re-acquired by Galapagos. In 2012, the product was licensed to Abbott for development and marketing. In January 2013, Abbott spun-off its research-based pharmaceutical business into a newly-formed company AbbVie. The license agreement between Galapagos and Abbott was terminated in September 2015, Galapagos regaining all rights to the product. The same year, Galapagos and Gilead entered into a global partnership and Gilead obtained the global rights of codevelopment and commercialization for the treatment of inflammatory diseases

Filgotinib (GLPG0634), by the Belgian biotech company Galápagos NV, is a drug which is currently under investigation for the treatment of rheumatoid arthritis and Crohn’s disease.

Filgotinib (GLPG0634) is an orally-available, selective inhibitor of JAK1 (Janus kinase 1) for the treatment of rheumatoid arthritis and potentially other inflammatory diseases. Filgotinib (GLPG0634) dose-dependently inhibited Th1 and Th2 differentiation and to a lesser extent the differentiation of Th17 cells in vitro. GLPG0634 was well exposed in rodents upon oral dosing, and exposure levels correlated with repression of Mx2 expression in leukocytes. The JAK1 selective inhibitor GLPG0634 (Filgotinib) is a promising novel therapeutic with potential for oral treatment of rheumatoid arthritis and possibly other immune-inflammatory diseases. Filgotinib (GLPG0634) is currently in a Phase 2 study in Crohn’s disease.

3D

Mechanism of action

Filgotinib is a Janus kinase inhibitor with selectivity for subtype JAK1 of this enzyme. It is considered a promising agent as it inhibits JAK1 selectively. Less selective JAK inhibitors (e.g. tofacitinib) are already being marketed. They show long-term efficacy in the treatment of various inflammatory diseases. However, their lack of selectivity leads to dose-limiting side effects.[1] It is thought that inhibition of all JAK isoenzymes is beneficial in rheumatoid arthritis. However, pan-JAK inhibition might also lead to unwanted side effects that might not outweigh its benefits. This is the rationale for the development of newer and more selective inhibitors like filgotinib.

The signal transmission of large numbers of proinflammatory cytokines is dependent on JAK1. Inhibition of JAK2 may also contribute to the efficacy against RA. Nonetheless it is thought that JAK2 inhibition might lead to anemia and thrombopenia by interference witherythropoietin and thrombopoietin and granulocyte-macrophage colony-stimulating factor. Therefore one might prefer to choose a more selective JAK1 inhibitor as a primary therapeutic option. Filgotinib exerts a 30-fold selectivity for JAK1 compared to JAK2.[2] It is however still to be seen to what extent JAK2 inhibition should be avoided.

Novel crystalline forms of filgotinib salts, particularly hydrochloride salt, useful for treating JAK-mediated diseases eg inflammatory diseases, autoimmune diseases, proliferative diseases, allergy and transplant rejection.  Galapagos and licensee AbbVie are developing filgotinib, a selective JAK-1 inhibitor, for treating rheumatoid arthritis (RA) and Crohn’s disease (CD). In August 2015, the drug was reported to be in phase 2 clinical development for treating RA and CD. The drug is also being investigated for the treatment of colitis and was discovered as part of the company’s arthritis alliance with GSK; however in August 2010 Galapagos reacquired the full rights. See WO2013189771, claiming use of filgotinib analog for treating inflammatory diseases. Also see WO2010010190 (co-assigned with GSK and Abbott) and WO2010149769 (assigned to Galapagos) claiming filgotinib, generically and specifically, respectively.

Clinical trials and approval

The efficacy of filgotinib is currently studied in a phase2b program (DARWIN trial 1, 2) with involvement of 886 rheumatoid arthritis patients and 180 Crohn’s disease patients.

Phase 1 study

It was shown in phase 1 studies that the pharmacokinetics of filgotinib metabolism is independent of hepatic CYP450 enzymatic degradation. The drug metabolism is however mediated by carboxylesterases. There is no interference reported with the metabolism of methotrexate nor with any of the investigated transport proteins.[3]

Phase 2 study: Proof of concept (2011)

In november 2011 Galápagos released the results of their phase 2 study (identification: NCT01384422, Eudract: 2010-022953-40) in which 36 patients were treated who showed a suboptimal clinical response to methotrexate treatment. Three groups of twelve patients were treated either with 200 mg filgotinib in a single dose, 200 mg divided in two doses or placebo. The primary end-point was the ACR20 score, which monitors improvements in the symptomatology of the patient. After the scheduled 4 weeks of treatment, 83% of the respondents showed an improved ACR20-score. Half of the treated patients showed a complete (or near complete) remission of the disease. There were no reports ofanemia nor changes in lipidemia. The company stated in their press release that filgotinib is the first selective JAK1 inhibitor that shows clinical efficacy. As a result of this study, the company stated that “GLPG0634 shows one of the highest initial response rates ever reported for rheumatoid arthritis treatments”.[4]

DARWIN 1 trial

The DARWIN 1 trial is a 24 week double blind placebo-controlled trial with 599 rheumatoid arthritis patients enrolled. All participants have moderate to severe RA and showed an insufficient response to standard methotrexate treatment. The trial compares three dosages of filgotinib as a once or twice per day regimen. During the trial all participants remain on their methotrexate treatment. According to the company, the results of this trial are expected in July 2015.[5]

DARWIN 2 trial

The DARWIN 2 trial is a double blind placebo-controlled trial with 280 rheumatoid arthritis patients enrolled who show an insufficient response to standard methotrexate treatment. This trial, in contrast to the previous DARWIN 1 trial, methotrexate is discontinued. Therefore, this trial investigates filgotinib as a monotherapy.[6] The recruitment of DARWIN trial 2b ended in november 2014.[7] Preliminary results are expected in the second quarter of 2015 and a full completion of the study is expected in the third quarter of 2015.

DARWIN 3 trial

Patients who complete DARWIN 1 and 2 will be eligible for DARWIN 3.

COSY PREDICT

COSY NMR prediction (26)

Time line

  • june 2011: results of first phase 2 trial
  • november 2014: initiation of DARWIN 1 and 2 trials
  • april 2015: expected date of DARWIN 1 trial results
  • june 2015: expected date of DARWIN 2 trial results

ChemSpider 2D Image | Filgotinib | C21H23N5O3S

NMR FROM NET….ABMOLE, DMSOD6

NMR ABMOLE

NMR MEDKOO DMSOD6

NMR MEDKOO

CHEMIETEK

1H NMR PREDICT
1H NMR MOLBASE GRAPH 1H NMR MOLBASE VAL

13C NMR PREDICT

13C NMR MOLBASE GRAPH 13C NMR MOLBASE VAL

……………………

MORE PREDICTS

FIL CHEMDDOODLE

1H NMR PREDICT

1H NMR DB GRAPH

H EXPLODED

1H NMR DB VAL

13C NMR PREDICT

13C NMRDB GRAPH 13C NMRDB VAL

PRODUCT PATENT

http://www.google.com/patents/WO2010149769A1?cl=en

Applicants: GALAPAGOS NV [BE/BE]; Generaal De Wittelaan L11/A3 B-2800 Mechelen (BE) (For All Designated States Except US).
MENET, Christel Jeanne Marie [FR/BE]; (BE) (For US Only).
SMITS, Koen Kurt [BE/BE]; (BE) (For US Only)
Inventors: MENET, Christel Jeanne Marie; (BE).
SMITS, Koen Kurt; (BE)

PRODUCT PATENT SYN 1

WO2010149769

International Filing Date: 25.06.2010

ESTIMATED EXP 2030

Condensation of 2-amino-6-bromopyridine (I) with ethoxycarbonyl isothiocyanate (II) in CH2Cl2 gives 1-(6-bromopyridin-2-yl)-3-carboethoxythiourea (III), which upon cyclization with hydroxylamine hydrochloride (IV) in the presence of DIEA in EtOH/MeOH yields 2-amino-5-bromo[1,2,4]triazolo[1,5-a]pyridine (V). N-Acylation of amine (V) with cyclopropanecarbonyl chloride (VI) using Et3N in acetonitrile, and subsequent treatment with methanolic ammonia furnishes the carboxamide (VII) (1-3), which upon Suzuki coupling with 4-(hydroxymethyl)phenylboronic acid (VIII) in the presence of PdCl2(dppf) and K2CO3 in dioxane/H2O at 90 °C, followed by bromination with PBr3 in CHCl3 affords intermediate (IX). Condensation of benzyl bromide derivative (IX) with thiomorpholine-1,1-dioxide (X) using DIEA in CH2Cl2/MeOH yields filgotinib (1,2). Alternatively, condensation of (4-bromomethylphenyl)-4,4,5,5-tetramethyl-[1,3,2]dioxaborolane (XI) with thiomorpholine 1,1-dioxide (X) in the presence of DIEA in CH2Cl2/MeOH gives intermediate (XII), which undergoes Suzuki coupling with aryl bromide (VII) in the presence of PdCl2(dppf) and K2CO3 in dioxane/H2O at 90 °C to afford the target filgotinib

The present invention is based on the discovery that the compound of the invention is able to act as an inhibitor of JAK and that it is useful for the treatment of inflammatory conditions, autoimmune diseases, proliferative diseases, transplantation rejection, diseases involving impairment of cartilage turnover, congenital cartilage malformations, and/or diseases associated with hypersecretion of IL6. In a specific aspect the compound is an inhibitor of JAKl and JAK2. The present invention also provides methods for the production of this compound, a pharmaceutical composition comprising this compound and methods for treating inflammatory conditions, autoimmune diseases, proliferative diseases, transplantation rejection, diseases involving impairment of cartilage turnover, congenital cartilage malformations, and/or diseases associated with hypersecretion of IL6 by administering the compound of the invention.

Accordingly, in a first aspect of the invention, a compound of the invention is provided having a formula (I):

[0017] The compound of the invention is a novel inhibitor of JAK that appears to exhibit a dramatically improved in vivo potency as compared to structurally similar compounds. In a particular embodiment the compound of the invention is an inhibitor of JAKl and JAK2. In particular it appears to exhibit this increase in potency at lower in vivo exposure levels compared to structurally similar compounds. The use of a compound with these improvements is expected to result in a lower dosage requirement (and therefore an improved dosing schedule).

General Synthetic Method Scheme 1

1. RCOCI, Et3N 2. NH3 / MeOH CH3CN, 20 0C 2O 0C


wherein Ar represents phenyl-Ll-heterocycloalkyl, where Ll is a bond, -CH2– or -CO- and the heterocycloalkyl group is optionally substituted.

General

1.1.1 l-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2)

(2)

[00117] To a solution of 2-amino-6-bromopyridine (1) (253.8 g, 1.467 mol) in DCM (2.5 L) cooled to 5 0C is added ethoxycarbonyl isothiocyanate (173.0 mL, 1.467 mol) dropwise over 15 min. The reaction mixture is then allowed to warm to room temp. (20 0C) and stirred for 16 h. Evaporation in vacuo gives a solid which may be collected by filtration, thoroughly washed with petrol (3×600 mL) and air-dried to afford (2). The thiourea may be used as such for the next step without any purification. 1H (400 MHz, CDCl3) δ 12.03 (IH, br s, NH), 8.81 (IH, d, J 7.8 Hz, H-3), 8.15 (IH, br s, NH), 7.60 (IH, t, J 8.0 Hz, H-4), 7.32 (IH, dd, J 7.7 and 0.6 Hz, H-5), 4.31 (2H, q, J 7.1 Hz, CH2), 1.35 (3H, t, J 7.1 Hz, CH3).

7.7.2 5-Bromo-[l, 2, 4]triazolo[l, 5-a]pyridin-2-ylamine (3)

[00118] To a suspension of hydroxylamine hydrochloride (101.8 g, 1.465 mol) in EtOH/MeOH

(1 :1, 900 mL) is added N,N-diisopropylethylamine (145.3 mL, 0.879 mol) and the mixture is stirred at room temp. (20 0C) for 1 h. l-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2) (89.0 g, 0.293 mol) is then added and the mixture slowly heated to reflux (Note: bleach scrubber is required to quench H2S evolved). After 3 h at reflux, the mixture is allowed to cool and filtered to collect the precipitated solid. Further product is collected by evaporation in vacuo of the filtrate, addition Of H2O (250 mL) and filtration. The combined solids are washed successively with H2O (250 mL), EtOH/MeOH (1 : 1, 250 mL) and Et2O (250 mL) then dried in vacuo to afford the triazolopyridine derivative (3) as a solid. The compound may be used as such for the next step without any purification. 1H (400 MHz, DMSO-t/β) δ 7.43-7.34 (2H, m, 2 x aromatic-H), 7.24 (IH, dd, J 6.8 and 1.8 Hz, aromatic-H), 6.30 (2H, br, NH2); m/z 213/215 (1 :1, M+H+, 100%).

7.7.3 General procedure for mono-acylation to afford intermediate (4):


[00119] To a solution of the 2-amino-triazolopyridine (3) (7.10 g, 33.3 mmol) in dry CH3CN

(150 mL) at 5 0C is added Et3N (11.6 mL, 83.3 mmol) followed by cyclopropanecarbonyl chloride (83.3 mmol). The reaction mixture is then allowed to warm to ambient temperature and stirred until all starting material (3) is consumed. If required, further Et3N (4.64 mL, 33.3 mmol) and cyclopropanecarbonyl chloride (33.3 mmol) is added to ensure complete reaction. Following solvent evaporation in vacuo the resultant residue is treated with 7 N methanolic ammonia solution (50 mL) and stirred at ambient temp, (for 1-16 h) to hydro lyse any bis-acylated product. Product isolation is made by removal of volatiles in vacuo followed by trituration with Et2O (50 mL). The solids are collected by filtration, washed with H2O (2x50mL), acetone (50 mL) and Et2O (50 mL), then dried in vacuo to give the required bromo intermediate (4).

Method A

Preparation of compounds of the invention via Suzuki coupling (5):

[00120] An appropriate boronic acid (2eq.) is added to a solution of bromo intermediate (4) in

1 ,4-dioxane/water (5:1). K2CO3 (2 eq.) and PdCl2dppf (5%) are added to the solution. The resulting mixture is then heated in a microwave at 140 0C for 30 min (this reaction can also be carried out by traditional heating in an oil bath at 900C for 16h under N2). Water is added and the solution is extracted with ethyl acetate. The organic layers are dried over anhyd. MgSθ4 and evaporated in vacuo. The final compound is obtained after purification by flash chromatography or preparative HPLC. HPLC: Waters

XBridge Prep Cl 8 5μm ODB 19mm ID x 100mm L (Part No.186002978). All the methods are using

MeCN/H2O gradients. H2O contains either 0.1% TFA or 0.1% NH3.

Method B

Bl. 4 4-[2-(Cyclopropanecarbonyl-amino)-[ 1 , 2, 4]triazolo[l, 5-a] pyridin-5-yl] -benzoyl chloride

[00121] 2 Drops of DMF are added to a solution of 4-[2-(cyclopropanecarbonyl-amino)- [l,2,4]triazolo[l,5-a]pyridin-5-yl]-benzoic acid (1 eq) obtained by Method A using 4-carboxyphenylboronic acid in DCM under N2 atmosphere. Then oxalyl chloride (2 eq) is added dropwise to this resulting solution (gas release). The mixture is stirred at room temperature for 2 hours. After completion of the reaction by LCMS, the solvent is removed. The crude acid chloride is used without further purification in next step.

B2. Amide formation (General Method)

[00122] An appropriate amine (1.1 eq) and Et3N (5 eq) are dissolved in DCM under N2 atmosphere and cooled at 00C. The acid chloride (Bl, 1 eq) dissolved in DCM is added dropwise to this solution. The reaction is stirred at room temperature for 16 h. After this time, reaction is complete. The compound is extracted with EtOAc and water, washed with brine and dried over anhyd. MgSO4. Organic layers are filtered and evaporated. The final compound is isolated by preparative HPLC. Preparative HPLC: Waters XBridge Prep C18 5μm ODB 19mm ID x 100mm L (Part No.186002978). All the methods are using MeCN/H2O gradients. H2O contains either 0.1% TFA or 0.1% NH3.

Method C

Wherein R3a or R3b together with the nitrogen atom to which they are attached, may form a heterocycloalkyl.

Reductive alkylation (general method)

[00123] An appropriate amine (2 eq.), cyclopropanecarboxylic acid (for example cyclopropanecarboxylic acid [5-(4-formyl-phenyl)-[l,2,4]triazolo[l,5-a]pyridine-2-yl]-amide) prepared by method A (1 eq.) and Ti(OPr)4 are mixed and stirred at room temperature for 3 hrs. The mixture is diluted in ethanol and Na(CN)BH3 (leq.) is added. The resulting solution is stirred at room temperature for 16 hrs. The mixture is diluted in water and filtered. The filtrate is washed with ethanol. The combined solvent phases are evaporated under vacuum. The final compound is isolated by preparative HPLC.

Method D 
wherein R1 and R2 together with the Nitrogen atom to which they are attached, may form a heterocycloalkyl.

Reaction ofalkylation

[00124] 2-(4-Bromomethyl-phenyl)-4,4,5,5-tetramethyl-[l,3,2]dioxaborolane (leq) and Et3N (2 eq) (or AgCO3) are dissolved in DCM/MeOH (4:1 v:v) under N2 and an amine (2 eq) is added dropwise. The resulting solution is stirred at room temperature for 16h. After this time, the reaction is complete. The solvent is evaporated. The compound is extracted with EtOAc and water, washed with brine and dried over anhyd. MgSθ4. Organic layers are filtered and evaporated. The final compound is isolated by flash chromatography.

Suzuki coupling

[00125] The obtained boronic acid (2eq.) is added to a solution of cyclopropanecarboxylic acid

(5-bromo-[l,2,4]triazolo[l,5-a]pyridin-2-yl)-amide (4) in 1 ,4-dioxane/water (5:1). K2CO3 (2 eq.) and PdCl2dppf (5%) are added to the solution. The resulting mixture is then heated in a microwave at 140 0C for 30 min (This reaction can also be carried out by traditional heating in an oil bath at 900C for 16h under N2). Water is added and the solution is extracted with ethyl acetate. The organic layers are dried over anhyd. MgSθ4 and evaporated in vacuo. The final compound is obtained after purification by flash chromatography or preparative HPLC. HPLC: Waters XBridge Prep C18 5μm ODB 19mm ID x 100mm L (Part No.186002978). All the methods are using MeCN/H2O gradients. H2O contains either 0.1% TFA or 0.1% NH3.

Synthesis of the compound of the invention and comparative examples

Compound l(the compound of the invention)

Step 1:

[00126] 2-(4-Bromomethyl-phenyl)-4,4,5,5-tetramethyl-[l,3,2]dioxaborolane (leq) and DIPEA

(2 eq) were dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1 -dioxide (2 eq) was added portionwise. The resulting solution was stirred at room temperature for 16h. After this time, the reaction was complete. The solvent was evaporated. The compound was extracted with EtOAc and water, washed with brine and dried over anhyd. MgS O4. Organic layers were filtered and evaporated. The final compound was isolated without further purification.

Step 2: Suzuki coupling

[00127] 4-[4-(4,4,5,5-Tetramethyl-[l,3,2]dioxaborolan-2-yl)-benzyl]-thiomorpholine-l,l-dioxide

(l.leq.) was added to a solution of cyclopropanecarboxylic acid (5-bromo-[l,2,4]triazolo[l,5-a]pyridin-2-yl)-amide in 1 ,4-dioxane/water (4:1). K2CO3 (2 eq.) and PdCl2dppf (0.03 eq.) were added to the solution. The resulting mixture was then heated in an oil bath at 900C for 16h under N2. Water was added and the solution was extracted with ethyl acetate. The organic layers were dried over anhyd. MgSθ4 and evaporated in vacuo. The final compound was obtained after purification by flash chromatography.

[00128] Alternatively, after completion of the reaction, a palladium scavenger such as 1,2-bis(diphenylphosphino)ethane, is added, the reaction mixture is allowed to cooled down and a filtration is performed. The filter cake is reslurried in a suitable solvent (e.g. acetone), the solid is separated by filtration, washed with more acetone, and dried. The resulting solid is resuspended in water, aqueous HCl is added, and after stirring at RT, the resulting solution is filtered on celite (Celpure P300). Aqueous NaOH is then added to the filtrate, and the resulting suspension is stirred at RT, the solid is separated by filtration, washed with water and dried by suction. Finally the cake is re-solubilised in a mixture of THF/H2O, treated with a palladium scavenger (e.g. SMOPEX 234) at 500C, the suspension is filtered, the organic solvents are removed by evaporation, and the resulting slurry is washed with water and methanol, dried and sieved, to obtain the title compound as a free base.

Alternative route to Compound l(the compound of the invention):

Step 1:

[00129] 4-(Hydroxymethyl)phenylboronic acid (l.leq.) was added to a s o luti o n o f cyclopropanecarboxylic acid (5-bromo-[l,2,4]triazolo[l,5-a]pyridin-2-yl)-amide in 1 ,4-dioxane/water (4:1). K2CO3 (2 eq.) and PdCl2dppf (0.03 eq.) were added to the solution. The resulting mixture was then heated in an oil bath at 900C for 16h under N2. Water was added and the solution was extracted with ethyl acetate. The organic layers were dried over anhyd. MgSθ4 and evaporated in vacuo. The resulting mixture was used without further purification.

Step 2:

[00130] To a solution of cyclopropanecarboxylic acid [5-(4-hydroxymethyl-phenyl)- [l,2,4]triazolo[l,5-a]pyridin-2-yl]-amide (1.0 eq) in chloroform was slowly added phosphorus tribromide (1.0 equiv.). The reaction mixture was stirred at room temperature for 20 hours, quenched with ice and water (20 mL) and extracted with dichloromethane. The organic layer was dried over anhyd. MgSθ4, filtered and concentrated to dryness. The resulting white residue was triturated in dichloromethane/diethyl ether 2:1 to afford the expected product as a white solid.

Step 3:

[00131] Cyclopropanecarboxylic acid [5-(4-bromomethyl-phenyl)-[l,2,4]triazolo[l,5-a]pyridin- 2-yl]-amide (leq) and DIPEA (2 eq) were dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1 -dioxide (1.1 eq) was added dropwise. The resulting solution was stirred at room temperature for 16h. After this time, the reaction was complete. The solvent was evaporated. The compound was dissolved in DCM, washed with water and dried over anhyd. MgSO^ Organic layers were filtered and evaporated. The final compound was isolated by column chromatography using EtOAc to afford the desired product.

PATENT

WO 2010010190

WO 2013173506

WO 2013189771

WO 2015117980

WO 2015117981

POLYMORPH

CN 105061420

CN105061420

https://encrypted.google.com/patents/CN105061420A?cl=en

JAK inhibitor N-(5-(4-(1,1-dioxothiomorpholinyl)methyl)phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl)cyclopropanecarboxamide, and methods for preparing the four crystal forms, wherein the four crystal forms respectively are a crystal form H1, a crystal form H2, a crystal form H3 and a crystal form H4,

POLYMORPH

E CRYSTAL

CN 105111206

D CRYSTAL

CN 105111207

H CRYSYAL

CN 105198876

G 

CN 105198877

F CN 105198878

C CN 105198880

POLYMORPH

WO 2016105453

POLYMORPH

POLYMORPH

CN 105669669

The present invention provides a crystal form A, B, D, G and M of N-[5-[4-[(1,1-dioxido-4-thiomorpholinyl)methyl]phenyl][1,2,4]triazolo[1,5-a]pyridin-2-yl]cyclopropanecarboxamide hydrochloride.

PAPER

Future Medicinal Chemistry (2015), 7(2), 203-235.  |  Language: English, Database: CAPLUSA review.  The discovery of the JAK-STAT pathway was a landmark in cell biol.  The identification of these pathways has changed the landscape of treatment of rheumatoid arthritis and other autoimmune diseases.  The two first (unselective) JAK inhibitors have recently been approved by the US FDA for the treatment of myelofibrosis and rheumatoid arthritis and many other JAK inhibitors are currently in clin. development or at the discovery stage.  Research groups have demonstrated the different roles of JAK member and the therapeutic potential of targeting them selectively. ………..

https://www.future-science.com/doi/10.4155/fmc.14.149

PAPER

Journal of Pharmaceutical Sciences (Philadelphia, PA, United States) (2018), 107(6), 1624-1632.

PATENT

US2010/331319 A1, ; Page/Page column 13-14

http://www.google.com/patents/US20100331319

Synthetic Preparation of the Compound of the Invention and Comparative Examples

The compound of the invention and the comparative examples can be produced according to the following scheme.

Figure US20100331319A1-20101230-C00003

wherein Ar represents phenyl-L1-heterocycloalkyl, where L1 is a bond, —CH2— or —CO— and the heterocycloalkyl group is optionally substituted.

General 1.1.1 1-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2)

Figure US20100331319A1-20101230-C00004

To a solution of 2-amino-6-bromopyridine (1) (253.8 g, 1.467 mol) in DCM (2.5 L) cooled to 5° C. is added ethoxycarbonyl isothiocyanate (173.0 mL, 1.467 mol) dropwise over 15 min. The reaction mixture is then allowed to warm to room temp. (20° C.) and stirred for 16 h. Evaporation in vacuo gives a solid which may be collected by filtration, thoroughly washed with petrol (3×600 mL) and air-dried to afford (2). The thiourea may be used as such for the next step without any purification. 1H (400 MHz, CDCl3) δ 12.03 (1H, br s, NH), 8.81 (1H, d, J=7.8 Hz, H-3), 8.15 (1H, br s, NH), 7.60 (1H, t, J=8.0 Hz, H-4), 7.32 (1H, dd, J 7.7 and 0.6 Hz, H-5), 4.31 (2H, q, J 7.1 Hz, CH2), 1.35 (3H, t, J 7.1 Hz, CH3).

1.1.2 5-Bromo-[1,2,4]triazolo[1,5-a]pyridin-2-ylamine (3)

Figure US20100331319A1-20101230-C00005

To a suspension of hydroxylamine hydrochloride (101.8 g, 1.465 mol) in EtOH/MeOH (1:1, 900 mL) is added N,N-diisopropylethylamine (145.3 mL, 0.879 mol) and the mixture is stirred at room temp. (20° C.) for 1 h. 1-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2) (89.0 g, 0.293 mol) is then added and the mixture slowly heated to reflux (Note: bleach scrubber is required to quench H2S evolved). After 3 h at reflux, the mixture is allowed to cool and filtered to collect the precipitated solid. Further product is collected by evaporation in vacuo of the filtrate, addition of H2O (250 mL) and filtration. The combined solids are washed successively with H2O (250 mL), EtOH/MeOH (1:1, 250 mL) and Et2O (250 mL) then dried in vacuo to afford the triazolopyridine derivative (3) as a solid. The compound may be used as such for the next step without any purification. 1H (400 MHz, DMSO-d6) δ 7.43-7.34 (2H, m, 2×aromatic-H), 7.24 (1H, dd, J 6.8 and 1.8 Hz, aromatic-H), 6.30 (2H, br, NH2); m/z 213/215 (1:1, M+H+, 100%).

1.1.3 General Procedure for Mono-Acylation to Afford Intermediate (4)

Figure US20100331319A1-20101230-C00006

To a solution of the 2-amino-triazolopyridine (3) (7.10 g, 33.3 mmol) in dry CH3CN (150 mL) at 5° C. is added Et3N (11.6 mL, 83.3 mmol) followed by cyclopropanecarbonyl chloride (83.3 mmol). The reaction mixture is then allowed to warm to ambient temperature and stirred until all starting material (3) is consumed. If required, further Et3N (4.64 mL, 33.3 mmol) and cyclopropanecarbonyl chloride (33.3 mmol) is added to ensure complete reaction. Following solvent evaporation in vacuo the resultant residue is treated with 7 N methanolic ammonia solution (50 mL) and stirred at ambient temp. (for 1-16 h) to hydrolyse any bis-acylated product. Product isolation is made by removal of volatiles in vacuo followed by trituration with Et2O (50 mL). The solids are collected by filtration, washed with H2O (2×50 mL), acetone (50 mL) and Et2O (50 mL), then dried in vacuo to give the required bromo intermediate (4).

Method A Preparation of Compounds of the Invention Via Suzuki Coupling (5):

An appropriate boronic acid (2 eq.) is added to a solution of bromo intermediate (4) in 1,4-dioxane/water (5:1). K2CO3 (2 eq.) and PdCl2dppf (5%) are added to the solution. The resulting mixture is then heated in a microwave at 140° C. for 30 min (this reaction can also be carried out by traditional heating in an oil bath at 90° C. for 16 h under N2). Water is added and the solution is extracted with ethyl acetate. The organic layers are dried over anhyd. MgSO4 and evaporated in vacuo. The final compound is obtained after purification by flash chromatography or preparative HPLC. HPLC: Waters XBridge Prep C18 5 μm ODB 19 mm ID×100 mm L (Part No. 186002978). All the methods are using MeCN/H2O gradients. H2O contains either 0.1% TFA or 0.1% NH3.

Method B

Figure US20100331319A1-20101230-C00007

B1. 4 4-[2-(Cyclopropanecarbonyl-amino)-[1,2,4]triazolo[1,5-a]pyridin-5-yl]-benzoyl chloride

Figure US20100331319A1-20101230-C00008

2 Drops of DMF are added to a solution of 4-[2-(cyclopropanecarbonyl-amino)-[1,2,4]triazolo[1,5-a]pyridin-5-yl]-benzoic acid (1 eq) obtained by Method A using 4-carboxyphenylboronic acid in DCM under N2 atmosphere. Then oxalyl chloride (2 eq) is added dropwise to this resulting solution (gas release). The mixture is stirred at room temperature for 2 hours. After completion of the reaction by LCMS, the solvent is removed. The crude acid chloride is used without further purification in next step.

B2. Amide Formation (General Method)

Figure US20100331319A1-20101230-C00009

An appropriate amine (1.1 eq) and Et3N (5 eq) are dissolved in DCM under N2 atmosphere and cooled at 0° C. The acid chloride (B1, 1 eq) dissolved in DCM is added dropwise to this solution. The reaction is stirred at room temperature for 16 h. After this time, reaction is complete. The compound is extracted with EtOAc and water, washed with brine and dried over anhyd. MgSO4. Organic layers are filtered and evaporated. The final compound is isolated by preparative HPLC. Preparative HPLC: Waters XBridge Prep C18 5 μm ODB 19 mm ID×100 mm L (Part No. 186002978). All the methods are using MeCN/H2O gradients. H2O contains either 0.1% TFA or 0.1% NH3.

…

Synthesis of the Compound of the Invention and Comparative Examples Compound 1 (the Compound of the Invention) Step 1:

Figure US20100331319A1-20101230-C00014

2-(4-Bromomethyl-phenyl)-4,4,5,5-tetramethyl-[1,3,2]dioxaborolane (1 eq) and DIPEA (2 eq) were dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1-dioxide (2 eq) was added portionwise. The resulting solution was stirred at room temperature for 16 h. After this time, the reaction was complete. The solvent was evaporated. The compound was extracted with EtOAc and water, washed with brine and dried over anhyd. MgSO4. Organic layers were filtered and evaporated. The final compound was isolated without further purification.

STEP 2: Suzuki coupling

Figure US20100331319A1-20101230-C00015

4-[4-(4,4,5,5-Tetramethyl-[1,3,2]dioxaborolan-2-yl)-benzyl]-thiomorpholine-1,1-dioxide (1.1 eq.) was added to a solution of cyclopropanecarboxylic acid (5-bromo-[1,2,4]triazolo[1,5-a]pyridin-2-yl)-amide in 1,4-dioxane/water (4:1). K2CO3 (2 eq.) and PdCl2dppf (0.03 eq.) were added to the solution. The resulting mixture was then heated in an oil bath at 90° C. for 16 h under N2. Water was added and the solution was extracted with ethyl acetate. The organic layers were dried over anhyd. MgSO4 and evaporated in vacuo. The final compound was obtained after purification by flash chromatography.

Alternatively, after completion of the reaction, a palladium scavenger such as 1,2-bis(diphenylphosphino)ethane, is added, the reaction mixture is allowed to cooled down and a filtration is performed. The filter cake is reslurried in a suitable solvent (e.g. acetone), the solid is separated by filtration, washed with more acetone, and dried. The resulting solid is resuspended in water, aqueous HCl is added, and after stirring at RT, the resulting solution is filtered on celite (Celpure P300). Aqueous NaOH is then added to the filtrate, and the resulting suspension is stirred at RT, the solid is separated by filtration, washed with water and dried by suction. Finally the cake is re-solubilised in a mixture of THF/H2O, treated with a palladium scavenger (e.g. SMOPEX 234) at 50° C., the suspension is filtered, the organic solvents are removed by evaporation, and the resulting slurry is washed with water and methanol, dried and sieved, to obtain the title compound as a free base.

Alternative Route to Compound 1 (the Compound of the Invention): Step 1:

Figure US20100331319A1-20101230-C00016

4-(Hydroxymethyl)phenylboronic acid (1.1 eq.) was added to a solution of cyclopropanecarboxylic acid (5-bromo-[1,2,4]triazolo[1,5-a]pyridin-2-yl)-amide in 1,4-dioxane/water (4:1). K2CO3 (2 eq.) and PdCl2dppf (0.03 eq.) were added to the solution. The resulting mixture was then heated in an oil bath at 90° C. for 16 h under N2. Water was added and the solution was extracted with ethyl acetate. The organic layers were dried over anhyd. MgSO4 and evaporated in vacuo. The resulting mixture was used without further purification.

Step 2:

Figure US20100331319A1-20101230-C00017

To a solution of cyclopropanecarboxylic acid [5-(4-hydroxymethyl-phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl]-amide (1.0 eq) in chloroform was slowly added phosphorus tribromide (1.0 equiv.). The reaction mixture was stirred at room temperature for 20 hours, quenched with ice and water (20 mL) and extracted with dichloromethane. The organic layer was dried over anhyd. MgSO4, filtered and concentrated to dryness. The resulting white residue was triturated in dichloromethane/diethyl ether 2:1 to afford the expected product as a white solid.

Step 3:

Figure US20100331319A1-20101230-C00018

Cyclopropanecarboxylic acid [5-(4-bromomethyl-phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl]-amide (1 eq) and DIPEA (2 eq) were dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1-dioxide (1.1 eq) was added dropwise. The resulting solution was stirred at room temperature for 16 h. After this time, the reaction was complete. The solvent was evaporated. The compound was dissolved in DCM, washed with water and dried over anhyd. MgSO4. Organic layers were filtered and evaporated. The final compound was isolated by column chromatography using EtOAc to afford the desired product.

…………………….

PATENT

WO 2015117981

Novel salts and pharmaceutical compositions thereof for the treatment of inflammatory disorders

Also claims a method for preparing filgotinib hydrochloride trihydrate. The present filing forms a pair with this week’s filing, WO2015117980, claiming a tablet composition comprising filgotinib hydrochloride.

The compound cyclopropanecarboxylic acid {5-[4-(l,l-dioxo-thiomorpholin-4-ylmethyl)-phenyl]-[l,2,4]triazolo[l,5-a]pyridin-2-yl -amide (Compound 1), which has the chemical structure:

is disclosed in our earlier application WO 2010/149769 (Menet C. J., 2010) as being an inhibitor of JAK and as being useful in the treatment of inflammatory conditions, autoimmune diseases, proliferative diseases, allergy, transplant rejection, diseases involving impairment of cartilage turnover, congenital cartilage malformations, and/or diseases associated with hypersecretion of IL6 or interferons. Hereafter this compound is named Compound 1. The data presented in WO 2010/149769 demonstrate that despite similar in vitro activities, Compound 1 has unexpectedly high in vivo potency compared with structurally similar compounds.

Example 1. Preparation of Compound 1

1.1. Route 1

1.1.1. 4-[4-(4,4,5,5-Tetramethyl-[l,3,2]dioxaborolan-2-yl)-benzyl]-thiomorpholine-l,l-dioxide

[00205] 2-(4-Bromomethyl-phenyl)-4,4,5,5-tetramethyl-[l,3,2]dioxaborolane (1 eq) and DIPEA (2 eq) are dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1 -dioxide (2 eq) is added portionwise. The resulting solution is stirred at room temperature for 16h. After this time, the reaction is complete. The solvent is evaporated. The compound is extracted with EtOAc and water, washed with brine and dried over anhydrous MgSO i. Organic layers are filtered and evaporated. The final compound is isolated without further purification.

1.1.2. Cyclopropanecarboxylic acid (5-bromo-[l,2,4]triazolo[l,5-a]pyridin-2-yl)-amide

1.1.2.1. Step i): l-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea

[00206] To a solution of 2-amino-6-bromopyridine (1) (253.8 g, 1.467 mol) in DCM (2.5 L) cooled to 5°C is added ethoxycarbonyl isothiocyanate (173.0 mL, 1.467 mol) dropwise over 15 min. The reaction

mixture is then allowed to warm to room temp. (20 °C) and stirred for 16 h. Evaporation in vacuo gives a solid which may be collected by filtration, thoroughly washed with petrol (3 x 600 niL) and air-dried to afford the desired product. The thiourea may be used as such for the next step without any purification. lH (400 MHz, CDC13) δ 12.03 (1H, br s), 8.81 (1H, d), 8.15 (1H, br s), 7.60 (1H, t), 7.32 (1H, dd), 4.31 (2H, q), 1.35 (3H, t).

1.1.2.2. Step ii): 5-Bromo-[l,2,4]triazolo[l,5-a]pyridin-2-ylamine

[00207] To a suspension of hydroxylamine hydrochloride (101.8 g, 1.465 mol) in EtOH/MeOH (1 : 1, 900 mL) is added NN-diisopropylethylamine (145.3 mL, 0.879 mol) and the mixture is stirred at room temp. (20 °C) for 1 h. l-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2) (89.0 g, 0.293 mol) is then added and the mixture slowly heated to reflux (Note: bleach scrubber is required to quench H2S evolved). After 3h at reflux, the mixture is allowed to cool and filtered to collect the precipitated solid. Further product is collected by evaporation in vacuo of the filtrate, addition of H20 (250 mL) and filtration. The combined solids are washed successively with H20 (250 mL), EtOH/MeOH (1 : 1, 250 mL) and Et20 (250 mL) then dried in vacuo to afford the triazolopyridine derivative (3) as a solid. The compound may be used as such for the next step without any purification. lH (400 MHz, DMSO-i¼) δ 7.43-7.34 (2H, m, 2 x aromatic-H), 7.24 (1H, dd, J 6.8 and 1.8 Hz, aromatic-H), 6.30 (2H, br, NH2); m/z 213/215 (1 : 1, M+H+, 100%).

1.1.2.3. Step Hi): Cyclopropanecarboxylic acid (5-bromo-[l ,2,4]triazolo[l ,5-a]pyridin-2-yl)-amide

[00208] To a solution of the 2-amino-triazolopyridine obtained in the previous step (7.10 g, 33.3 mmol) in dry MeCN (150 mL) at 5°C is added Et3N (11.6 mL, 83.3 mmol) followed by cyclopropanecarbonyl chloride (83.3 mmol). The reaction mixture is then allowed to warm to ambient temperature and stirred until all starting material is consumed. If required, further Et3N (4.64 mL, 33.3 mmol) and cyclopropanecarbonyl chloride (33.3 mmol) is added to ensure complete reaction. Following solvent evaporation in vacuo the resultant residue is treated with 7 N methanolic ammonia solution (50 mL) and stirred at ambient temp, (for 1-16 h) to hydro lyse any bis-acylated product. Product isolation is made by removal of volatiles in vacuo followed by trituration with Et20 (50 mL). The solids are collected by filtration, washed with H20 (2x50mL), acetone (50 mL) and Et20 (50 mL), then dried in vacuo to give the desired compound.

1.1.3. Compound 1

[00209] 4-[4-(4,4,5,5-Tetramethyl-[l ,3,2]dioxaborolan-2-yl)-benzyl] hiomoφholine , l -dioxide (l . l eq.) is added to a solution of cyclopropanecarboxylic acid (5-bromo-[l ,2,4]triazolo[l ,5-a]pyridin-2-yl)-amide in 1 ,4-dioxane/water (4: 1). K2CO3 (2 eq.) and PdC^dppf (0.03 eq.) are added to the solution. The resulting mixture is then heated in an oil bath at 90°C for 16h under N2. Water is added and the solution is extracted with ethyl acetate. The organic layers are dried over anhydrous MgS04 and evaporated in vacuo.

[00210] The final compound is obtained after purification by flash chromatography.

[00211] Alternatively, after completion of the reaction, a palladium scavenger such as 1 ,2-bis(diphenylphosphino)ethane, is added, the reaction mixture is allowed to cool down and a filtration is performed. The filter cake is reslurried in a suitable solvent (e.g. acetone), the solid is separated by filtration, washed with more acetone, and dried. The resulting solid is resuspended in water, aqueous HC1 is added, and after stirring at room temperature, the resulting solution is filtered on celite (Celpure P300). Aqueous NaOH is then added to the filtrate, and the resulting suspension is stirred at room temperature, the solid is separated by filtration, washed with water and dried by suction. Finally the cake is re-solubilised in a mixture of THF/H20, treated with a palladium scavenger (e.g. SMOPEX 234) at 50°C, the suspension is filtered, the organic solvents are removed by evaporation, and the resulting slurry is washed with water and methanol, dried and sieved, to obtain the desired compound as a free base.

1.2. Route 2

1.2.1. Step 1: cyclopropanecarboxylic acid [5-(4-hydroxymethyl-phenyl)-[l,2, 4]triazolo[l, 5- a] pyridin-2-yl] -amide

[00212] 4-(Hydroxymethyl)phenylboronic acid (l . l eq.) is added to a solution of cyclopropanecarboxylic acid (5-bromo-[l ,2,4]triazolo[l ,5-a]pyridin-2-yl)-amide in 1 ,4-dioxane/water

(4:1). K2CO3 (2 eq.) and PdC^dppf (0.03 eq.) are added to the solution. The resulting mixture is then heated in an oil bath at 90°C for 16h under N2. Water is added and the solution is extracted with ethyl acetate. The organic layers are dried over anhydrous MgS04 and evaporated in vacuo. The resulting mixture is used without further purification.

1.2.2. Step 2: Cyclopropanecarboxylic acid [5-(4-bromomethyl-phenyl)-[l,2,4]triazolo[l,5- a Jpyridin-2-ylJ -amide

[00213] To a solution of cyclopropanecarboxylic acid [5-(4-hydroxymethyl-phenyl)-[l,2,4]triazolo[l,5-a]pyridin-2-yl] -amide (1.0 eq) in chloroform is slowly added phosphorus tribromide (1.0 eq.). The reaction mixture is stirred at room temperature for 20 h, quenched with ice and water (20 mL) and extracted with dichloromethane. The organic layer is dried over anhydrous MgSO i, filtered and concentrated to dryness. The resulting white residue is triturated in dichloromethane/diethyl ether 2:1 to afford the desired product.

1.2.3. Step 3:

[00214] Cyclopropanecarboxylic acid [5-(4-bromomethyl-phenyl)-[l,2,4]triazolo[l,5-a]pyridin-2-yl]-amide (l eq) and DIPEA (2 eq) are dissolved in DCM/MeOH (5: 1 v:v) under N2 and thiomorpho line 1,1-dioxide (1.1 eq) is added dropwise. The resulting solution is stirred at room temperature for 16h. After this time, the reaction is complete. The solvent is evaporated. The compound is dissolved in DCM, washed with water and dried over anhydrous MgSO i. Organic layers are filtered and evaporated. The final compound is isolated by column chromatography using EtOAc to afford the desired product.

…………………

PATENT

http://www.google.co.in/patents/WO2013189771A1?cl=en

Example 1. Synthesis of the compounds

1.1. Route 1

1.1.1. Synthesis of 5-Bromo-[l,2,4]triazolo[l,5-a]pyridin-2-ylamine (Intermediate 3)

Figure imgf000030_0001

led to 5 °C was added ethoxycarbonyl isothiocyanate (173.0 mL, 1.467 mol) dropwise over 15 min. The reaction mixture was then allowed to warm to room temp. (20 °C) and stirred for 16 h. Evaporation in vacuo gave a solid which was collected by filtration, thoroughly washed with petrol (3×600 mL) and air-dried to afford (2). The thiourea was used as such in the next step without any purification.

[00157] lH (400 MHz, CDC13) δ 12.03 (IH, br s, NH), 8.81 (IH, d, J 7.8 Hz, H-3), 8.15 (IH, br s, NH), 7.60 (IH, t, J 8.0 Hz, H-4), 7.32 (IH, dd, J 7.7 and 0.6 Hz, H-5), 4.31 (2H, q, J 7.1 Hz, CH2), 1.35 (3H, t, J 7.1 Hz, CH3).

1.1.1.2. 5-Bromo-f 1,2, 4]triazolo[ 1 ,5-a] pyridin-2-ylamine (3)

[00158] To a suspension of hydroxylamine hydrochloride (101.8 g, 1.465 mol) in EtOH/MeOH (1 : 1, 900 mL) was added NN-diisopropylethylamine (145.3 mL, 0.879 mol) and the mixture was stirred at room temp. (20 °C) for 1 h. l-(6-Bromo-pyridin-2-yl)-3-carboethoxy-thiourea (2) (89.0 g, 0.293 mol) was then added and the mixture slowly heated to reflux (Note: bleach scrubber was required to quench H2S evolved). After 3 h at reflux, the mixture was allowed to cool and filtered to collect the precipitated solid. Further product was collected by evaporation in vacuo of the filtrate, addition of H20 (250 mL) and filtration. The combined solids were washed successively with H20 (250 mL), EtOH/MeOH (1 : 1, 250 mL) and Et20 (250 mL) then dried in vacuo to afford the triazolopyridine derivative (3) as a solid. The compound was used as such in the next step without any purification.

[00159] lH (400 MHz, DMSO-i¼) δ 7.43-7.34 (2H, m, 2 x aromatic-H), 7.24 (1H, dd, J 6.8 and 1.8 Hz, aromatic-H), 6.30 (2H, br, NH2); m/z 213/215 (1 : 1, M+H+, 100%).

1.1.2. Synthesis of 4-[ 4-(4, 4, 5, 5-Tetramethyl-f 1, 3,2] ‘ dioxaborolan-2-yl) -benzyl] ‘- thiomor holine- 1, 1 -dioxide (Intermediate 4)

Figure imgf000031_0001

[00160] 2-(4-Bromomethyl-phenyl)-4,4,5,5-tetramethyl-[l,3,2]dioxaborolane (1 eq) and DIPEA (2 eq) were dissolved in DCM/MeOH (5:1 v:v) under N2 and thiomorpholine 1,1 -dioxide (2 eq) was added portion wise. The resulting solution was stirred at room temperature for 16h. After this time, the reaction was complete. The solvent was evaporated. The compound was extracted with EtOAc and water, washed with brine and dried over anhydrous MgSO i. Organic layers were filtered and evaporated. The final compound was isolated without further purification.

1.1.3. Synthesis of 5-[4-(l, l-Dioxothiomorpholin-4-ylmethyl)-phenyl]-[l,2,4]triazolo[l,5- a ridin-2-ylamine (Formula I)

Figure imgf000031_0002

[00161] 4-[4-(4,4,5,5-Tetramethyl-[l,3,2]dioxaborolan-2-yl)-benzyl]-thiomorpholine-l,l-dioxide (l .leq.) was added to a solution of 5-bromo-[l,2,4]triazolo[l,5-a]pyrid in-2-ylamine (4: 1). K2CO3 (2 eq.) and PdC^dppf (0.03 eq.) were added to the solution. The resulting mixture was then heated in an oil bath at 90°C for 16h under N2. Water was added and the solution was extracted with ethyl acetate. The organic layers were dried over anhydrous MgSC>4 and evaporated in vacuo. The final compound was obtained after purification by flash chromatography.

[00162] lH (400 MHz, CDC13) δ 7.94-7.92 (d, 2H), 7.52-7.48 (m, 3H), 7.37-7.34 (m, 1H), 7.02-7.00 (m, 1H), 6.00 (d, 2H), 3.76 (d, 2H), 3.15-3.13 (m, 4H), 2.93-2.91 (m, 4H).

[00163] m/z 358.2 (M+H+, 100%). 1.2. Route 2

1.2.1. Cyclopropanecarboxylic acid {5-[4-(l, l-dioxo-thiomorpholin-4-ylmethyl)-phenylJ- [l,2,4]triazolo[l,5-a]pyridin-2-yl}-amide (Formula II)

[00164] The compound according to Formula II may be synthesized according to the procedure described in WO 2010/149769.

1.2.2. Synthesis of 5-[4-(l, l-Dioxothiomorpholin-4-ylmethyl)-phenyl]-[l,2,4]triazolo[l,5- aJpyridin-2-ylamine (Formula I)

[00165] The compound according to Formula I can also be produced by hydrolysis of the compound accor ing to Formula II:

Figure imgf000032_0001

[00166] Hydrochloric acid 30% aq (12.06 kg; 3.9 rel. volumes) was added to a slurry of the compound according to Formula II (3.45 kg; 1.0 equiv.) in demineralized water (10.0 kg; 3.0 rel. volumes). Subsequently, a line rinse was performed with demineralized water (3.4 kg; 1.0 rel. volumes). The reaction mixture was heated to 80±5°C for 14.5 h. After completion of the reaction (conversion > 99%>), the reaction mixture was cooled to 20±5°C. The reaction mixture was diluted with demineralized water (6.8 kg; 2.0 rel. volumes) and sodium hydroxide 33%> aq (9.52 kg; 3.7 rel volumes) was dosed at such a rate that the temperature of the reactor contents remained below 35°C. An additional amount of sodium hydroxide 33%> aq (2.55 kg; 1.0 rel. volumes) was needed to get the pH > 10. The product was filtered off, washed twice with demineralized water (1.5 rel. volumes) and dried under vacuum for 1 h, thus yielding the crude compound according to Formula I.

[00167] The crude compound according to Formula I (5.70 kg) was re-slurried in demineralized water (23.0 kg; 8.5 rel. volumes). Hydrochloric acid 30%> aq (1.65 kg; 0.7 rel. volumes) and demineralized water (4.3 kg; 1.6 rel. volumes) were added and the reaction mixture was stirred at 20±5°C for 45 min. As the compound according to Formula I was not dissolved completely, the reaction mixture was stirred at 45±5°C for 1 h. The reaction mixture was filtered and the residue was washed with demineralized water (2.0 kg 0.75 rel. volumes). Sodium hydroxide 33%> aq (1.12 kg; 0.6 rel volumes) was added to the filtrate. An additional amount of sodium hydroxide 33%> aq (1.01 kg) was needed to get the pH > 10. The resulting reaction mixture was stirred at 20±5°C for about 3 h. The product was filtered off, washed twice with demineralized water (4.1 kg; 1.5 rel. volumes), and twice with methyl tert-butyl ether (MTBE; 3.0 kg; 1.5 rel. volumes) and dried under vacuum for 15.5 h on the filter. The product was further dried in a vacuum oven at 40±5°C for 202 h, thus affording the desired compound according to Formula I.

Update

WO-2016179207

Scheme 1: General S nthesis of Compounds of Formula I or A

Formula A

Scheme 7.

(16) (17) (18)

(18a): R3a=R3b=R2a=R (18b): R3a=R3b=D; R2a 18c): R3a=R3b=H; R2a

References

  1.  Namour, Florence; Diderichsen, Paul Matthias; Cox, Eugène; Vayssière, Béatrice; Van der Aa, Annegret; Tasset, Chantal; Van’t Klooster, Gerben (2015-02-14). “Pharmacokinetics and Pharmacokinetic/Pharmacodynamic Modeling of Filgotinib (GLPG0634), a Selective JAK1 Inhibitor, in Support of Phase IIB Dose Selection”. Clin Pharmacokinet. Epub ahead of print.doi:10.1007/s40262-015-0240-z.
  2.  Van Rompaey, L; Galien, R; Van der Aar, E; Clement-Lacroix, P; Van der Aar, E; Nelles, L; Smets, B; Lepescheux, L; Cristophe, T; Conrath, K; Vandeghinste, N; Vayssiere, B; De Vos, S; Fletcher, S; Brys, R; Van’t Klooster, G; Feyen, J; Menet, C (2013-10-01). “Preclinical characterization of GLPG0634, a selective inhibitor of JAK1 for the treatment of inflammatory diseases”. J Immunol. 191(7). doi:10.4049/jimmunol.1201348.
  3.  http://acrabstracts.org/abstracts/phase-1-and-phase-2-data-confirm-that-glpg0634-a-selective-jak1-inhibitor-has-a-low-potential-for-drug-drug-interactions/
  4.  “Galapagos’ GLPG0634 shows excellent efficacy and safety in rheumatoid arthritis Phase II study” (PDF) (Press release). Retrieved 2015-02-26.
  5.  “Galapagos reports that the last patient in DARWIN 1 has completed 12 weeks of treatment” (PDF) (Press release). Retrieved 2015-02-26.
  6.  “Galapagos completes recruitment for Darwin 1 study with GLPG0634 (filgotinib) in RA”. EuroInvestor. Retrieved 2015-02-26.
  7.  NASDAQ OMX Corporate Solutions. “Galapagos completes recruitment for Darwin 2 monotherapy study with GLPG0634 (filgotinib) in RA”. Yahoo Finance. Retrieved 2015-02-26.
US8551980 Nov 17, 2010 Oct 8, 2013 Bayer Intellectual Property Gmbh Substituted triazolopyridines
US8796457 Jun 25, 2010 Aug 5, 2014 Galapagos Nv Compound useful for the treatment of degenerative and inflammatory diseases
Filgotinib
Filgotinib.png
Systematic (IUPAC) name
N-[5-[4-[(1,1-dioxo-1,4-thiazinan-4-yl)methyl]phenyl]-[1,2,4]triazolo[1,5-a]pyridin-2-yl]cyclopropanecarboxamide
Clinical data
Routes of
administration
Oral
Pharmacokinetic data
Biological half-life 6 hours[1]
Identifiers
CAS Registry Number 1206161-97-8 Yes
ATC code L01XE18
IUPHAR/BPS 7913
ChemSpider 28189566 Yes
UNII 3XVL385Q0M Yes
ChEMBL CHEMBL3301607 
Chemical data
Formula C21H23N5O3S
Molecular mass 425.50402 g/mol
Patent Submitted Granted
Compound useful for the treatment of degenerative and inflammatory diseases [US8088764] 2010-12-30 2012-01-03
NOVEL COMPOUNDS USEFUL FOR THE TREATMENT OF DEGENERATIVE AND INFLAMMATORY DISEASES [US2011190260] 2011-08-04

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Anthony Melvin Crasto Dr.

 amcrasto@gmail.com

09b37-misc2b027LIONEL MY SON

He was only in first standard in school when I was hit by a deadly one in a million spine stroke called acute transverse mylitis, it made me 90% paralysed and bound to a wheel chair, Now I keep him as my source of inspiration and helping millions, thanks to millions of my readers who keep me going and help me to keep my son happy

सुकून उतना ही देना प्रभू, जितने से

जिंदगी चल जाये।

औकात बस इतनी देना,

कि औरों का भला हो जाये।

Read all about Organic Spectroscopy on ORGANIC SPECTROSCOPY INTERNATIONAL  

/////////Galapagos,  GLPG0634, Filgotinib, PHASE 2, orphan drug designation, PHASE 3,  Crohn’s disease, Rheumatoid arthritis, Ulceraticolitis

ve SMILES code: O=C(C1CC1)NC2=NN3C(C4=CC=C(CN5CCS(CC5)(=O)=O)C=C4)=CC=CC3=N2

SD-809, Deutetrabenazine


SD-809,  Deutetrabenazine

  • Tetrabenazine-d6

(3RS,11Brs)-9,10-di((2H3)methoxy)-3-(2-methylpropyl)-1,3,4,6,7,11b-hexahydro-2H-benzo(a)quinolizin-2-one

2H-​Benzo[a]​quinolizin-​2-​one, 1,​3,​4,​6,​7,​11b-​hexahydro-​9,​10-​di(methoxy-​d3)​-​3-​(2-​methylpropyl)​-​, (3R,​11bR)​-​rel–

2H-Benzo(a)quinolizin-2-one, 1,3,4,6,7,11b-hexahydro-9,10-di(methoxy-d3)-3-(2-methylpropyl)-, (3R,11bR)-rel-

2H-Benzo(a)quinolizin-2-one, 1,3,4,6,7,11b-hexahydro-9,10-di(methoxy-d3)-3-(2-methylpropyl)-, (3R,11bR)-rel-

(RR,SS)-1,3,4,6,7,11b-Hexahydro-9,10-di(methoxy-d3)-3-(2-methylpropyl)-2H-benzo[a]quinolizin-2-one

(3RS,11Brs)-9,10-di((2H3)methoxy)-3-(2-methylpropyl)-1,3,4,6,7,11b-hexahydro-2H-benzo(a)quinolizin-2-one
Treatment of Chorea Associated with Huntington Disease

MF C19-H21-D6-N-O3

  • C19-H27-N-O3
Molecular Weight, 323.4629
CAS 1392826-25-3
UNII P341G6W9NB
Chemistry Review(s) (PDF) fda approved 2017

Deutetrabenazine

TEVA

Deutetrabenazine.svg

Image result for deutetrabenazineImage result for deutetrabenazineImage result for deutetrabenazine

LINK……………https://newdrugapprovals.org/2015/08/15/sd-809-deutetrabenazine-nda-submitted-by-teva/

Austedo FDA 4/3/2017 For the treatment of chorea associated with Huntington’s disease
Drug Trials Snapshot   Chemistry Review(s) (PDF)

STR1STR2str3


SD-809 was granted Orphan Drug Designation for the treatment of HD by the FDA in November 2014 and became part of Teva’s CNS portfolio with the acquisition of Auspex Pharmaceuticals in May 2015.

Teva announced that the New Drug Application (NDA) for SD-809 (deutetrabenazine) has been accepted by the U.S. Food and Drug Administration (FDA) for the treatment of chorea associated with Huntington disease (HD), a rare and fatal neurodegenerative disorder caused by the progressive breakdown of nerve cells in the brain that affects about five to seven people per 100,000 in western countries, according to the World Health Organization.

(3RS,11Brs)-9,10-di((2H3)methoxy)-3-(2-methylpropyl)-1,3,4,6,7,11b-hexahydro-2H-benzo(a)quinolizin-2-one.png

…………………….

Patent for preparing tetrabenazine

http://www.google.com/patents/WO2012081031A1?cl=en

Chemically tetrabenazine is cis rac -1, 3, 4, 6, 7, 1 lb-hexahydro-9, 10-dimethoxy-3-(2- methylpropyl)-2Hbenzo[a]quinolizin-2-one and it is represented by compound of structural formula I.

Formula 1

The proprietary name of tetrabenazine is Xenazine and is marketed by Biovail Americas. Xenazine is indicated for the treatment of chorea associated with Huntington’s disease. U.S. patent no. 2,830,993 discloses a process for the preparation of tetrabenazine compound of structural formula I wherein 1 -carbethoxymethyl-6, 7-dimethoxy-l , 2, 3, 4- tetrahydroisoquinoline compound of structural formula IV is being reacted with mono- isobutylmalonic acid dimethyl ester compound of structural formula V and paraformaldehyde in methanol solvent to get l-carbethoxymethyl-2 (2, 2-dicarbomethoxy-4-methyl-n-pentyl)-6, 7- dimethoxy-1, 2, 3, 4-tetrahydroisoquinoline compound of structural formula VI. The 1- carbethoxymethyl-2(2,2-dicarbomethoxy-4-methyl-n-pentyl)-6,7-dimethoxy-l ,2,3,4- tetrahydroisoquinoline compound of structural formula VI is subjected to Dieckmann cyclization , hydrolysis and decarboxylation to get tetrabenazine compound of structural formula I, which is recrystallized from di-isopropyl ether solvent.

Formula I

Scheme I

U. S. patent no. 4,678,792 discloses a process for the preparation of 6, 7-dimethoxy-3, 4- dihydroisoquinoline compound of structural formula VII wherein 2-(3, 4-dimethoxyphenyl)- ethylamine compound of structural formula II is being reacted with chloral hydrate at 120°C to get N-formyl-2-(3, 4-dimethoxyphenyl)-ethylamine compound of structural formula III. The N- formyl-2-(3, 4-dimethoxyphenyl)-ethylamine compound of structural formula III is further reacted with polyphosphoric acid to get 6, 7-dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII. The 6, 7-dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII is being used as an intermediate for the preparation of tetrabenazine compound of structural formula I.

Formula III

Formula II

Polyphosphoric acid

Formula VII

Scheme II

Bull. Korean Chem. Soc. 2002 Volume (23). No. l , page no. 149 discloses N-formylation of various amines and alcohols with formic acid in toluene.

U.S. patent publication no. 2010/0130480 discloses a process for the preparation of 6, 7- dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII by reacting 2-(3, 4- dimethoxyphenyl)-ethylamine compound of structural formula II with hexamethylenetetramine in presence of acetic acid or trifluoroacetic acid.

Hexamethylenetetramine

Formula II Formula VII

U.S. patent publication no. 2008/0167337 discloses a process for the preparation of tetrabenazine compound of structural formula I wherein 6, 7-dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII is reacted with 3-dimethylaminomethyl-5-methyl-hexan-2-one methiodide compound of structural formula VIII to get crude tetrabenazine compound. The crude tetrabenazine compound was purified by employing flash column chromatography technique and

Formula VIII Formula I

The prior-art processes for preparing N-formyl-2-(3, 4-dimethoxyphenyl)-ethylamine compound of structural formula III produces below mentioned compound of structural formula XVII, XVIII, XIX, XX, XXI and XXII as a by-product of the reaction due to the demethylation and formylation of resulting hydroxy compounds.

Formula XX Formula XXI Formula XXII

The compounds of structural formula XVII, XVIII, XIX, XX, XXI and XXII are being carry- forwarded into the further steps of reactions of preparing tetrabenazine compound of structural formula I and therefore there is a need in the art to develop an improved process of preparing 6, 7-dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII, which obviates the prior-art problems. Accordingly there is provided a process of preparing tetrabenazine compound of structural formula I wherein 6, 7-dimethoxy-3, 4-dihydroisoquinoline compound of structural formula VII is being formed without the formation of above mentioned compounds of structural formula XVII, XVIII, XIX, XX, XXI and XXII.

EXAMPLE: PROCESS FOR THE PREPARATION OF SUBSTANTIAL PURE CRYSTALLINE FORM A OF TETRABENAZINE

Stage A: Process for the preparation of 6, 7-dimethoxy-3, 4-dihydroisoquinoIine

Step 1 : Process for the preparation of N-formyl-2-(3, 4-dimethoxyphenyl)-ethylamine

A solution of 2-(3, 4-dimethoxyphenyl)-ethylamine (500gm) in toluene (2000ml) was added formic acid (150gm) at 25°C, the resulting reaction mixture was diluted with toluene (500ml) and heated up to 45°C. The reaction mixture was maintained at 40-45°C for 5 hours and then the resulting reaction mixture was concentrated under reduced pressure at 50°C to get the title compound

Yield: 570gm

Purity: 99.98% (By HPLC)

Step 2: Process for the preparation of 6, 7-dimethoxy-3, 4-dihydroisoquinoline

A solution of N-formyl-2-(3, 4-dimethoxyphenyl)-ethylamine (250gm) obtained from step 1 in toluene (500ml) and polyphosphoric acid (50gm) was heated at 110°C for 5 hours. The resulting reaction mixture was cooled to 50°C, quenched with water (500ml) and pH of the resulting solution was adjusted to about 8.3 with aqueous solution of sodium hydroxide [sodium hydroxide (690gm) + water (690ml)]. The resulting reaction mass was extracted by ethyl acetate (2 1250ml), dried over anhydrous sodium sulfate (50gm) and concentrated under reduced pressure to get 6, 7-dimethoxy-3, 4-dihydroisoquinoline (190gm).

Yield: 215gm

Purity: 99.67% (By HPLC)

Stage B: Process for the preparation of 3-((dimethylamino) methyi)-5-methylhexan-2-one methiodide

Step 1 : Process for the preparation of 3-((dimethylamino) methyl)-5-methylhexan-2-one Dimethylamine hydrochloride (180gm) and paraformaldehyde (lOOgm) were added to a solution of 5-methylhexan-2-one (900ml) in methanol (1600ml). The resulting reaction mass was heated at reflux for 12 hours, and then the pH was adjusted to about 8.75 with aqueous solution of sodium hydroxide [sodium hydroxide(90gm) + water (900ml)] at 25 °C. The resulting reaction solution was extracted by toluene (2x1234ml). The organic layer was dried over anhydrous sodium sulfate (50gm) and concentrated under reduced pressure to get title compound.

Yield: 900gm

Purity: 99.80% (By HPLC)

Step 2: Process for the preparation of 3-((dimethylamino) methyl)-5-methylhexan-2-one methiodide

Methyl iodide (323gm) was added dropwise to a solution of 3-((dimethylamino) methyl)-5- methylhexan-2-one (195gm) obtained from step 1 , in ethyl acetate (1650ml) at 25-30°C in 30 minutes. The resulting reaction mixture was stirred at 25 °C for 12 hours and then the resulting solids were filtered, washed with water (200ml) and suck-dried to get wet compound (400gm). The wet compound was slurried with water (1000ml) at 25°C for 1 hour and then it was again filtered, washed with water (200ml) and dried at 45-50°C to get title compound

Yield: 300gm

Purity: 99.86% (By HPLC)

Stage C: Preparation of substantial pure crystalline form A of Tetrabenazine

3-((Dimethylamino) methyl)-5-methylhexan-2-one methiodide (80gm) was added to the solution of 6, 7-dimethoxy-3, 4-dihydroisoquinoline (40gm) in isopropanol (288ml) at 25°C and the resulting reaction mass was heated at 40-45°C for 15 hours. The resulting insoluble material was filtered, washed with isopropanol (80ml) and filtrate was concentrated under reduced pressure up to the 150ml reaction volume. The reaction solution was diluted with methylene dichloride (1200ml) and water (1000ml) and pH was adjusted to 8.5 with sodium hydroxide solution [10%, 100ml]. The organic layer was separated, washed with water (3 x 1000ml) and concentrated under reduced pressure to obtain residue. The residue was dissolved in methanol (300ml) at 50°C, and resulting solution was treated with an activated carbon (20gm) at 50-60°C for 30minutes and then it was filtered and filtrate was further stirred at 20-25°C for 2 hours. The resulting solids were filtered, washed with methanol (150ml), dried at 50-55°C for 8 hours. The resulting solids were milled, sifted through 40 mesh sieve and micronized.

Yield: 65gm

Purity: 99.96% (By HPLC)

………………………

PAPER

Org. Lett., 2011, 13 (24), pp 6500–6503
DOI: 10.1021/ol202792q
Abstract Image

A concise synthesis of tetrabenazine and dihydrotetrabenazine is described. The key feature of this synthesis is the intramolecular aza-Prins-type cyclization of an amino allylsilane via oxidative C–H activation.

T1 T2 T3 T4

http://www.hgxb.com.cn/EN/abstract/abstract12047.shtml

……………
PAPER

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126153/

An external file that holds a picture, illustration, etc. Object name is nihms279693f2.jpg

The TBZ (4) for these reactions was prepared by reacting 3,4-dihydro-6,7-dimethoxyisoquinoline (3) and the Mannich base (2) as shown in Scheme 1.14 The α,β-unsaturated TBZ (5), which was the original substrate, was obtained by further treatment with chloranil in refluxing benzene.

Tetrabenazine (4a)

To a solution of 3,4-dihydro-6,7-dimethoxyisoquinoline hydrochloride (3, 3.5 g, 15.4 mmol) in cold H2O (20 mL) in an ice water bath, was added 3-(dimethylaminomethyl)-5-methyl-2-hexanone (2, 3.15 g, 18.3 mmol) as the free base with stirring. Precipitate formed within 3 h, and stirring was continued until the solid-gummy precipitate prevented stirring. The mixture was allowed to stand at RT (room temperature) for 3 days. The solid–gum mixture was filtered, and the yellow solid–gum mixture was dissolved in hot MeOH. The solution was chilled at −10°C for 18 h. The pale yellow solid was filtered to give 2.1 g (43%) of TBZ (4a).
TLC: Rf = 0.62; silica gel; 4% MeOH/96% CH2Cl2.
MS: (DCl-NH3) m/z 318 (M+H).
UV: (EtOH) λmax 282.0 nm (ε4431).
1H NMR: (300 MHz, CDCl3) δ 6.61 (s, 1H), 6.55 (s, 1H), 3.85 (s, 3H), 3.82 (s, 3H), 3.51 (br dd, 1H), 3.29 (dd, 1H), 3.13 (m, 2H), 2.90 (dd, 1H), 2.75 (m, 2H), 2.57 (m, 2H), 2.35 (t, 1H), 1.81 (ddd, 1H), 1.65 (m, 1H), 1.04 (ddd, 1H), 0.92 (d, 3H), 0.89 (d, 3H) ppm.
13C NMR: (75 MHz, CDCl3) δ 210.00, 147.86, 147.54, 128.60, 126.11, 111.53, 107.94, 62.48, 61.52, 56.01, 55.92, 50.58, 47.62, 47.57, 36.09, 29.38, 25.44, 23.21, 22.11 ppm.
EA: Anal. Calc for C19H17NO3: C, 71.89; H, 8.57; N, 4.41. Found C, 72.15; H, 8.69; N, 4.47.
HPLC: Brownlee 25 cm × 4.6 mm silica gel column; 30% isopropanol/70% hexane; 1 mL/min; ret. time 5.94 min; purity >99.5%.

…………….

http://www.google.ga/patents/WO2008154243A1?cl=en

Example 10 Removal The Boc Protecting Group From First Intermediate 12 And Amino Cyclization Provide (+)-Tetrabenazine XVII

[0063] First intermediate 12 (1.0 eq) was dissolved in 10% Me2S- dichloromethane to provide an 82 mM solution. The solution was cooled to 0 0C and triisopropylsilane (1.1 eq.) followed by TFA (precooled to 0 0C) was added to the reaction mixture to provide a final concentration of 41 mM. The reaction mixture was permitted to stir at 0 0C for 1 h. Following the allotted time the reaction mixture was quenched at 0 0C by the addition of saturated aqueous potassium carbonate solution and concentrated under reduced pressure to remove the majority of the dimethylsulfide. The mixture was extracted with five portions of dichloromethane, and the combined organic extracts were washed with brine, dried (MgSO4), filtered and concentrated under reduced pressure to provide the crude product as a yellow solid. The crude product was recrystallized from 3.5% dimethoxyethane in hexanes. The resulting colorless crystals were washed with hexanes to provide pure (+)- tetrabenazine (XVII) 46%: mp 126.0 0C (3.5% DME-hexanes) (a crystal polymorph was observed at 116 0C); [α]26 D +37.2 (c 0.41, CH2Cl2); 1H NMR (CD2Cl2) δ 0.89 (apparent t, J = 7.2 Hz, 6H), 0.98 (ddd, J = 12, 6.0, 4.0 Hz, IH), 1.59-1.68 (m, IH), 1.74 (ddd, J = 12, 5.9, 5.7 Hz, IH), 2.32 (apparent t, J = 11.7 Hz, IH), 2.46 (apparent t, J = 12.3 Hz, IH), 2.55 (ddd, J = 12, 10.0, 3.8 Hz, IH), 2.65-2.73 (m, 2H), 2.83 (dd, J = 5.5, 2.8Hz, IH), 2.97-3.07 (m, IH), 3.07-3.14 (m, IH), 3.25 (dd, J =9.7, 6.3 Hz, IH), 3.47 (apparent d, J = 12Hz, IH), 3.75 (s, 3H), 3.77 (s, 3H), 6.55 (s, IH), 6.60 (s, IH) 13C NMR (CD2Cl2) δ 21.98, 23.02, 25.51, 29.46, 35.16, 47.47, 47.63, 50.47, 55.87, 56.01, 61.47, 62.46, 108.46, 111.72, 126.37, 128.96, 147.65, 147.98, 209.72; HRMS-(ESI+) calcd for (C19H27NO3 + H) ([M+H]+ 318.2069, found 318.2082.

…………….

US 20150152099

d1 d2 d3

………….

WO 2015077520

NBI-98854 (CAS # 1025504-59-9), (S)-(2R,3R,l lbR)-3-isobutyl-9,10-dimethoxy-2,3,4,6,7,1 lb-hexahydro-lH-pyrido[2,l-a]isoquinolin-2-yl 2-amino-3-methylbutanoate, is a VMAT2 inhibitor. NBI-98854 is currently under investigation for the treatment of movement disorders including tardive dyskinesia. WO 2008058261; WO 2011153157; and US 8,039,627. NBI-98854, a valine ester of (+)-a-dihydrotetrabenazine, in humans is slowly hydrolyzed to (+)-a-dihydrotetrabenazine which is an active metabolite of tetrabenazine.

NBI-98854

 

EXAMPLE 1

D6-(±)-3-Isobutyl-9,10-dimethoxy-3,4,6,7-tetrahydro-lH-pyrido[2,l-a]isoquinolin-2(l lbH)-one ((±)-Tetrabenazine-<d6)

Step 1

[0193] Jgrt-butyl 3,4-dihydroxyphenethylcarbamate : A solution of dopamine

hydrochloride (209 g, 1.11 mol, 1.00 equiv), sodium carbonate (231 g, 2.75 mol, 2.50 equiv) and di-tert-butyl dicarbonate (263 g, 1.21 mol, 1.10) in 2.4 L tetrahydrofuran / water (5: 1) was stirred at 20°C for 2.5 h. After the starting material was consumed completedly, the reaction was diluted with ethyl acetate (2 L) and washed with water (2×600 mL). The organic phase was dried over sodium sulfate, filtered and concentrated under reduced pressure until two volumes of solvent was left. The precipitated solid was isolated by filtration and dried under vacuum to give 254 g (91%) of ieri-butyl 3,4-dihydroxyphenethylcarbamate as white solid. Ή-ΝΜΪ (300 MHz, CDC13) 8.72 (s, 1H), 8.62 (s, 1H), 6.79 (m, 1H), 6.62 (m, 1H), 6.51 (m, 1H), 6.40 (m, 1H), 3.03 (m, 2H), 2.50 (m, 2H), 1.37 (s, 1H). LC-MS: m /z = 254 (MH) +.

Step 2

[0194] D6-fert-butyl 3,4-dimethoxyphenethylcarbamate: A solution of ieri-butyl 3,4-dihydroxyphenethylcarbamate (127 g, 397 mmol, 1.00 equiv), potassium carbonate (359.3 g, 2.604 mmol, 3.00 equiv) and 18-crown-6 (1,4,7,10,13,16-hexaoxacyclooctadecane ) (68.64 g, 0.26 mmol, 0.03 equiv) in acetone (800 mL) was stirred at 38°C. After 30 min., CD3I (362 g, 2.604 mmol, 3.00 equiv) was added to the reaction, and the mixture was stirred at 38°C for 12 h. Then an additional CD3I (120 g, 0.868 mmol, 1.00 equiv) was added to the solution and the solution was stirred for 5 h. Then the mixture was cooled to room temperature and the solid was filtered. The filtrate was concentrated under vacuum. The resultant solid was dissolved in H2O (300 mL) and extracted with EA (3×300 mL), the organic layers was combined and concentrated under vacuum to give 114 g (79%) of de-tert-butyl 3,4-dimethoxyphenethylcarbamate as white

solid. ^-NMR (300 MHz, CDC13) <Π.39 (m, 5H), 6.82 (m, 1H), 6.73 (m, 2H), 5.12 (s, 1H), 3.45 (m, 2H), 2.77 (m, 2H). LC-MS: m /z = 288 (MH) +.

Step 3

[0195] D6-2-(3,4-dimethoxyphenyl)ethanamine: A solution of de-tert-butyl 3,4-dimethoxyphenethylcarbamate (128 g, 455.26 mmol, 1.00 equiv) in ethyl acetate (1.5 L) was stirred at room temperature. Then HC1 gas was introduced into the reaction mixture for 2h. The precipitated solid was isolated by filtration. The solid was dissolved in 300 mL of water. The pH value of the solution was adjusted to 12 with sodium hydroxide (solid). The resulting solution was stirred for 1 h at 5-10°C. The resulting solution was extracted with 6×800 mL of ethyl acetate and the organic layers combined, dried over sodium sulfate, and concentrated under vacuum to give 64 g (78%) of d6-2-(3,4-dimethoxyphenyl)ethanamine as yellow oil.

^-NMR (300 MHz, CDC ) 6.77 (m, 3H), 3.89 (s, 3H), 3.87 (s, 3H), 2.96 (m, 2H), 2.71 (m, 2H), 1.29 (s, 2H). LC-MS: m /z = 182 (MH) +.

Step 4

[0196] D6-N-r2-(3,4-dimethoxy-phenyl)ethyllformamide: A solution of d6-2-(3,4-dimethoxyphenyl)ethanamine (69 g, 368 mmol, 1.00 equiv) in ethyl formate(250 mL) was heated under reflux overnight. The solution was concentrated under vacuum to give 71 g (91%) of d6-N-[2-(3,4-dimethoxy-phenyl)ethyl]formamide as yellow solid. The crude solid was used in next step without purification. ^-NMR (300 MHz, CDCb) £8.17 (s, 1H), 6.81 (m, 3H), 5.53 (br, 1H).3.59 (m, 2H), 2.81 (t, 2H, / = 6.9 Hz). LC-MS: m /z = 216 (MH) +.

Step 5

[0197] D6-6,7-dimethoxy-3,4-dihvdroisoguinoline: A solution of d6-N-[2-(3,4-dimethoxy-phenyl)ethyl]formamide (71 g, 329 mmol, 1.00 equiv) in phosphorus oxychloride (100 mL) was stirred at 105°C for 1 h. Then the solution was concentrated under vacuum to remove

phosphorus oxychloride. The residual oil was dissolved in ice / water. The solution was made basic with potassium carbonate with cooling. The basic aqueous solution was extracted with dichloromethane. The collected organic phase was dried using sodium sulfate and then filtered. The dichloromethane was removed by concentration under vacuum to give an orange oil.

Purification by silica gel (ethyl acetate:petroleum ether = 1: 1 ~ ethyl acetate) to give 43 g (66%) of d6-6,7-dimethoxy-3,4-dihydroisoquinoline as orange solid (yield 66%). Ή-ΝΜΡ (300 MHz, CDC13) 8.24 (s, 1H), 6.82 (s, 1H), 6.68 (s, 1H), 3.74 (m, 2H), 2.69 (t, 2H, J = 12 Hz). LC-MS: m /z = 198 (MH) +.

Step 6

[0198] Trimethyl(5-methylhex-2-en-2-yloxy)silane: To a cold (-78°C), stirred solution of j-PrMgBr (500 mL of 2 M solution in tetrahydrofuran, 1 mol, 1.00 equiv) in anhydrous tetrahydrofuran (1 L) was added Cul (19.02 g, 0.1 mol, 0.10 equiv) and the resultant mixture was stirred for 15 min at -78°C. Anhydrous hexamethylphosphorous triamide (358.4 g, 2 mmol, 2 equiv) was added and after 20 min, a solution of methyl vinyl ketone (70 g, 0.1 mol, 1.00 equiv), trimethylsilyl chloride (217 g, 0.2 mol, 2.00 equiv), in tetrahydrofuran (200 mL) was added dropwise over 30 min. After the reaction mixture was stirred at -78 °C for lh, triethylamine (20.2g, 200 mmol, 2.00 equiv) was added and the resulting mixture stirred for 10 min at 0 °C. To this was added ie/ -butyl methyl ether (2 L), and the solution was washed with 5% ammonia solution (6×300 mL). Then the organic phase was dried over sodium sulfate and concentrated under vacuum at 25°C to give 155 g crude product as yellow liquid. The liquid was purified by distilling (64-68°C/40 mmHg) to provide 118 g (63.3%) of trimethyl(5-methylhex-2-en-2-

yloxy)silane (E:Z = 56 : 44) as a colorless oil. XH-NMR (300 MHz, J6-DMSO) 4.58 (m, 0.56H), 4.43 (m, 0.44H), 1.73 (s, 1.69H), 1.66 (s, 1.32H), 1.53 (m, 1H), 0.84 (m, 6 H), 0.15(m, 9H).

Step 7

[0199] 3-r(Dimethylamino)methyl1-5-methylhexan-2-one: To a stirred solution of trimethyl(5-methylhex-2-en-2-yloxy)silane (118 g, 633 mmol, 1.00 equiv) in anhydrous acetonitrile (800 mL) was added N-methyl-N-methylenemethanaminium iodide (128.8 g, 696.3 mmol, 1.10 equiv) in several batches and the resultant mixture was stirred at 20°C overnight. Then the solution was concentrated under vacuum to remove the solvent. The residue was dissolved in 400 mL 1 N HC1 (aq.) and extracted with ieri-butyl methyl ether. Then the water phase was basiced with 2 N aq. NaOH and extracted with ie/ -butyl methyl ether. The organic phase was dried and concentrated under vacuum. The liquid was purified by distilling (80°C/0.5 mmHg) to provide 50 g (46%) of 3-[(dimethylamino)methyl]-5-methylhexan-2-one as a colorless oil. XH-NMR (300 MHz, J6-DMSO) £0.92 (d, 3H), 0.98 (d, 3H), 1.11-1.23 (m, 1H), 1.23-1.38 (m, 1H), 1.54-1.70 (m, 1H), 2.30 (s, 3H), 3.01 (s, 9H), 3.10-3.32 (m, 2H), 3.81-3.88 (m, 1H).

Step 8

[0200] 2-Acetyl-N,N V,4-tetramethylpentan-l-aminium iodide: A solution of 3-[(dimethylamino)methyl]-5-methylhexan-2-one (50 g, 15.00 mmol, 1.00 equiv) and methyl iodide (4.26 g, 30.00 mmol, 2.00 equiv) in 50 mL diethyl ether was stirred overnight at room temperature. The precipitated solid was isolated by filtration and dried under vacuum to give 79 g (86%) of 2-acetyl-N,N,N,4-tetramethylpentan-l-aminium iodide as white solid. XH-NMR (300 MHz, Je-DMSO) 0.89-0.98 (m, 6H), 1.11-1.20 (m, 1H), 1.40 (m, 1H), 1.66 (m, 1H), 2.30 (s, 3H), 3.01(s, 9H), 3.21 (m, 2H), 3.85 (m, 1H).

Step 9

[0201] Ρό- (±) -tetrabenazine : A solution of d6-6,7-dimethoxy-3,4-dihydroisoquinoline (33.4 g, 169 mmol, 1.10 equiv) and 2-acetyl-N,N,N,4-tetramethylpentan-l-aminium iodide (48 g, 153 mmol, 1.00 equiv) in 300ml of methanol was heated under reflux for 48 h. Then 150 mL water was added. The solution was cooled to room temperature. The precipitated solid was isolated by filtration and dried under vacuum to give 38 g of crude d6-tetrabenazine as yellow solid. The crude tetrabenazine was dissolved in ieri-butyl methyl ether (15 volumes), the mixture was heated until the solid was almost dissolved. The yellow solid which was unsolvable was filtered. The filtrate was concentrated under vacuum until 2 volumes ieri-butyl methyl ether was left. The solid was filtered and collected. The above solid was dissolved in ethanol (4 volumes), then the mixture was heated until the solid was dissolved. The solution was stirred and cooled to room temperature at the rate of 20°C/h. Then the mixture was stirred at 0°C for lh. The precipitated solid was isolated by filtration and dried under vacuum to give 25 g (50.4%) of tetrabenazine-<d6 as white solid.

^-NMR (300 MHz, CD2C12) £6.61 (s, 1H), 6.55 (s, 1H), 3.84 (s, 3H), 3.82 (s, 3H), 3.50 (d, 1H, / = 12 Hz), 3.27 (dd, 1H, / = 11.4Hz, / = 6.3 Hz), 3.11 (m, 2H), 2.84 (dd, 1H, / = 10.5 Hz, / = 3 Hz), 2.74 (m, 2H), 2.56 (m, 2H), 2.31 (t, 1H, J = 12 Hz), 1.76 (m, 1H), 1.63 (m, 1H), 0.98 (m, 1H), 0.89 (m, 6H).

LC-MS: m /z = 324 (MH) +.

………………

NMR PREDICT

C1

D2

D3

Watch out will be updated……………….

Rob Koremans, MD, President and CEO of Global Specialty Medicines at Teva.

Michael Hayden, M.D., Ph.D., President of Global R&D and Chief Scientific Officer at Teva

 

 

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US8053578 16 juil. 2008 8 nov. 2011 General Electric Company Alpha-fluoroalkyl dihydrotetrabenazine imaging agents and probe

 

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Cited Patent Filing date Publication date Applicant Title
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1 * BROSSI, A. ET AL: “Synthesis in the emetine series. I. 2-Oxohydrobenzo[a]quinolizines“, HELVETICA CHIMICA ACTA, vol. 41, 1958, pages 119-139, XP002659731,
2 BULL. KOREAN CHEM. SOC. vol. 23, no. 1, 2002, page 149
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13 * DATABASE CA [Online] CHEMICAL ABSTRACTS SERVICE, COLUMBUS, OHIO, US; WANG, CHENG-XUE ET AL: “Synthesis of rutaecarpine and quinazolone compounds“, XP002659737, retrieved from STN Database accession no. 2009:92700
14 * RISHEL, MICHAEL J. ET AL: “Asymmetric Synthesis of Tetrabenazine and Dihydrotetrabenazine“, JOURNAL OF ORGANIC CHEMISTRY, vol. 74, no. 10, 2009, pages 4001-4004, XP002659732,
15 * SCHWARTZ, D. E. ET AL: “Metabolic studies of tetrabenazine, a psychotropic drug in animals and man“, BIOCHEMICAL PHARMACOLOGY, vol. 15, no. 5, 1966, pages 645-655, XP002659733,

 

update on 2018

Novel Process for Preparation of Tetrabenazine and Deutetrabenazine

Lupin Research Park, Lupin Limited, 46 & 47A, Village Nande, Taluka Mulshi, Pune-412115, Maharashtra, India
Org. Process Res. Dev., Article ASAP
DOI: 10.1021/acs.oprd.8b00011

Abstract

Abstract Image

A novel process for the synthesis of tetrabenazine (1) and deutetrabenazine (2), two well-known drugs used for the treatment of chorea associated with Huntington’s disease, has been developed. All of the reaction parameters were optimized through a series of reactions and by using Design of Experiment techniques. The newly developed methods are industrially scalable and employ cheap, commercially available raw materials and hence are highly efficient. The added advantage is that the developed processes evade the use of genotoxic alkylating agents and therefore could be considered as safe and viable alternatives to the existing methods.

Tetrabenazine (1) was invented by Hoffmann-La-Roche (Nutley, NJ, USA). It was also known as Ro 1-9569, Nitoman, and Xenazine. It is a benzoquinolizine derivative with the chemical name 1,3,4,6,7,11b-hexahydro-9,10-dimethoxy-3-(2-methylpropyl)-2H-benzo[α]quinolizin-2-one . Initially it was developed as an antipsychotic agent.Despite 50 years of medicinal background, the U.S. Food and Drug Administration (FDA) approved 1 on August 15, 2008, for the treatment of chorea associated with Huntington’s disease.

Figure

 Chemical structures of 1 and 2.

Deutetrabenazine (2) (trade name Austedo) is a stable, nonradioactive deuterium analogue of the approved drug tetrabenazine in which the six hydrogen atoms of the 9- and 10-methoxy (−OCH3) substituents have been replaced by deuterium atoms . Deutetrabenazine was found to be more effective for the treatment of chorea associated with Huntington’s disease because of improved pharmacokinetic properties compared with the nondeuterated drug tetrabenazine. Deutetrabenazine was originally developed by Auspex Pharmaceuticals (La Jolla, CA, USA). In 2015, Teva acquired Auspex Pharmaceuticals and submitted a new drug application (NDA) in the United States for the treatment of Huntington’s disease. On April 3, 2017, Teva Pharmaceutical received approval from the FDA to market deutetrabenazine as the first deuterated drug for the treatment of chorea associated with Huntington’s disease.(4) Both 1 and 2 are racemic mixtures .
  1. (a) Brossi, A.; Lindlar, H.; Walter, M.; Schnider, O. Helv. Chim. Acta 1958, 41, 119– 139, DOI: 10.1002/hlca.660410117

    .

    (b) Brossi, A.; Schnider, O.; Walter, M. Quinolizine derivatives.U.S. Patent 2,830,993, 1958.

  2. Pletscher, A.; Brossi, A.; Gey, K. F. Int. Rev. Neurobiol. 1962, 4, 275– 306, DOI: 10.1016/S0074-7742(08)60024-0
  3. Mestre, T.; Ferreira, J.; Coelho, M. M.; Rosa, M.; Sampaio, C. Cochrane Database Syst. Rev. 2009, 3,CD006456, DOI: 10.1002/14651858.CD006456.pub2

  4. U.S. Food and Drug Administration. Novel Drug Approvals for 2017.https://www.fda.gov/Drugs/DevelopmentApprovalProcess/DrugInnovation/ucm537040 (accessed Jan 15, 2018).
  5. Brossi, A. Preparation of substituted 2-oxobenzoquinolizines. U.S. Patent 3,045,021, 1962.

  6. Gant, T. G.; Shahbaz, M. M. Benzoquinoline inhibitors of vesicular monoamine transporter-2. U.S. Patent 8,524,733, 2013.

Large-Scale Preparation of Tetrabenazine (1)

1 (262.3 g, 96%). FTIR (in KBr): 2942, 2919, 1701, 1516, 1465, 1370, 1263, 1159, 1010, 860, 749 cm–1. 1H NMR (500 MHz, CDCl3): δ 6.63 (s, 1H), 6.57 (s, 1H), 3.87 (s, 3H), 3.84 (s, 3H), 3.52 (d, 1H, J = 11.2 Hz), 3.32 (dd, 1H, J = 11.6, 6.4 Hz), 3.13–3.10 (m, 2H), 2.93–2.90 (m, 1H), 2.77–2.73 (m, 2H), 2.64–2.53 (m, 2H), 2.37 (t, 1H, J = 11.6 Hz), 1.83–1.80 (m, 1H), 1.69–1.66 (m, 1H), 1.08–1.04 (m, 1H), 0.94–0.91 (m, 6H). ESI-MS: m/z 318.3 [M + H]+.

Purification of 1

1 (9.6 g, 96%). HPLC purity: 99.75%.

FTIR (in KBr): 2942, 2919, 1701, 1516, 1465, 1370, 1263, 1159, 1010, 860, 749 cm–1. 

1H NMR (500 MHz, DMSO-d6): δ 6.70 (s, 1H), 6.69 (s, 1H), 3.72 (s, 6H), 3.46 (d, 1H, J = 10.0 Hz), 3.24 (dd, 1H, J = 11.5, 6.0 Hz), 3.15–3.11 (m, 1H), 2.95–2.89 (m, 1H), 2.85 (dd, 1H, J = 13.0, 3.0 Hz), 2.69–2.65 (m, 2H), 2.52–2.46 (m, 2H), 2.28 (t, 1H, J= 12.0 Hz), 1.66–1.63 (m, 2H), 0.94–0.85 (m, 7H).

ESI-MS: m/z 318.3 [M + H]+.

Large-Scale Preparation of Deutetrabenazine (2)FTIR (in KBr): 2942, 2920, 2246, 2067, 1700, 1513, 1269, 1113, 990, 747 cm–1. 1H NMR (500 MHz, CDCl3): δ 6.63 (s, 1H), 6.56 (s, 1H), 3.53 (d, 1H, J = 10.5 Hz), 3.32–3.30 (m, 1H), 3.17–3.13 (m, 2H), 2.92 (dd, 1H, J = 13.5,3.0 Hz), 2.77–2.73 (m, 2H), 2.64–2.53 (m, 2H), 2.37 (t, 1H, J = 11.5 Hz), 1.84–1.79 (m, 1H), 1.69–1.67 (m, 1H), 1.08–1.04 (m, 1H), 0.94–0.91 (m, 6H). ESI-MS: m/z 324.4 [M + H]+

Large-Scale Purification of 2

Mp: 128.75–129.42 °C.

FTIR (in KBr): 2942, 2920, 2246, 2067, 1700, 1513, 1269, 1113, 990, 747 cm–1. 

1H NMR (500 MHz, DMSO-d6): δ 6.69 (s, 2H), 3.46 (d, 1H, J = 10.0 Hz), 3.25 (dd, 1H, J = 11.5, 6.0 Hz), 3.15–3.11 (m, 1H), 2.95–2.89 (m, 1H), 2.85 (dd, 1H, J = 13.5, 3.0 Hz), 2.70–2.64 (m, 2H), 2.52–2.44 (m, 2H), 2.28 (t, 1H, J = 11.5 Hz), 1.66–1.63 (m, 2H), 0.93–0.85 (m, 7H).

ESI-MS: m/z 324.4 [M + H]+.

[α]D −0.3 [c 0.3, DCM at 25 °C].

सुकून उतना ही देना प्रभू, जितने से जिंदगी चल जाये। औकात बस इतनी देना, कि औरों का भला हो जाये।
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Verubecestat (MK-8931)


Verubecestat.pngV1

Verubecestat (MK-8931)

Merck Alzheimer’s drugs Verubecestat (MK-8931) is an oral β- amyloid precursor protein cleaving enzyme (BACE1 or β-secretase enzyme) inhibitor, is currently in Phase III clinical trials

Verubecestat
MK 8931, MK-8931, SCH 900931
2-Pyridinecarboxamide, N- (3 – ((5R) -3-amino-5,6-dihydro-2,5-dimethyl-1 , 1-dioxido-2H-1,2,4-thiadiazin-5-yl) -4-fluorophenyl) -5-fluoro-

N-[3-[(5R)-3-amino-2,5-dimethyl-1,1-dioxo-6H-1,2,4-thiadiazin-5-yl]-4-fluorophenyl]-5-fluoropyridine-2-carboxamide

CAS : 1286770-55-5

C17 H17 F2 N5 O3 S, 409.41
Mechanism: Oral β- amyloid precursor protein cleavage enzyme (BACE) inhibitors
Indications: Alzheimer’s disease
Development progress: phase III clinical
Companies: Merck

Verubecestat (MK-8931) is a small-molecule inhibitor of beta-secretase cleaving enzyme (BACE) 1 and BACE2 in development by Merck for the treatment of Alzheimer’s Disease.

MK-8931 is a beta-secretase 1 (BACE1) inhibitor in phase III development for the treatment of amnestic mild cognitive impairment (aMCI) due to Alzheimer’s disease at Merck & Co. The company is also conducting phase II/III trials for the treatment of Alzheimer’s type dementia.

Alzheimer’s disease (AD) is a devastating, progressive neurodegenerative disease that is associated with up to 80% of the estimated 47 million cases of dementia worldwide and is a leading cause of death in the United States.(1, 2) As the elderly population increases, the worldwide incidence of dementia is expected to nearly triple to approximately 132 million by 2050, creating an unsustainable socioeconomic burden.(1) Currently available therapies, which include acetylcholinesterase inhibitors and the N-methyl-d-aspartate receptor antagonist memantine, produce modest and transient improvement in cognitive function but do not alter the progression of AD.(3) Treatments that delay or halt disease progression by targeting the underlying causes of AD would have lasting impacts on patient function and quality of life and would address an urgent unmet medical need.
Two histopathological hallmarks are invariably observed in the brains of AD patients, namely, extracellular amyloid plaques composed primarily of β-amyloid (Aβ) peptides and intraneuronal neurofibrillary tangles composed primarily of aggregates of abnormally phosphorylated tau protein. Aβ peptides are formed by two sequential cleavages of the amyloid precursor protein (APP), first by β-site amyloid precursor protein cleaving enzyme 1 (BACE1) followed by cleavage of the resulting C-terminal fragment C99 by γ-secretase. This cleavage sequence results in production of a family of Aβ peptides, of which Aβ40 is the most abundant isoform and Aβ42 is more highly prone to aggregate into neurotoxic, oligomeric species.(4) According to the amyloid hypothesis, aberrant production and/or accumulation of Aβ peptides, principally Aβ42, over a period of decades is causative of the underlying disease pathogenesis that ultimately leads to neuronal cell death.(4, 5) In addition to the invariant presence of amyloid plaques in the brains of AD patients, the amyloid hypothesis is underpinned by several other lines of evidence. First, many distinct neurodegenerative diseases are associated with the invariant presence of abnormal protein aggregates analogous to amyloid plaques. Second, low levels of Aβ42 in the CSF are a reasonably good diagnostic/prognostic biomarker for AD. Finally, and most significantly, early onset autosomal dominant familial AD is associated with mutations in APP and the presenilin proteins (which are components of the γ-secretase enzyme), and all of these mutations share the common phenotype of increasing total Aβ levels or the relative proportion of Aβ42.(6) Given this multifaceted evidence supporting the role of Aβ peptides in AD progression, substantial efforts have been invested in the development of amyloid-lowering therapies as a disease-modifying approach to AD treatment.(7) Prominent among these has been inhibition of BACE1 to reduce or prevent production of the Aβ peptides. This approach has been further supported by the recent finding that a rare mutation (A673T) near the BACE1 cleavage site in APP reduces Aβ peptide production and is associated with reduced risk of developing AD and improved cognitive function in the elderly.(8)
BACE1 is a membrane-bound aspartyl protease expressed primarily in the central nervous system (CNS), is the sole enzymatic activity responsible for the initial β-site APP cleavage, and is required for Aβ peptide production in vivo.(9) In the brain, BACE1 is expressed mainly in neurons and cleaves APP predominantly in the endosomal compartments where the acidic pH is near the optimum for its enzymatic activity (pH 5).(10) Since the characterization of BACE1 more than 15 years ago,(11) there have been intensive efforts to overcome the challenges of identifying small molecule inhibitors that can penetrate the CNS and inhibit the formation of centrally derived Aβ peptides.(12) These efforts have been driven by evidence that BACE1 inhibition, in comparison with γ-secretase inhibition and antiamyloid immunotherapy, may be an inherently safer amyloid-lowering approach,(7) a notion that has been informed by an evolving understanding of BACE1 biology. In this regard, Bace1 knockout mice have been reported to have a number of subtle phenotypes, including reduction of central and peripheral nerve myelination, and several putative BACE1 substrates other than APP have recently been proposed.(10, 13, 14) However, many of these phenotypes and substrates remain to be independently confirmed, have little if any functional consequence, are not recapitulated by pharmacological inhibition of BACE, or may be mitigated through partial BACE1 inhibition.(8, 10, 13-15)
.

Smiles: C [C @] 1 (CS (= O) (= O) N (C (= N1) N) C) c2cc (ccc2F) NC (= O) c3ccc (cn3) F

COSY PREDICT

V0COSY

https://www.google.co.in/patents/CN102639135A?cl=en

Scheme 3b:

Figure CN102639135AD00931

The amine A (Scheme 3a, step 4) (13.7 g) in n-butanol (150 mL) was added a slurry solution of cyanogen bromide (5M, in MeCN). The resulting mixture was heated to reflux for 4 hours. The mixture was concentrated to 1/3 of original volume. To this mixture was added Et20 (200 mL). The resulting solid was removed by filtration, and the solid was washed with Et20 (2x). The solid was partitioned between EtOAc and saturated Na2CO3 (aq). The aqueous layer was extracted with EtOAc (3x). The combined organic layers were washed with brine, dried over Na2SO4, filtered and concentrated to give 10.6 g

Scheme 10:

Figure CN102639135AD00982

The nitro compound (Scheme 3b) (2. 50 g, 6. 0 mmol) of Et0H (150 mL) was degassed (To this solution was bubbled with nitrogen time 3 min). To this solution was added Pd / C (10% w / w, 50% water, 698 mg). The mixture was placed in a nitrogen atmosphere. Exhaust, and backfilled with H2 (3x). The obtained mixture at room temperature, followed by stirring under H2 balloon for 2 hours. Bubbling nitrogen gas, and the mixture was purged, filtered through Celite, and concentrated.Small plug filtered through a silica gel column, eluting with EtOAc, and the product was purified to give the aniline (2. 2g, 97%).

SEE

PATENT

http://www.google.co.in/patents/WO2011044181A1?cl=en

veb

SNAPSHOT

WP_000366

SYNTHESIS CONSTUCTION

V9AND

V8ON RXN WITH WITH BuLi GIVES

V7THIS GIVES

V6THIS ON TREATMENT WITH BrCN

V5ON BOC2O TREATMENT GIVES

V4GIVES ON HYDGN

V2

REACTION WITH

V3

GIVES

FINAL COMPD Verubecestat

V1

1H NMR PREDICT

V0

V01H GRAPH

V01H

13C NMR PREDICT

V013C GRAPH

V013C

 

Updated…….WATCH OUT FOR MORE

https://www.google.co.in/patents/US8729071?cl=en

 

Steps 1-4:

These steps were performed using similar procedures to those described in steps 1-4 of Scheme 1a.

Step 5:

To a solution of the amine from step 4 (10.5 g, 36 mmol) in CH2Cl2 (200 mL) was added benzoylisothiocyanate (4.3 mL, 1.1 eq.). The resulting solution was stirred at RT for 2.5 days. Additional benzoylisothiocyanate (0.86 mL, 0.2 eq.) was added and the solution was stirred at RT for an additional 2 hours. The solution was then concentrated in vacuo.

A portion of this material (6.5 g, ˜14 mmol) was dissolved in MeOH (200 mL). To this solution was added Na2CO3 (s) (1.52 g, 14 mmol). The resultant mixture was stirred at RT for 45 min. After that time, a slight excess of HOAc was added to the solution. The mixture was then concentrated. The residue was partitioned between CH2Cl2 and ½ sat. NaHCO3 (aq.). The aqueous layer was extracted with CH2Cl2 (3×). The combined organic layers were dried over Na2SO4, filtered and concentrated. The thiourea (˜4.9 g) was carried onto the next reaction without further purification.

Step 6:

Example 15 was prepared using a method similar to that described in Scheme 1a step 6.

To a shiny of amine A (Scheme 3a step 4) (13.7 grams) in n-butanol (150 mL) was added a solution of cyanogen bromide (5M in MeCN). The resultant mixture was heated to reflux for 4 hours. The mixture was concentrated to ⅓ of the original volume. To the mixture was added Et2O (200 mL). The resultant solid was removed via filtration and the solid was washed with Et2O (2×). The solid was partitioned between EtOAc and sat. Na2CO3 (aq.). The aqueous layer was extracted with EtOAc (3×). The combined organic layers were washed with brine, dried over Na2SO4, filtered and concentrated to afford 10.6 grams of Ex. 15. This material was converted to the t-butyl carbamate using a procedure similar to that described in Scheme 3.

Step 7:

A mixture of the bromide (3.00 g, 6.92 mmol), benzophenone imine (1.39 mL, 8.30 mmol), Pd2(dba)3 (0.634 g, 0.692 mmol), John-Phos (0.413 g, 1.38 mmol), sodium tert-butoxide (2.13 g, 22.1 mmol), and toluene (51 mL) was degassed (vacuum/N2). The mixture was then stirred at 65° C. under nitrogen for 3 h. After this time, the reaction mixture was cooled to room temperature and filtered through a pad of Celite and rinsed with ethyl acetate (100 mL). The filtrate was concentrated under reduced pressure. The residue was then dissolved in methanol (76 mL) and the resulting solution was charged with hydroxyl amine hydrochloride (2.16 g, 31.1 mmol) and sodium acetate (2.55 g, 31.1 mmol). The reaction mixture was stirred at room temperature for 40 min. After this time, the reaction mixture was concentrated under reduced pressure. The resulting residue was dissolved in ethyl acetate (200 mL) and washed with saturated aqueous sodium bicarbonate (100 mL), water (100 mL), and brine (100 mL). The organic layer was then dried over anhydrous sodium sulfate, filtered, and concentrated under reduced pressure. The residue was purified by column chromatography (silica, 0-100% ethyl acetate/heptane) to afford the amino pyridine (0.880 g, 34%).

To a flame-dried flask was added a pyridyl bromide (Table IIb, Entry 15, 1.5 g, 3.3 mmol), Pd2(dba)3 (305 mg, 0.3 mmol), (2-biphenyl)di-tert-butylphosphine (200 mg, 0.7 mmol), sodium tert-butoxide (1.02 g, 0.011 mmol), benzophenone imine (670 ul, 4 mmol), and toluene (21 mL). The mixture was evacuated under vacuum and back-filled with N2 (3×). The mixture was stirred at 60° C. for 1 h. After filtration through celite, the filtrate was concentrated. The crude residue was dissolved in 36 mL of methanol, and hydroxyl amine hydrochloride (458 mg, 6.6 mmol) and sodium acetate (541 mg, 6.6 mmol) were added. The reaction was stirred for 35 min and then quenched with saturated aqueous sodium bicarbonate. The mixture was extracted with ethyl acetate, and the combined organic portions were dried over magnesium sulfate and concentrated. The crude residue was purified by a flash silica column (50% ethyl acetate/hexane) to get an aminopyridine product (730 mg, 68%).

A solution of the nitro compound (Scheme 3b) (2.50 g, 6.0 mmol) in EtOH (150 mL) was degassed by bubbling N2 through the solution for 3 min. To this solution was added Pd/C (10% w/w, 50% H2O, 698 mg.). The mixture was placed under an atmosphere of N2. The atmosphere was evacuated and back-filled with H2 (3×). The resulting mixture was stirred at RT under a H2 balloon for 2 h. The mixture was purged by bubbling N2 through it, filtered through Celite and concentrated. The product was purified by filtering through a small plug of silica gel column eluting with EtOAc to afford the aniline (2.2 g, 97%).

 

ENTRY 25

MH+: 410.0, HPLC1.79 min, LCMSMETHOD D

Method D:

  • Column: Agilent Zorbax SB-C18 (3.0×50 mm) 1.8 uM

Mobile phase: A: 0.05% Trifluoroacetic acid in water

    • B: 0.05% Trifluoroacetic acid in acetonitrile

Gradient: 90:10 (A:B) for 0.3 min, 90:10 to 5:95 (A:B) over 1.2 min, 5:95 (A:B) for 1.2 min.

Flow rate: 1.0 mL/min

UV detection: 254 and 220 nm

Mass spectrometer: Agilent 6140 quadrupole

 

update…………..

Discovery of the 3-Imino-1,2,4-thiadiazinane 1,1-Dioxide Derivative Verubecestat (MK-8931)–A β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Inhibitor for the Treatment of Alzheimer’s Disease

Departments of †Discovery Chemistry, ‡Neuroscience, §Pharmacokinetics, Pharmacodynamics, and Drug Metabolism, ΔTranslational Medicine, #Structural Chemistry, ⊥Molecular and Materials Characterization, ∥Pharmaceutical Sciences and Clinical Supply, and Toxicological Sciences, MRL, Merck & Co. Inc., 2015 Galloping Hill Road, Kenilworth, New Jersey 07033, United States
∇ Albany Molecular Research Inc., 26 Corporate Circle, Albany, New York 12203, United States
J. Med. Chem., Article ASAP
DOI: 10.1021/acs.jmedchem.6b00307
Publication Date (Web): November 18, 2016
Copyright © 2016 American Chemical Society
*Phone: 908-740-4729. E-mail: jack.scott@merck.com., *Phone: 973-868-2088. E-mail: andy.stamford1@gmail.com.

ACS Editors’ Choice – This is an open access article published under an ACS AuthorChoice License, which permits copying and redistribution of the article or any adaptations for non-commercial purposes.

Abstract

Abstract Image

Verubecestat 3 (MK-8931), a diaryl amide-substituted 3-imino-1,2,4-thiadiazinane 1,1-dioxide derivative, is a high-affinity β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor currently undergoing Phase 3 clinical evaluation for the treatment of mild to moderate and prodromal Alzheimer’s disease. Although not selective over the closely related aspartyl protease BACE2, verubecestat has high selectivity for BACE1 over other key aspartyl proteases, notably cathepsin D, and profoundly lowers CSF and brain Aβ levels in rats and nonhuman primates and CSF Aβ levels in humans. In this annotation, we describe the discovery of 3, including design, validation, and selected SAR around the novel iminothiadiazinane dioxide core as well as aspects of its preclinical and Phase 1 clinical characterization.

 

N-[3-[(5R)-3-Amino-5,6-dihydro-2,5-dimethyl-1,1-dioxido-2H-1,2,4-thiadiazin-5-yl]-4-fluorophenyl]-5-fluoro-2-pyridinecarboxamide (3)

 3 (2.70 g, 89% yield) as a white solid. 1H NMR (400 MHz, DMSO-d6) δ 10.57 (s, 1H), 8.73 (d, J = 2.8 Hz, 1H), 8.22 (dd, J = 8.8, 4.8 Hz, 1H), 8.03–7.95 (m, 2H), 7.79 (m, 1H), 7.14 (dd, J = 11.6, 8.8 Hz, 1H), 6.03 (br s, 2H), 3.78 (s, 1H), 3.34 (s, 1H), 3.05 (s, 3H), 1.61 (s, 3H). ESI MS m/z 410.2 [M + H]+. [α]D20 37.2° (c 0.367, CH3OH).
To generate its hydrochloride salt, 3prepared above was added to CH2Cl2 (50 mL) followed by a solution of HCl (2 N in Et2O, 3.6 mL, 7.2 mmol), and the mixture was concentrated in vacuo. The product was slurried in distilled water (50 mL) and lyophilized to afford the HCl monohydrate salt of 3 (2.58 g, 79% yield, 3 steps) as a white solid. 1H NMR (400 MHz, CD3OD) δ 8.59 (d, J = 2.8 Hz, 1H), 8.26 (dd, J = 8.8, 4.8 Hz, 1H), 8.02 (dd, J = 7.6, 2.8 Hz, 1H), 7.82–7.75 (m, 2H), 7.22 (dd, J = 12.0, 8.8 Hz, 1H), 4.49 (dd, J = 14.4, 0.8 Hz, 1H), 4.30 (d, J = 14.4 Hz, 1H), 3.30 (s, 3H), 1.96 (s, 3H). ESI MS m/z410.2 [M + H]+. Anal. Calcd (C17H20ClF2N5O4S): C, 44.02; H, 4.35; N, 15.10; Cl, 7.64; S, 6.91. Found: C, 43.77; H, 4.32; N, 14.81; Cl, 7.84; S, 7.04.

 

References

 

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    (a) Wortmann, M.Dementia: a global health priority – highlights from an ADI and World Health Organization report Alzheimer’s Res. Ther. 2012, 4, 40– 43, DOI: 10.1186/alzrt143

    (b) Alzheimer’s Disease International. World Alzheimer Report 2015. http://www.alz.co.uk/research/WorldAlzheimerReport2015.pdf.

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    Alzheimer’s Association. 2015 Alzheimer’s disease facts and figures. Alzheimers Dement. 2015, 332– 384.

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    Haass, C.; Selkoe, D. J.Soluble protein oligomers in neurodegeneration: Lesson from the Alzheimer’s amyloid β-peptide Nat. Rev. Mol. Cell Biol. 2007, 8, 101– 112, DOI: 10.1038/nrm2101

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    (a) Hardy, J.; Selkoe, D. J.The amyloid hypothesis of Alzheimer’s disease: Progress and problems on the road to therapeutics Science 2002, 297, 353– 356, DOI: 10.1126/science.1072994

    (b) Karran, E.; Mercken, M.; De Strooper, B.The amyloid cascade hypothesis for Alzheimer’s disease: an appraisal for the development of therapeutics Nat. Rev. Drug Discovery 2011, 10, 698– 712, DOI: 10.1038/nrd3505

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    Citron, M.Alzheimer’s disease: strategies for disease modification Nat. Rev. Drug Discovery 2010, 9, 387– 398, DOI: 10.1038/nrd2896

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    Jonsson, T.; Atwal, J. K.; Steinberg, S.; Snaedal, J.; Jonsson, P. V.; Bjornsson, S.; Stefansson, H.; Sulem,P.; Gudbjartsson, D.; Maloney, J.; Hoyte, K.; Gustafson, A.; Liu, Y.; Lu, Y.; Bhangale, T.; Graham, R. R.; Huttenlocher, J.; Bjornsdottir, G.; Andreassen, O. A.; Jönsson, E. G.; Palotie, A.; Behrens, T. W.; Magnusson, O. T.; Kong, A.; Thorsteinsdottir, U.; Watts, R. J.; Stefansson, K.A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline Nature 2012, 488, 96– 99, DOI: 10.1038/nature11283

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    Roberds, S. L.; Anderson, J.; Basi, G.; Bienkowski, M. J.; Branstetter, D. G.; Chen, K. S.; Freedman, S. B.; Frigon, N. L.; Games, D.; Hu, K.; Johnson-Wood, K.; Kappenman, K. E.; Kawabe, T. T.; Kola, I.; Kuehn,R.; Lee, M.; Liu, W.; Motter, R.; Nichols, N. F.; Power, M.; Robertson, D. W.; Schenk, D.; Schoor, M.; Shopp, G. M.; Shuck, M. E.; Sinha, S.; Svensson, K. A.; Tatsuno, G.; Tintrup, H.; Wijsman, J.; Wright, S.; McConlogue, L.BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer’s disease therapeutics Hum. Mol. Genet. 2001, 10, 1317– 1324

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    Vassar, R.; Kuhn, P.-H.; Haass, C.; Kennedy, M. E.; Rajendran, L.; Wong, P. C.; Lichtenthaler, S. F.Function, therapeutic potential and cell biology of BACE proteases: current status and future prospectsJ. Neurochem. 2014, 130, 4– 28, DOI: 10.1111/jnc.12715

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    (a) Oehlrich, D.; Prokopcova, H.; Gijsen, H. J. M.The evolution of amidine-based brain penetrant BACE1 inhibitors Bioorg. Med. Chem. Lett. 2014, 24, 2033– 2045, DOI: 10.1016/j.bmcl.2014.03.025

    (b) Yuan, J.; Venkatraman, S.; Zheng, Y.; McKeever, B. M.; Dillard, L. W.; Singh, S. B.Structure-based design of β-site APP cleaving enzyme 1 (BACE) inhibitors for the treatment of Alzheimer’s disease. disease J. Med. Chem. 2013, 56, 4156– 4180, DOI: 10.1021/jm301659n

    (c) Probst, G.; Xu, Y. z.Small-molecule BACE1 inhibitors: a patent literature review (2006 – 2011) Expert Opin. Ther. Pat. 2012, 22, 511– 540, DOI: 10.1517/13543776.2012.681302

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    (a) Willem, M.; Garratt, A. N.; Novak, B.; Citron, M.; Kaufmann, S.; Rittger, A.; DeStrooper, B.; Saftig, P.; Birchmeier, C.; Haass, C.Control of peripheral nerve myelination by the β-Secretase BACE1 Science2006, 314, 664– 666, DOI: 10.1126/science.1132341

    (b) Hu, X.; Hicks, C. W.; He, W.; Wong, P.; Macklin, W. B.; Trapp, B. D.; Yan, R.Bace1 modulates myelination in the central and peripheral nervous system Nat. Neurosci. 2006, 9, 1520– 1525, DOI: 10.1038/nn1797

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    McConlogue, L.; Buttini, M.; Anderson, J. P.; Brigham, E. F.; Chen, K. S.; Freedman, S. B.; Games, D.; Johnson-Wood, K.; Lee, M.; Zeller, M.; Liu, W.; Motter, R.; Sinha, S.Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP transgenic mice J. Biol. Chem. 2007,282, 26326– 26334, DOI: 10.1074/jbc.M611687200

  14. 17.

    The CAS name represents the 3-aminothiadiazine tautomer, and the structures depicted in the manuscript represent the 3-iminothiadiazinane tautomer.

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Toremifene


Toremifene.svg

Toremifene

2-[4-[(Z)-4-chloro-1,2-diphenylbut-1-enyl]phenoxy]-N,N-dimethylethanamine

(Z)-2-[4-(4-Chloro-1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine
(Z)-4-Chloro-1,2-diphenyl-1-[4-[2-(N,N-dimethylamino)ethoxy]phenyl]-1-butene
(Z)-Toremifene
2-({4-[(1Z)-4-chloro-1,2-diphenylbut-1-en-1-yl]phenyl}oxy)-N,N-dimethylethanamine
4-chloro-1,2-diphenyl-1-[4-[2-(N ,N-dimethylamino)ethoxy]phenyl]-1-butene

Toremifene; Acapodene; Farestone; Z-Toremifene; Toremifeno; Toremifenum

Molecular Formula: C26H28ClNO
Molecular Weight: 405.95962 g/mol

cas 89778-26-7

 

Launched – 1988.Orion (FI), greast cancer

  1. Citrate, Toremifene, GTx-006
    NK-622

  2. Fareston
  3. FC 1157a
  4. FC-1157a
  5. FC1157a
  6. Toremifene
  7. Toremifene Citrate
  8. Toremifene Citrate (1:1)
  9. Toremifene, (E)-Isomer
    • C26H28ClNO · C6H8O7
    • Molecular Weight 598.08Toremifene citrate salt ≥98% (HPLC)Toremifene Citrate

Toremifene is a first generation selective estrogen receptor modulator (SERM). Like TAMOXIFEN, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue.

The company GTx is conducting phase III clinical trials for the prevention of prostate cancer in men who have been diagnosed with high grade prostatic intraepithelial neoplasia (PIN).

Toremifene citrate is an oral selective estrogen receptor modulator (SERM) which helps oppose the actions of estrogen in the body. Licensed in the United States under the brand name Fareston, toremifene citrate is FDA-approved for use in advanced (metastatic)breast cancer. It is also being evaluated for prevention of prostate cancer under the brand name Acapodene.[1]

ChemSpider 2D Image | Toremifene | C26H28ClNO

In 2007 the pharmaceutical company GTx, Inc was conducting two different phase 3 clinical trials; First, a pivotal Phase clinical trial for the treatment of serious side effects of androgen deprivation therapy (ADT) (especially vertebral/spine fractures and hot flashes, lipid profile, and gynecomastia) for advanced prostate cancer, and second, a pivotal Phase III clinical trial for the prevention of prostate cancer in high risk men with high grade prostatic intraepithelial neoplasia, or PIN. Results of these trials are expected by first quarter of 2008[2]

An NDA for the first application (relief of prostate cancer ADT side effects) was submitted in Feb 2009,[3] and in Oct 2009 the FDA said they would need more clinical data, e.g. another phase III trial.[4]

Originally developed at Orion, toremifene was subsequently licensed to Nippon Kayaku in Japan and to Asta Medica (now, part of Meda) in Germany.

toremifene.png

Synthesis

 ……….

PATENT

http://www.google.com/patents/CN104230723A?cl=en

Toremifene (Toremifene), chemical name (Z) -4- chloro-1,2-diphenyl–1- [4- (2- (N, N- dimethylamino) ethoxy yl) phenyl] -1-butene, having the structure I.Toremifene to tamoxifen (Tamoxifen) analogues with anti-estrogenic activity, can be used in the treatment of hormone-dependent breast cancer, and its E-isomer has the presence of estrogenic activity, E isomers toremifene may counteract anti-estrogenic activity, and therefore isomeric purity is essential toremifene.Toremifene was developed in 1983 by the Finnish Famos company, listed in 1996 by the Orion company in the EU, the trade name Fareston, 2002 to enter the country, the trade name of toremifene.

 

Figure CN104230723AD00051

RJ Toivola et al., European Patent EP95875, disclosed in U.S. Patent US4696949A synthetic route toremifene, that following a synthetic route, the synthetic route to phenol as a raw material, by acylation, rearrangement, alkyl group and an addition reaction to give 1,2-diphenyl -1- [4- [2- (N, N- dimethylamino) ethoxyphenyl]] – 1,4-diol (Compound 5) as the key intermediate, further HCl in ethanol or hydrochloric acid elimination reaction occurs, then get toremifene thionyl chloride reaction. The main problem with this approach is that the elimination reaction of the compound 5 in ethanol occurs when hydrochloric acid or concentrated hydrochloric acid, the resulting triaryl alcohol butyrate (Compound 6) having a Z / E configuration, both the ratio of 1: 2 ~ 2: 1, stereo selectivity is not high, and there are 5% of the cyclization by-product; on the Z / E configuration Miyoshi butyric fractional crystallization of alcohol, you can get pure Z-type Miyoshi butyric alcohol , but the yield is only 41%; then, Z-type Miyoshi butyric alcohol chlorination reaction occurs in the action of thionyl chloride, the purified product toremifene.

 

Figure CN104230723AD00061

 U.S. Patent US5491173A also reported another synthetic route toremifene namely the following two synthetic routes. The route to the aryl ketone (Compound 7) with a phenyl Grignard reagent addition reaction of ketone carbonyl groups to give triaryl-butanediol (compound 5), which is the elimination of toremifene and chlorinated reaction products happen again.

 

Figure CN104230723AD00062

 Chinese Patent Publication No. CN1125716A application reported an efficient synthesis of Z-type Miyoshi butyric alcohol (compound 6) method, US4696949A compared with the US patent, the method mild conditions, reduce the acid concentration and reaction temperature, reaction time, triarylphosphine butanediol (Compound 5) in concentrated hydrochloric acid or concentrated hydrochloric isopropanol or ethanol effect of concentrated hydrochloric acid, can be 60-78% selectivity and 95% yield of type 2 Miyoshi butyric alcohol But after Publication No. 0 02,126,969 attached eight patent applications after the inventor repeated experiments show that the technique disclosed in the patent application programs can not achieve their claimed technical effect.

 Publication No. CN102126969A of Chinese patent applications through the intermediate Miyoshi butyric alcohol occurs at a catalytic converter configuration of concentrated hydrochloric acid, while taking advantage of differences in solubility, so E- type Miyoshi butyric alcohol continuously into Z-type Miyoshi butyric alcohol (compound 6) precipitates, thereby undermining the balance, so that one of the E-type Miyoshi butyric alcohol continuously into Z-type Miyoshi butyric alcohol (compound 6) to give the Z-Miyoshi butyric alcohol ( Compound 6) and then get toremifene thionyl chloride after chlorination. Although to some extent, improve the yield, but increased operating procedure, is not conducive to industrial production.

Currently, the key intermediate is patent protected, and z-type Miyoshi butyric alcohol (compound 6) stereoselective low yield and isolated intermediates, to solve this problem, to overcome technical barriers to foreign pharmaceutical companies, urgent need to find a simple process, low cost, easy to separate and viable for large-scale production of synthetic routes.

To achieve the above object, according to one aspect of the present invention, there is provided a method of synthesizing toremifene, synthetic method comprising: a step S1, so that a compound having the structural formula II with a compound B having the structural formula III C occurs Mike Murray to give compound D having the structural formula IV; step S2, the Compound D and Compound E or Compound E of the hydrochloride salt of the formula V having a phenolic hydroxyl group on the occurrence of a selective alkylation reaction, to give a compound having the structural formula VI F; step S3, the compound F is reacted with thionyl chloride to give toremifene, wherein,

 Formula II is:

Figure CN104230723AD00071

Structural formula III as follows:

Figure CN104230723AD00072

Formula IV is

Figure CN104230723AD00073

Of formula V is C1CH2CH2N (CH 3) 2; formula VI is

Figure CN104230723AD00074

FIG. 1 illustrates the present invention obtained in Example 1 H NMR spectrum of compound D of implementation;

TORE 1

FIG. 2 shows the 1 H NMR spectrum of the present invention, the compound obtained in Example F;

TORE 2

FIG. 3 shows the present invention is a proton nuclear magnetic resonance spectrum of toremifene obtained in Example.

TORE 3

Figure 1, which shows a spectrum of results for Che bandit? (400 cm take, 01 ^ 0) 3 = 9.20 (! 8,1 1), 7.37 (^ = 7.4 to take, 2 1!), 7.30- 7. 23 (m, 3H), 1.22- 7. 15 (m, 2H), 7. 15 – 7. 06 ( m, 3H), 6. 61 (dd, J = 9. 0, 2. 2Hz, 2H), 6. 49 -. 6. 32 (m, 2H), 4 48 (s, 1H), 3 30 (. m, 2H), 2 55 (t, J = 7. 5Hz, 2H);. F proton nuclear magnetic resonance spectrum of the compound attached to the

Figure 2, showing spectrum results Che NMR (400MHz, DMSO) δ = 7. 36 (d, J = 7. 3Hz, 2H), 7. 31 – 7. 25 (m, 3H), 7. 21 – 7. 10 (m, 5H), 6. 75 – 6. 69 (m , 2H), 6. 59 (d, J = 8. 8Hz, 2H), 4. 49 (s, 1H), 3. 88 (t, J = 5. 8Hz, 2H), 3. 31 (d, J = 4. 3Hz, 2H), 2. 57 (t, J = 7.5Hz, 2H), 2.52 (t, J = 4.6Hz, 2H), 2 15 (s, 6H);.

Tommy remifentanil NMR hydrogen spectrum in Figure 3 attached, showing spectrum results Che NMR (400MHz, CDC13) δ = 7. 41 -. 7. 33 (m, 2H), 7 29 (dt, J = 7. 1, 2. 9Hz, 3H), 7. 20 (dd, J = 10. 0, 4. 3Hz, 2H), 7. 13 (dd, J = 7. 1, 4. 3Hz, 3H), 6.87- 6. 72 (m, 2H), 6. 57 (dd, J = 6. 8, 4. 8Hz, 2H), 3. 92 (t, J = 5. 8Hz, 2H), 3. 41 (t, J = 7. 5Hz, 2H), 2. 92 (t, J = 7. 5Hz, 2H), 2. 63 (t, J = 5. 8Hz, 2H), 2. 28 (s, 6H).

The synthetic routes above synthetic method are as follows:

 

Figure CN104230723AD00094

Synthesis of toremifene:

To a 2L reaction flask 1. 1L of toluene, 110g (0. 28mol) obtained in the above step Z configuration compound F, mixed to obtain a sixth system, the cooling system to the sixth mixed 0~5 ° C , was slowly added dropwise 99. 93g (0. 84mol) thionyl chloride addition was complete the formation of the seventh mixed system, the mixed system was slowly warmed to a seventh ll〇 ° C, for 1 hour to obtain a third product system, stop The third product heating and cooling system to 15~25 ° C, the third product system slowly poured into 1L of water, adding NaOH solution to a pH 9~10 and get the second system, the second in and a system for liquid separation, and the resulting aqueous phase to obtain a second solution was extracted with 1L toluene extraction, the organic phase of the second extraction solution and liquid separation were combined and concentrated to give crude toremifene, the crude product was mass ratio of 1 : mixed solvent of ethyl acetate and acetone 1 crystals to give 103. 7g toremifene products.

Synthesis of toremifene:

[0062] To a 5L reaction flask 3. 3L of toluene, 110g (0. 28mol) obtained in the above step Z configuration compound F, mixed to obtain a sixth system, the cooling system to the sixth mixed 0~5 ° C , was slowly added dropwise 33. 31g (0. 28mol) thionyl chloride addition was complete the formation of the seventh mixed system, the mixed system was slowly warmed to a seventh ll〇 ° C, after the reaction for 6 hours to obtain a third product system, stop The third product heating and cooling system to 15~25 ° C, the third product system slowly poured into 1L of water, potassium carbonate solution to a pH 9~10 and get the second system, the second and system for liquid separation, and the resulting aqueous phase to obtain a second solution was extracted with 1L ethyl acetate, the organic phase after the second extraction solution and liquid separation were combined and concentrated to give crude toremifene, the crude product was quality ratio was crystallized from acetone to give 92. 2g toremifene products.

Purity of toremifene following method:

[0107] to take the product, add the mobile phase dissolved and diluted into 1ml of 1. Omg solution containing, according to HPLC octadecylsilane bonded silica as a filler to square 1% trifluoroacetic acetic acid aqueous solution (A) and acetonitrile (B) as the mobile phase gradient elution (T = Omin 10% B; T = lOmin 95% B; T = 12min 100% B; T = 15min 10% B), detection wavelength 210nm; area normalization method to calculate the Z configuration purity compound F, where F Z configuration compound retention time of 6. 76min. The purity of the above calculation or Z configuration detection obtained compound D, compound D Z configuration and E configuration of the weight ratio, toremifene yield and purity are reported in Table 1 below.

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PATENT

http://www.google.com/patents/US5491173

c) 4-chloro-1,2-diphenyl-1-[4-[2-(N ,N-dimethylamino)ethoxy]phenyl]-1-butene (Z and E)

(Z)-isomer: The reaction is performed under dry conditions. 42.4 g of (Z)-1,2-diphenyl-1-[4-[2-(N,N-dimethylamino )ethoxy]phenyl]-1-buten-4-ol are dissolved in 250 ml of chloroform. Then 23.8 g of thionyl chloride areadded dropwise. The mixture is refluxed 3 h. The solvent is evaporated, after which the product is recrystallized from ethyl acetate. The yield ofthe hydrochloride salt is 36.7 g (83%), m.p. 194°-6° C. The base can be liberated from the Salt with 1M sodium carbonate solution, after which the base is extracted in toluene. The toluene solution is dried and the solvent is evaporated. The free base has m.p. 108°-10° C. (from acetone).

1 H-NMR-spectrum (CDCl3): δ 2.27 (6H, s), 2.63 (2H, t), 2.91 (2H, t), 3.41 (2H, t), 3.92 (2H, t), 6.54 (2H, d), 6.79 (2H. d), 7.15(5H, s), 7.31 (5H, s). MS: m/z 405/407 (M+, 7/3), 72 (20), 58 (100).

The citric acid salt can be prepared as follows: 40.6 g of the (Z)-isomer as a free base are dissolved in 175 ml of warm acetone and 24.3 g of citric acid are dissolved in 100 ml of warm acetone. The solutions are combined and the mixture is allowed to cool. The citrate, m.p. 160°-162° C., is collected by filtration.

(E)-isomer: The compound is prepared from (E)-1,2-diphenyl-1-[4-[2-(N ,N-dimethylamino)ethoxy]phenyl]-1-buten-4-ol in the same manner as the corresponding (Z)-isomer. The hydrochloride salt is crystallized from toluene. The yield is 35.8 g (81%) of a product having m.p. 183°-5° C. The base can be liberated from the salt in the same manner as the corresponding (Z)-isomer. It has m.p. 69°-71° C. (from hexane).

1 H-NMR-spectrum (CDCl3): b 2.34 (6H, s), 2.74 (2H, t), 2.97 (2H,t), 3.43 (2H, t), 4.08 (2H, t), 6.80-7.30 (14H, m).

MS: m/z 405/407 (M+, 7/3) 72 (19) 58 (100)

 

EXAMPLE 4

4-chloro-1,2-diphenyl-1-[4-[2-(N ,N-diethylamino)ethoxy]phenyl ]-1-butene (Z and E)

43.3 g of 1,2-diphenyl-1-[4-[2-(N,N-diethylamino)ethoxy]phenyl]butane-1,4-diol (pureenantiomer pairs or their mixture: m.p. of (RR,SS)-pair is 107°-9° C.)is suspended in 250 ml of toluene, after which 25ml toluene is distilled off to dry the solution. The mixture is cooled to 0° C. with stirring. While stirring and keeping the temperature at 0° C. or a little below, 47.6 g of thionyl chloride of good qualityare added. The mixture is stirred for 1 h at 0° C. and the temperature is then allowed to rise to 22° C. The mixture is stirred at 80° C. until the reaction is completed (about 3 h). After that, water is added to decompose the excess of thionyl chloride followed by 20% sodium hydroxide solution to liberate the product from itshydrochloride salt. The aqueous layer is discarded and the toluene layer iswashed with water. Then the solvent is evaporated to leave a mixture of (Z)- and (E)isomers (Z:E 7:3) as an oil in quantitative yield.

(Z)-isomer: The (Z)-isomer is isolated from the isomer mixture above as thehydrochloride salt because of the low melting point of the free base. The m.p. of the hydrochloride salt is 178°-80° C. The (Z)-isomermay be freed from its salt by any normal method.

1 H-NMR-spectrum (CDCl3): δ 1.01 (6H, t), 2.57 (4H, q), 2.77 (2H, t), 2.91 t), 3.41 (2H, t), 3.90 t), 6.53 (2H, d), 6.78 (2H, d), 7.15 (5H, s), 7.31 (5H, s). (E)-isomer:

1 H-NMR-spectrum (CDCl3): δ 1.07 (6H, t), 2.66 (4H, q), 2.89 (2H, t), 2.97 (2H, t), 3.42 (2H, t), 4.07 (2H, t), 6.90-7.20 (10H, m).

……………….

SEE

http://www.google.co.ug/patents/EP0095875B1?cl=en

………….

http://www.intechopen.com/books/topics-on-drug-metabolism/electrochemical-methods-for-the-in-vitro-assessment-of-drug-metabolism

References

  1.  Price N, Sartor O, Hutson T, Mariani S. Role of 5a-reductase inhibitors and selective estrogen receptor modulators as potential chemopreventive agents for prostate cancer. Clin Prostate Cancer 2005;3:211-4. PMID 15882476
  2.  “GTx’s Phase III Clinical Development of ACAPODENE on Course Following Planned Safety Review” (Press release). GTx Inc. 2007-07-12. Retrieved 2006-07-14.
  3.  “GTx Announces Toremifene 80 mg NDA Accepted for Review by FDA” (Press release).
  4.  “GTx and Ipsen End Prostate Cancer Collaboration due to Costs of FDA-Requested Phase III Study”. 2 Mar 2011
Toremifene
Toremifene.svg
Systematic (IUPAC) name
2-{4-[(1Z)-4-chloro-1,2-diphenyl-but-1-en-1-yl]phenoxy}-N,N-dimethylethanamine
Clinical data
AHFS/Drugs.com monograph
MedlinePlus a608003
Pharmacokinetic data
Protein binding more than 99.5%
Biological half-life 5 days
Identifiers
CAS Registry Number 89778-26-7 Yes
ATC code L02BA02
PubChem CID: 3005573
IUPHAR/BPS 4325
DrugBank DB00539 Yes
ChemSpider 2275722 Yes
UNII 7NFE54O27T Yes
KEGG D08620 Yes
ChEBI CHEBI:9635 Yes
ChEMBL CHEMBL1655 Yes
Chemical data
Formula C26H28ClNO
Molecular mass 405.959 g/mol
Patent Submitted Granted
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