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ORGANIC SPECTROSCOPY

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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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Silevertinib


Silevertinib

CAS 2607829-38-7

MF C30H30ClFN6O2 MW561.0 g/mol

(E)-N-[4-(3-chloro-2-fluoroanilino)-7-[2-[(1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl]quinazolin-6-yl]-4-morpholin-4-ylbut-2-enamide

(2E)-N-[4-(3-chloro-2-fluoroanilino)-7-{[(1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl}quinazolin-6-yl]-4-(morpholin-4-yl)but-2-enamide
epidermal growth factor receptor tyrosine kinase inhibitor, antineoplastic, BDTX-1535, BDTX 1535, CANCER, Glioblastoma, Black Diamond Therapeutics, RP9F537KVY

Silevertinib is an investigational new drug that is being evaluated by Black Diamond Therapeutics for the treatment of glioblastoma and non-small cell lung cancer.[1] It is a EGFR protein tyrosine kinase inhibitor.[1][2]

Silevertinib (formerly known as BDTX-1535) is an investigational, orally bioavailable, fourth-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) developed by Black Diamond Therapeutics. It is specifically engineered to be brain-penetrant and to target a broad spectrum of both classical and non-classical EGFR mutations, as well as resistance mutations, while sparing wild-type EGFR to reduce side effects.

Silevertinib is an orally bioavailable, brain penetrating, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, silevertinib selectively targets, irreversibly binds to, and inhibits the activity of various EGFR alterations and mutations, including certain intrinsic and acquired resistance mutations. This prevents EGFR-mediated signaling in susceptible tumor cells. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.

Mechanism of Action

Silevertinib works by selectively and irreversibly binding to mutated EGFR receptors. EGFR is a receptor tyrosine kinase that, when mutated, triggers uncontrolled cell division and tumor vascularization. By shutting down this signaling cascade, silevertinib induces tumor cell death and inhibits further growth.

A major clinical advantage of the drug is its ability to cross the blood-brain barrier, allowing it to target central nervous system (CNS) tumors and brain metastases that many traditional therapies fail to reach.

Target Indications & Clinical Data

Silevertinib is primarily being studied for two aggressive types of cancer:

  • Non-Small Cell Lung Cancer (NSCLC): It targets frontline patients with classical and over 50 non-classical EGFR driver mutations, as well as patients who have developed the acquired C797S resistance mutation from prior treatments. Phase 2 clinical trial data presented at the American Society of Clinical Oncology (ASCO) 2026 Annual Meeting showcased robust efficacy:
    • Objective Response Rate (ORR): 60% in treatment-naïve patients.
    • CNS Response Rate: An impressive 86% intracranial ORR in patients presenting with brain metastases.
    • Disease Control Rate (DCR): 91%.
  • Glioblastoma Multiforme (GBM): In May 2026, a randomized Phase 2 trial was initiated for newly diagnosed patients with EGFRvIII-positive, MGMT-negative glioblastoma, evaluating silevertinib in combination with temozolomide.

Safety Profile & Side Effects

The adverse events of silevertinib are consistent with the broader class of EGFR inhibitors. The most frequently reported treatment-related adverse events (TRAEs) include:

  • Rash
  • Diarrhea
  • Stomatitis (mouth sores)
  • Paronychia (nail bed inflammation)

While a high percentage of patients (up to 77–84%) require dose reductions to manage these side effects, data shows that 86% of responding patients maintained or deepened their clinical response even after dropping to a lower dose. The treatment discontinuation rate remains low at roughly 9–14%, indicating the drug is manageable for long-term therapy.

Regulatory Status

As an investigational drug, silevertinib is not yet approved for commercial use by global regulatory agencies. However, the manufacturer anticipates regulatory feedback from the US FDA regarding its registration pathway for first-line NSCLC therapy.

  • OriginatorBlack Diamond Therapeutics
  • Class2 ring heterocyclic compounds; Amides; Amines; Aniline compounds; Antineoplastics; Halogenated hydrocarbons; Morpholines; Quinazolines; Small molecules
  • Mechanism of ActionErbB receptor antagonists
  • Phase IIGlioblastoma
  • Phase I/IINon-small cell lung cancer
  • Phase 0Glioma
  • 06 Aug 2026Black Diamond Therapeutics anticipates regulatory feedback from the US FDA on registration path of silevertinib for Non-small cell lung cancer (First-line therapy) in the fourth quarter of 2026 (Black Diamond pipeline, May 2026)
  • 02 Jun 2026Efficcay and adverse event data from phase I/II trial in Non-small cell lung cancer presented at the 62nd Annual Meeting of the American Society of Clinical Oncology (ASCO-2026)
  • 21 May 2026Efficacy and adverse events data from a phase I/II trial in Non small cell lung cancer released by Black Diamond Therapeutics

SYN

PAT

[WO2021030711]

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2021030711&_cid=P21-MU6CBO-49598-1

Example 33. Synthesis of Compound No. 37 ((E)-N-(4-((3-chloro-2-fluorophenyl)amino)-7-(((1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl)ethynyl)quinazolin-6-yl)-4-morpholinobut-2-enamide)

PAT

WO2026064728

https://patentscope.wipo.int/search/en/detail.jsf;jsessionid=2A0850BB19B29C599F589233A4E61A49.wapp2nB?docId=WO2026064728&_cid=P21-MU6C38-37561-1

PAT

US20220298120

https://patentscope.wipo.int/search/en/detail.jsf?docId=US375116378&_cid=P21-MU6C60-41372-1

Example 33. Synthesis of Compound No. 37 ((E)-N-(4-((3-chloro-2-fluorophenyl)amino)-7-(((1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl)ethynyl)quinazolin-6-yl)-4-morpholinobut-2-enamide)

Step 1. To a solution of (E)-4-bromobut-2-enoic acid (5.00 g, 30.3 mmol) and dimethylformamide (22.2 mg, 303 umol) in dichloromethane (20 mL) was added (COCl) 2 (3.85 g, 30.3 mmol) dropwise at 0° C. under N 2. The mixture was stirred at 0-25° C. for 4 h. On completion, the reaction mixture was concentrated in vacuo to give (E)-4-bromobut-2-enoyl chloride (5.8 g, crude) as a yellow oil.
      Step 2. To a solution of N4-(3-chloro-2-fluoro-phenyl)-7-[2-[(1S,5R)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl]quinazoline-4,6-diamine (4.00 g, 9.81 mmol) and triethylamine (2.98 g, 29.4 mmol) in dichloromethane (70 mL) was added a solution of (E)-4-bromobut-2-enoyl chloride (3.60 g, 19.6 mmol) in dichloromethane (15 mL) dropwise at 0° C. and the mixture was stirred at 0° C. for 10 min. On completion, the reaction mixture was concentrated under vacuum to give (E)-4-bromo-N-(4-((3-chloro-2-fluorophenyl)amino)-7-4(1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl)ethynyl)quinazolin-6-yl)but-2-enamide (5.44 g, crude) as a yellow solid, which was used for next step directly. m/z ES+ [M+H] + 556.0
      Step 3. A mixture of (E)-4-bromo-N-[4-(3-chloro-2-fluoro-anilino)-7-[2-[(1S,5R)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl]quinazolin-6-yl]but-2-enamide (5.44 g, 9.80 mmol), morpholine (1.71 g, 19.6 mmol), triethylamine (992 mg, 9.80 mmol) in dichloromethane (1.5 mL) was degassed and purged with N 2 for 3 times, and then the mixture was stirred at 25° C. for 12 hrs under N 2 atmosphere. On completion, the reaction mixture was concentrated in vacuo to give a residue. The residue was purified by reverse phase flash [acetonitrile/(0.1% formic acid in water), 0% to 90%] to give 2.8 g crude product. Then it was purified by Prep-HPLC [column: Waters Xbridge BEH C18 250*50 mm*10 um; mobile phase: [water (0.05% ammonium hydroxide v/v)-acetonitrile]; B %: 35%-55%, 22 min] to give 2.2 g crude product. Then the crude product was triturated with EA/petroleum ether=5/1 (200 mL) twice to give (E)-N-[4-(3-chloro-2-fluoro-anilino)-7-[2-[(1S,5R)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl]quinazolin-6-yl]-4-morpholino-but-2-enamide (1.84 g, 33% yield) as a yellow solid. m/z ES+ [M+H] + 561.3; 1H NMR (400 MHz, DMSO-d 6) δ 10.06 (s, 1H), 9.78 (s, 1H), 8.67 (s, 1H), 8.48 (s, 1H), 7.80 (s, 1H), 7.50 (s, 2H), 7.29 (t, J=7.6 Hz, 1H), 6.81 (td, J=5.6, 15.6 Hz, 1H), 6.45 (d, J=15.6 Hz, 1H), 3.65-3.60 (m, 4H), 3.17 (d, J=5.2 Hz, 2H), 3.11 (d, J=8.4 Hz, 1H), 2.93 (d, J=9.0 Hz, 1H), 2.46-2.38 (m, 6H), 2.26 (s, 3H), 1.98-1.90 (m, 1H), 1.38 (t, J=4.4 Hz, 1H), 1.03 (dd, J=4.0, 8.0 Hz, 1H).

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References

  1.  “Silevertinib”. AdisInsight. Springer Nature Switzerland AG. Retrieved 5 July 2026.
  2.  Joshi H, Sheikh MS (August 2025). “Cell Death, Molecular Targeted Therapies, and Metabolic Reprogramming in EGFR-Mutant Lung Cancer”. Cancers. 17 (17). Basel: 2791. doi:10.3390/cancers17172791. PMC 12427363. PMID 40940888.

PAT

Clinical data
Other namesRVU-120
Identifiers
IUPAC name
CAS Number2607829-38-7
PubChem CID156071569
IUPHAR/BPS13371
UNIIRP9F537KVY
KEGGD13300
Chemical and physical data
FormulaC30H30ClFN6O2
Molar mass561.06 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

///////////silevertinib, anax labs, epidermal growth factor receptor tyrosine kinase inhibitor, antineoplastic, BDTX-1535, BDTX 1535, CANCER, Glioblastoma, Black Diamond Therapeutics, RP9F537KVY

#silevertinib, #anax labs, #epidermal growth factor receptor tyrosine kinase inhibitor, #antineoplastic, #BDTX-1535, #BDTX 1535, #CANCER, #Glioblastoma, #Black Diamond Therapeutics, #RP9F537KVY

Iodofalan (131I)


Iodofalan (131I)

CAS 76641-05-9

MFC9H10131INO2

Molecular FormulaC9H10INO2

Molecular Weight295.09

4-(131I)iodo-L-phenylalanine

(2S)-2-amino-3-(4-iodophenyl)propanoic acid
radiopharmaceutical, antineoplastic, Phase 2, Glioblastoma, 606VTF676Y, 131I-TLX-101, ACD 101

  • 4-Iodophenylalanine I-131
  • 4-(131I)Iodo-L-phenylalanine
  • 4-Iodo-L-phenylalanine-131I
  • ACD-101
  • L-Phenylalanine, 4-(iodo-131I)-
  • OriginatorTherapeia
  • DeveloperTelix Pharmaceuticals; Therapeia
  • ClassAmino acids; Antineoplastics; Radioisotopes; Radiopharmaceutical diagnostics; Radiopharmaceuticals; Small molecules
  • Mechanism of ActionApoptosis stimulants; Positron-emission tomography enhancers
  • Orphan Drug StatusYes – Glioblastoma
  • Phase IIGlioblastoma
  • 14 Oct 2025Telix Pharmaceuticals receives IND approval for TLX 101 in Glioblastoma
  • 27 Jul 2025Telix Pharmaceuticals plans a phase III IPAX BrIGHT trial for Glioblastoma (Monotherapy, Combination therapy, Recurrent, Second-line therapy or greater) in Australia(IV) (NCT07100730)(EudraCT2025-521785-10) in September 2025
  • 16 Apr 2025Telix has submitted for ethics approval a registration-enabling study of TLX101 in recurrent glioblastoma.

Iodofalan (131I) is a radiopharmaceutical that has garnered significant attention in oncological research due to its targeted therapeutic potential. This compound, which includes the radioactive isotope Iodine-131, has been explored for its efficacy in treating certain types of cancers, particularly those associated with the thyroid. Various research institutions worldwide have been studying Iodofalan (131I) to better understand its clinical benefits, optimize its usage, and minimize potential side effects. As a drug type, Iodofalan (131I) is categorized as a targeted radiopharmaceutical therapy, which leverages the properties of radioactive isotopes to destroy cancer cells with precision. Currently, its primary indications include differentiated thyroid cancer and non-resectable metastatic thyroid cancer, among other investigational uses.

Iodofalan (131I) Mechanism of Action

The mechanism of action for Iodofalan (131I) centers on the properties of Iodine-131, a beta-emitting isotope. When administered, Iodofalan (131I) is selectively absorbed by thyroid cells. This selectivity is due to the thyroid gland’s natural ability to uptake iodine, a key element required for the production of thyroid hormones. Cancerous thyroid tissues retain this ability, making them ideal targets for Iodofalan (131I) therapy.

Once absorbed by the thyroid cancer cells, the radioactive decay of Iodine-131 begins. This decay process emits beta particles, which possess sufficient energy to destroy nearby cells. The radiation from these beta particles causes direct DNA damage, leading to cell death. Additionally, the gamma radiation emitted by Iodine-131 can be used diagnostically to track the distribution and uptake of the compound in the body via imaging techniques such as SPECT (Single Photon Emission Computed Tomography).

The dual role of Iodofalan (131I) in both treatment and diagnostic contexts underscores its importance in managing thyroid cancers. By delivering a localized radiation dose to thyroid cancer cells, Iodofalan (131I) minimizes damage to surrounding healthy tissues, which is a significant advantage over traditional external beam radiotherapy.

What is the indication of Iodofalan (131I)?

The primary indication for Iodofalan (131I) is the treatment of differentiated thyroid cancer, a category that includes papillary and follicular thyroid cancers. These subtypes are characterized by their ability to absorb iodine, making them particularly amenable to radioiodine therapy. Iodofalan (131I) is typically used in cases where the thyroid cancer is not amenable to surgical removal or has metastasized to other parts of the body. In such scenarios, the radiopharmaceutical offers a non-invasive therapeutic option that can target and destroy cancer cells even in distant metastatic sites.

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=US42129729&_cid=P21-MHE8B5-15309-1

EXAMPLE 1

      4-Bromo-L-phenylalanine (4-BrPA), 3-bromo-L-phenylalanine (3-BrPA), 4-iodo-L-phenylalanine (4-IPA), 4-ter.butyltinn-L-phenylalanine (4-TBSnPA), 3-ter.butyltinn-L-phenylalanine (3-TBSnPA), 4-methylsilyl-L-phenylalanine (4-Me 3SiPA) and 3-methylsilyl-L-phenylalanine (3-Me 3SiPA) used as starting materials (precursor) for radiolabeling were either purchased commercially or prior synthesized in analogy to the literature. Unless stated otherwise, all other chemicals and solvent were of analytical grade and obtained commercially or via our local hospital pharmacy. Sodium [ 124I]iodide, sodium [ 125I]iodide, sodium [131I]iodide, sodium [ 77Br]bromide, sodium [ 82Br]bromide, and sodium [ 211At]astatine for radiolabeling was obtained in the highest obtainable radiochemical purity, generally in 0.01 N NaOH or in phosphate buffered saline (PBS) from different suppliers. HPLC purification was performed on a Hewlett Packard HPLC system consisting of a binary gradient pump (HP 1100), a Valco 6-port valve with 2500 μl loop, a variable wavelength detector (HP 1100) with a UV detection at 254 nm and a sodium iodide scintillation detector (Berthold, Wildbad, Germany), using reversed-phased column (250×4 mm, Nucleosil-100). The column was eluted at different flow rates in with water/ethanol/acetic acid (89:10:1; v/v) or PBS/ethanol (90:10; v/v).
      The proposed radiolabeled phenylalanines were obtained either by non-isotopic halogen exchange (carrier-added/c.a.) or by radio-demetalation of the corresponding precursor as described in the general scheme 1, resulting to no-carrier-added (n. c. a) products after HPLC separation.

EXAMPLE 2

General synthesis of 3,4-[124I]iodo-L-phenylalanine (m, p-IPA-124), 3,4-[125I]iodo-L-phenylalanine (m,p-IPA-125) and 3,4-[131I]iodo-L-phenylalanine (m,p-IPA-131) by non-isotopic radioiodo-debromination

      A solution of carrier free sodium [ 124I]iodide, sodium [ 125I]iodide or sodium [ 131I]iodide (up to 5 GBq) and 5 μl aqueous Na 2S 2O 5 (4.0 mg Na 2S 2O 5/ml) was evaporated to dryness by passing a stream of nitrogen through a reaction vessel at 100° C., followed by addition of 200 μl of the corresponding L-bromophenylalanine (0.25-0.5 mg/ml 0.1 N H 3PO 4), 20 μl aqueous L-ascorbic acid (10 mg/ml) and 20 μl aqueous Cu(II) sulphate (0.10 mol/l). The reaction vessel was heated for 30 min at 170° C., cooled and the mixture diluted with up to 500 μl water. The radioiodinated product was separated from unreacted starting materials and radioactive impurities by HPLC.
      Generally, 3/4-IPA-124, 3/4-IPA-125 and m/p-IPA-131 were obtained in 88±10% radiochemical yield, with a specific activity >500 GBq/μmol. The fraction containing the radioiodinated products was collected into a sterile tube, buffered with 0.5 M phosphate buffered saline (pH 7.0; Braun, Melsungen, Germany), and sterile filtered through a 0.22 μm sterile membrane (Millex GS, Millipore, Molsheim, France) to an isotonic and injectable radiopharmaceutical for in vitro and in vivo investigations.

PAT

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//////////Iodofalan (131I), radiopharmaceutical, antineoplastic, Phase 2, Glioblastoma, 606VTF676Y, 131I-TLX-101, ACD 101

BQ-788


BQ-788.svg

ChemSpider 2D Image | BQ-788 | C34H50N5NaO7

Image result for bq-788

Image result for bq-788

BQ-788

  • Molecular FormulaC34H50N5NaO7
  • Average mass663.780 Da

SP ROT +3.8 ° Conc: 1.032 g/100mL; methanol; Wavlenght: 589.3 nm, Development of an efficient strategy for the synthesis of the ETB receptor antagonist BQ-788 and some related analogues
Peptides (New York, NY, United States) (2005), 26, (8), 1441-1453., https://doi.org/10.1016/j.peptides.2005.03.022

FOR FREE FORM +19.6 °, Conc: 0.998 g/100mL; : N,N-dimethylformamide; 589.3 nm

CAS 156161-89-6 [RN]
CAS 173326-37-9 FREE ACID
2,6-Dimethylpiperidinecarbonyl-γ-Methyl-Leu-Nin-(Methoxycarbonyl)-D-Trp-D-Nle
BQ 788 sodium salt
BQ788
D-Norleucine, N-(((2R,6S)-2,6-dimethyl-1-piperidinyl)carbonyl)-4-methyl-L-leucyl-1-(methoxycarbonyl)-D-tryptophyl-, monosodium salt
D-Norleucine, N-((cis-2,6-dimethyl-1-piperidinyl)carbonyl)-4-methyl-L-leucyl-1-(methoxycarbonyl)-D-tryptophyl-, monosodium salt
D-Norleucine, N-[[(2R,6S)-2,6-dimethyl-1-piperidinyl]carbonyl]-4-methyl-L-leucyl-1-(methoxycarbonyl)-D-tryptophyl-, sodium salt (1:1)
MFCD00797882
N-[N-[N-[(2,6-Dimethyl-1-piperidinyl)carbonyl]-4-methyl-L-leucyl]-1-(methoxycarbonyl)-D-tryptophyl]-D-norleucine sodium salt
 
Sodium N-{[(2R,6S)-2,6-dimethylpiperidin-1-yl]carbonyl}-4-methyl-L-leucyl-N-[(1R)-1-carboxylatopentyl]-1-(methoxycarbonyl)-D-tryptophanamide
2,6-Dimethylpiperidinecarbonyl-γ-Methyl-Leu-Nin-(Methoxycarbonyl)-D-Trp-D-Nle

BQ-788 is a selective ETB antagonist.[1]

presumed to be under license from Banyu , was investigating BQ-788, a selective endothelin receptor B (ETRB) antagonist, for treating metastatic melanoma. By December 2009, the drug was in validation.

Also claimed is their use as an ETBR antagonist and for treating cancers, such as brain cancer, pancreas cancer, colon cancer, breast cancer, ovary cancer, prostate cancer, glioblastoma, solid tumor, melanoma and squamous cell carcinoma. Represent a first filing from ENB Therapeutics Inc and the inventors on these deuterated forms of BQ-788. Melcure SarL ,

SYN

By Brosseau, Jean-Philippe et alFrom Peptides (New York, NY, United States), 26(8), 1441-1453; 2005

CONTD…………

PAPER

https://pubs.acs.org/doi/pdf/10.1021/jo00130a028

N-(cw-2,6-Dimethylpiperidinocarbonyl)-y-methylleucylD-l-(methoxycarbonyl)tryptophanyl-D-norleucine Sodium Salt (1, BQ-788). To a solution of 15 (3.5 g, 5.5 mmol) in methanol (50 mL) was slowly added 5% aqueous NaHCOs (300 mL) over a period of 30 min. The solution was stirred until clarity was achieved (30 min, 23 °C). The solution was diluted with water (200 mL), and the resulting solution was passed through a C18 (60 mL) cartridge preequilbrated in water. BQ-788 (1) was eluted with methanol (2 x 50 mL), concentrated under reduced pressure, resuspended in water (50 mL), and lyophilized to quantitatively yield compound 1 as a white powder:

HPLC £r = 16.4 (gradient A, > 99%);

NMR (400 MHz, DMSO-d6) ó 0.80 (s, 9H), 0.74-0.85 (m, 3H), 1.00 (d, 3H), 1.02 (d, 3H), 1.10-1.25 (m, 6H), 1.30-1.55 (m, 6H), 1.60-1.75 (m, 2H), 2.92 (dd, 1H), 3.12 (dd, 1H), 3.78 (m, 1H), 3.95 (s, 3H), 4.08 (m, 1H), 4.13 (m, 1H), 4.29 (m, 1H), 4.50 (m, 1H), 5.98 (d, 1H), 7.22 (t, 1H), 7.32 (t, 1H), 7.50 (s, 1H), 7.58 (br d, 1H), 7.65 (d, 1H), 8.05 (d, 1H), 8.15 (br d, 1H) ESMS m/z 640.6 (M).

PATENT

WO-2019140324

Novel deuterated analogs of a substituted heterocyclic compound, particularly BQ-788 , processes for their preparation and compositions and combinations comprising them are claimed.

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2019140324&tab=PCTDESCRIPTION&_cid=P22-JYJK98-13819-1

PAPER

https://www.sciencedirect.com/science/article/abs/pii/S0196978105001415

Image result for bq-788

PAPER

By He, John X.; Cody, Wayne L.; Doherty, Annette M., From Journal of Organic Chemistry (1995), 60(25), 8262-6

Journal of medicinal chemistry (1996), 39(12), 2313-30.

References

  1. ^ Okada, M; Nishikibe, M (Winter 2002). “BQ-788, a selective endothelin ET(B) receptor antagonist”. Cardiovascular drug reviews. 20 (1): 53–66. PMID 12070534.
BQ-788
BQ-788.svg
Names
Systematic IUPAC name

Sodium N-{[(2R,6S)-2,6-dimethyl-1-piperidinyl]carbonyl}-4-methyl-L-leucyl-N-[(1R)-1-carboxylatopentyl]-1-(methoxycarbonyl)-D-tryptophanamide
Identifiers
3D model (JSmol)
ChemSpider
PubChem CID
Properties
C34H50N5NaO7
Molar mass 663.792 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

///////////BQ-788, BQ 788, BQ788, ETBR antagonist, cancers,  brain cancer, pancreas cancer, colon cancer, breast cancer, ovary cancer, prostate cancer, glioblastoma, solid tumor, melanoma, squamous cell carcinoma, PEPTIDE

CCCC[C@H](C(=O)O)NC(=O)[C@@H](Cc1cn(c2c1cccc2)C(=O)OC)NC(=O)[C@H](CC(C)(C)C)NC(=O)N3[C@@H](CCC[C@@H]3C)C