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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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Direclidine

January 18, 2026 2:41 am / Leave a comment


Direclidine

CAS 1803346-98-6

MF C19H30N4O2 MW346.5 g/mol

ethyl 2-[4-(2-methylpyrazol-3-yl)piperidin-1-yl]-6-azaspiro[3.4]octane-6-carboxylate

6-Azaspiro[3.4]octane-6-carboxylic acid, 2-[4-(1-methyl-1H-pyrazol-5-yl)-1-piperidinyl]-, ethyl ester, cis-

ethyl (2r,4s)-2-[4-(1-methyl-1H-pyrazol-5-yl)piperidin-1-yl]-6-azaspiro[3.4]octane-6-carboxylate
muscarinic M4 receptor positive allosteric modulator, TXB4V44U24, NBI-1117568, NBI 1117568

Direclidine (INNTooltip International Nonproprietary Name;[2] developmental code names NBI-1117568, HTL-0016878)[1] is an investigational antipsychotic drug for schizophrenia[3] that was out-licensed from Nxera Pharma to Neurocrine Biosciences, a United States-based pharmaceutical company.[4][1][5] It is an oral small molecule.[6][7]

Direclidine (NBI-1117568) is an investigational, oral drug in Phase 3 trials for schizophrenia, developed by Neurocrine Biosciences, working as a selective M4 muscarinic receptor agonist to treat psychosis by modulating dopamine indirectly. It’s an innovative small molecule with potential for neuropsychiatric disorders, showing promise in early trials and aiming to offer a new treatment approach beyond traditional antipsychotics. 

Key aspects of Direclidine:

  • Drug Class: Small molecule, muscarinic M4 receptor agonist, antipsychotic.
  • Mechanism: Acts as a selective agonist for the M4 receptor, which indirectly helps improve dopamine levels, targeting schizophrenia symptoms.
  • Developer: Originally from Nxera Pharma, licensed to Neurocrine Biosciences.
  • Status: In Phase 3 clinical trials for schizophrenia.
  • Significance: Offers a novel mechanism for treating schizophrenia, potentially with fewer side effects than current treatments.
  • Other Uses: Also being explored for bipolar mania and other neuropsychiatric conditions. 

Development Timeline & Data:

  • Positive Phase 2 data was announced in August 2024, showing promise for its use in schizophrenia.
  • Topline data from ongoing Phase 3 studies is expected around 2027. 

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2015118342&_cid=P20-MKJ4D7-04370-1

Typical procedure for the preparation of piperidines via sodium triacetoxyborohydride reductive amination, Boc-deprotection and ethylcarbamate formation as exemplified by the preparation of Example 1 -7, ethyl 2-[4-(1 -methyl-1 H-imidazol-2-yl)piperidin-1 -yl]-6-aza s p i ro [3.4] octa n e -6 -ca rb oxy late

Example 1-7

4-(1 -Methylimidazol-2-yl)piperidine hydrochloride (0.244 g, 1 .21 mmol) and 6-Boc-2-oxo-6-azaspiro[3,4]octane (0.273 g, 1 .21 mmol) were dissolved in DCM (10 mL) at rt and titanium isopropoxide (0.4 mL, 2.42 mmol) was added. The reaction mixture was stirred at rt for 1 h. The reaction mixture was cooled to -5 °C, then STAB (0.513 g, 2.42 mmol) and acetic acid (27 pL, 480 pmol) were added and the reaction mixture was stirred overnight under nitrogen while warming to rt. The reaction mixture was quenched with the addition of NaHC03 (sat aq.) (10 mL) and diluted with DCM then filtered through a pad of celite. The layers were separated and the aqueous layer was extracted with DCM. The combined DCM layers were washed with brine, then dried over MgS04. The solvents were removed in vacuo, and the residue was purified by column chromatography (normal phase, [Biotage SNAP cartridge KP-sil 25g , 40-63 μΠΊ, 60 A, 50 mL per min, gradient 1 % to 10% MeOH in DCM]) to give an inseparable mixture of isomers of terf-butyl 2-[4-(1 -methyl-1 H-imidazol-2-yl)piperidine]-6-azaspiro[3.4]octane-6-carboxylate (0.330 g, 72%) as a yellow gum.

LCMS (Method A): m/z 374 (M+H)+ (ES*), at 1.68 min, UV inactive.

Terf-butyl 2-[4-(1-methyl-1 H-imidazol-2-yl)piperidine]-6-azaspiro[3.4]octane-6-carboxylate (0.326 g, 0.87 mmol) was dissolved in 4 M hydrogen chloride in dioxane (1 .2 mL, 5.2 mmol). The reaction mixture was stirred at rt for 18 h. The volatiles were then removed in vacuo and the residue dissolved DCM (17 mL) and triethylamine (0.49 mL, 3.49 mmol). Ethyl chloroformate (125 μί, 1.31 mmol) was added dropwise and the solution stirred at rt for 18 h. The mixture was then poured into NaHC03 (aq) (75 mL) and DCM (75 mL), extracted (2 x 75 mL) , and the combined DCM extracts washed with brine (20 mL) then dried over MgSO*. After concentration, the residue was purified by column chromatography (normal phase, [Biotage SNAP cartridge KP-sil 25 g, 40-63 μΐη, 60 A, 50 mL per min, gradient 1 % to 10% MeOH in DCM]) to provide ethyl 2-[4-(1 -methyl-1 H-imidazol-2-yl)piperidine]-6-azaspiro[3.4]octane-6-carboxylate as a brown oil as a mixture of diastereomers (0.25 g, 83%). Preparative HPLC was used to separate the diastereomers, using a Phenomenex Gemini-N C18 column, 150 x 21 mm, eluting with 38 to 48% MeCN/H20 at 18 mL/min and collecting fractions by monitoring at 218 nm to give ethyl 2-[4-(1 -methyl-1 H-imidazol-2-yl)piperidine]-6-azaspiro[3.4]octane-6-carboxylate, Example 1-7 Isomer 1 , (0.044 g, 15%) as a colourless oil and ethyl 2-[4-(1 -methyl-1 /-/-imidazol-2-yl)piperidine]-6-azaspiro[3.4]octane-6-carboxylate, Example 1 -7 Isomer 2, (0.031 g, 10%) as a colourless oil. The data for Isomer 2 are in Table 3

PAT

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Overview

It is a selective muscarinic acetylcholine M4 receptor agonist that indirectly modulates dopamine as the basis for its putative improvement of schizophrenia.[6] In April 2016, the compound was out-licensed from Nxera Pharma to Allergan, an Irish pharmaceutical company, as part of Nxera’s wider muscarinic agonist portfokio. By September 2017, it had advanced to Phase I clinical trial for the indication of “neuropsychiatric symptoms associated with Alzheimer’s disease and other dementias”[8] Following Allergan’s acquisition by AbbVie, the license was returned to Nxera in January 2021.[9] In November 2021, the compound was newly out-licensed to Neurocrine Biosciences, a U.S. pharmaceutical company.[5] It has been under development as a treatment for schizophrenia, and is currently in Phase III clinical trials.[10][11]

History

  • 2016
    • April: The rights to develop Nxera Pharma’s muscarinic agonist portfolio, including NBI-1117568 were transferred to Allergan.[9]
  • 2017
    • September: Allergan initiated Phase I clinical trials for NBI-1117568 to treat “neurobehavioral symptoms related to Alzheimer’s disease and other conditions.”[8]
  • 2021
    • January: Allergan returned the rights to its muscarinic agonist portfolio, including, NBI-1117568 to Nxera Pharma.[9]
    • November: The rights for the muscarinic agonist portfolio were then transferred to Neurocrine Biosciences, which took over the development of NBI-1117568.[5]
  • 2022
    • October: Phase II clinical trial of NBI-1117568 for the treatment of adults with schizophrenia was initiated.[12]
  • 2024
    • April: Neurocrine Biosciences announced that NBI-1117568 had met the requirements of long-term preclinical toxicity tests.[6]
    • August: Neurocrine Biosciences released the results of the Phase II clinical trial.[13][11]
  • 2025
    • May: Neurocrine Biosciences initiated a Phase III registrational program for NBI-1117568 for the treatment of adults with schizophrenia.[14]

Clinical trials

Phase II clinical trial

The Phase II clinical trial was conducted in 15 sites across the U.S. with 200 adult patients diagnosed with schizophrenia.[15] The primary endpoint was assessed by the change in the total score of the Positive and Negative Syndrome Scale (PANSS) after six weeks of treatment. The 20 mg once-daily group showed a statistically significant improvement of 7.5 points compared to the placebo group (improvement of 18.2 points from baseline, p = 0.011, effect size = 0.61).[16] However, the 40 mg once-daily group, 60 mg once-daily group, and 30 mg twice-daily group did not show statistically significant differences compared to the placebo group (p-values: 40 mg group: 0.282, 60 mg group: 0.189, 30 mg twice-daily group: 0.090).[16]

Market reaction to phase II clinical trial

With a PANSS improvement of 7.5, NBI-111758 lagged behind xanomeline/trospium (KarXT) (Karuna Therapeutics) with 8.4 and emraclidine (Cerevel Therapeutics) with 12.7, both of which were in clinical trials at the same time. Moreover, the lack of dose-dependency led to disappointment in the stock market.[17] Neurocrine Biosciences’ share price dropped 19% on the day following the announcement of the Phase II clinical trial results.[18]

References

  1.  “Delving into the Latest Updates on Direclidine with Synapse”. Synapse. 30 June 2025. Retrieved 27 July 2025.
  2.  https://cdn.who.int/media/docs/default-source/international-nonproprietary-names-(inn)/pl133.pdf [bare URL PDF]
  3.  Ye N, Wang Q, Li Y, Zhen X (March 2025). “Current emerging therapeutic targets and clinical investigational agents for schizophrenia: Challenges and opportunities”. Medicinal Research Reviews. 45 (2): 755–787. doi:10.1002/med.22086. PMID 39300769.
  4.  “HTL 0016878”. AdisInsight. 2 September 2024. Retrieved 21 October 2024.
  5.  “ニューロクライン社との統合失調症およびその他の精神神経疾患を対象とした新規ムスカリン受容体作動薬に関するライセンス契約締結のお知らせ” [Announcement of License Agreement with Neurocrine for Novel Muscarinic Receptor Agonist for Schizophrenia and Other Neuropsychiatric Disorders] (in Japanese). PR TIMES. 2021-11-22. Retrieved 2024-09-17.
  6.  “ネクセラファーマ株価6.5%高 薬候補で毒性試験成功 – 日本経済新聞” [NexThera Pharma shares rise 6.5% as drug candidate passes toxicity test – Nikkei]. 日本経済新聞 電子版 (Nikkei Electronic Edition) (in Japanese). 日本経済新聞社 (Nikkei Inc.). 2024-04-17. Retrieved 2024-09-17.
  7.  “当社提携先のニューロクライン社が、統合失調症を対象にしたNBI-1117568の第II相臨床試験の開始を発表［そーせいグループ］ | NIKKEI COMPASS – 日本経済新聞” [Our partner Neurocrine, Inc. announces initiation of Phase II clinical trial of NBI-1117568 for schizophrenia [Sosei Group] | NIKKEI COMPASS – Nikkei Newspaper]. 日経コンパス (Nikkei Compass) (in Japanese). 日本経済新聞社 (Nikkei Inc.). 2022-10-28. Retrieved 2024-09-17.
  8.  “アルツハイマー病等の主要症状の治療薬として開発中の新薬候補、 選択的ムスカリンM4受容体作動薬の第I相臨床試験で最初の被験者への投与を実施” [First subjects dosed in Phase I clinical trial of selective muscarinic M4 receptor agonist, a potential new drug candidate for treating major symptoms of Alzheimer’s disease] (PDF) (in Japanese). ネクセラファーマ（旧そーせいグループ株式会社）. 2017-09-01. Retrieved 2024-09-17.
  9.  “ムスカリン作動薬プログラムのグローバルな研究開発権・販売権が返還” [Global R&D and commercial rights to muscarinic agonist program returned]. プレスリリース・ニュースリリース配信シェアNo.1｜PR TIMES (in Japanese). PR Times. 2021-01-05. Retrieved 2024-09-17.
  10.  日経バイオテクONLINE (2024-09-02). “ネクセラファーマ、統合失調症治療薬候補 NBI-1117568の第II相臨床試験の良好な結果によりニューロクライン社より35百万米ドルのマイルストンを受領” [Nexella Pharma Receives $35 Million Milestone Payment from Neurocrine Following Positive Results of Phase II Clinical Trial of NBI-1117568, a Potential Treatment for Schizophrenia]. 日経バイオテクONLINE (in Japanese). 日本経済新聞社. Retrieved 2024-09-17.
  11.  “ネクセラ—大幅反落、ニューロクラインの株価下落に追随売り | 個別株 – 株探ニュース” [Nexella – Sharp decline, selling follows fall in Neurocrine stock price | Individual stocks – Kabutan News]. kabutan.jp (in Japanese). MINKABU THE INFONOID, Inc. 2024-08-29. Retrieved 2024-09-17.
  12.  “当社提携先のニューロクライン社が、統合失調症を対象にしたNBI-1117568の第Ⅱ相臨床試験の開始を発表” [Our Partner Neurocrine Announces Initiation of Phase 2 Clinical Trial of NBI-1117568 for Schizophrenia]. プレスリリース・ニュースリリース配信シェアNo.1｜PR TIMES (in Japanese). PR TIMES. 2022-10-28. Retrieved 2024-09-17.
  13.  日経バイオテク (Nikkei Biotech) ONLINE (2024-09-02). “ネクセラファーマ、統合失調症治療薬候補 NBI-1117568の第II相臨床試験の良好な結果によりニューロクライン社より35百万米ドルのマイルストンを受領” [Nexella Pharma Receives $35 Million Milestone Payment from Neurocrine Following Positive Results of Phase II Clinical Trial of NBI-1117568, a Potential Treatment for Schizophrenia]. 日経バイオテクONLINE (in Japanese). 日本経済新聞社. Retrieved 2024-09-17.
  14.  “ネクセラファーマの統合失調症薬、最終治験を開始”. 日本経済新聞. 日本経済新聞社. 2025-05-01. Retrieved 2025-05-02.
  15.  “Neurocrine Biosciences Initiates Phase 2 Clinical Study Evaluating NBI-1117568 in Adults with Schizophrenia”. ニューロクライン. 2022-10-27. Retrieved 2024-09-17.
  16.  “ネクセラファーマ[4565]：ニューロクライン社との提携プログラムである統合失調症治療薬候補NBI-1117568の第2相臨床試験で良好な結果 2024年8月28日(適時開示) ：日経会社情報DIGITAL：日本経済新聞” [Nexella Pharma [4565]: Positive results in Phase 2 clinical trial of NBI-1117568, a candidate for the treatment of schizophrenia, a collaboration program with Neurocrine, Inc. August 28, 2024 (timely disclosure) : Nikkei Company Information DIGITAL: Nikkei Shimbun]. 日本経済新聞 電子版 (in Japanese). 日本経済新聞社. Retrieved 2024-09-17.
  17.  “Nxera Pharma Official IR Blog 「ニューロクライン社から35百万米ドルのマイルストン受領」” [Received $35 million milestone payment from Neurocrine]. soseiheptares.blogspot.com. ネクセラファーマ. 2024-09-02. Retrieved 2024-09-19.
  18.  “Neurocrine Stock Down 19% on Mixed Schizophrenia Study Results”. Zacks Investment Research. Zacks Investment. 2024-08-29. Retrieved 2024-09-17.
Clinical data
Other namesHTL-0016878; NBI-1117568; NBI-568[1]
Routes of
administration		Oral
Drug classMuscarinic acetylcholine M4 receptor agonist
Identifiers
IUPAC name
CAS Number1803346-98-6
PubChem CID118295270
ChemSpider133319625
UNIITXB4V44U24
KEGGD13221
Chemical and physical data
FormulaC19H30N4O2
Molar mass346.475 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

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/////direclidine, ANAX, BLUE JET, ADVECT, muscarinic M4 receptor positive allosteric modulator, TXB4V44U24, NBI-1117568, NBI 1117568

Brexanolone caprilcerbate

January 12, 2026 2:55 am / Leave a comment


Brexanolone caprilcerbate

CAS 2681264-65-1

MFC48H78O12 MW 847.1 g/mol

1-O-[[(3R,5S,8R,9S,10S,13S,14S,17S)-17-acetyl-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxycarbonyloxymethyl] 5-O-[1,3-di(octanoyloxy)propan-2-yl] 3-methylpentanedioate

1-[1,3-bis(octanoyloxy)propan-2-yl] 5-[({[(20-oxo-5α-pregnan3α-yl)oxy]carbonyl}oxy)methyl] 3-methylpentanedioate
GABAA receptor positive allosteric modulator, K3KLQ9T6WM, PHASE 2,

Brexanolone caprilcerbate (INNTooltip International Nonproprietary Name; developmental code names LYT-300, SPT-300) is an orally active prodrug of brexanolone (allopregnanolone) which is under development for the treatment of anxiety disorders.[1][2][3][4] It is a absorbed via the lymphatic system with oral administration.[5] The drug is being developed by Seaport Therapeutics and PureTech Health.[1][2] As of January 2025, it is in phase 2 clinical trials.[1]

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=US335021515&_cid=P22-MKAJEO-33027-1

PAT

str1

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References

  1.  “Allopregnanolone prodrug”. AdisInsight. 28 January 2025. Retrieved 26 February 2025.
  2.  “Delving into the Latest Updates on Brexanolone caprilcerbate with Synapse”. Synapse. 15 February 2025. Retrieved 26 February 2025.
  3.  “Proposed INN: List 131 International Nonproprietary Names for Pharmaceutical Substances (INN)” (PDF). WHO Drug Information. 38 (2): 270. 2024. brexanolonum caprilcerbas brexanolone caprilcerbate 1-[1,3-bis(octanoyloxy)propan-2-yl] 5-[({[(20-oxo-5α-pregnan3α-yl)oxy]carbonyl}oxy)methyl] 3-methylpentanedioate GABAA receptor positive allosteric modulator C48H78O12 2681264-65-1
  4.  Carlini SV, Osborne LM, Deligiannidis KM (December 2023). “Current pharmacotherapy approaches and novel GABAergic antidepressant development in postpartum depression”. Dialogues in Clinical Neuroscience. 25 (1): 92–100. doi:10.1080/19585969.2023.2262464. PMC 10557560. PMID 37796239.
  5.  Alashal N, Hussain N (2025). “Approach to the use of rescue medications in children for prolonged epileptic seizures in the community”. Paediatrics and Child Health. 35 (4): 113–117. doi:10.1016/j.paed.2025.01.004.
Clinical data
Other namesLYT-300; LYT300; SPT-300; SPT300; Allopregnanolone 3-O-caprilcerbate
Routes of
administration		Oral[1]
Drug classGABAA receptor positive allosteric modulator; Neurosteroid
Identifiers
IUPAC name
CAS Number2681264-65-1
PubChem CID158098654
UNIIK3KLQ9T6WM
Chemical and physical data
FormulaC48H76O12
Molar mass845.124 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

/////////////Brexanolone caprilcerbate, GABAA receptor positive allosteric modulator, K3KLQ9T6WM, PHASE 2,

Balinatunfib

January 7, 2026 2:58 am / Leave a comment


Balinatunfib

CAS 2248726-53-4

MF C27H24F2N6O2, 502.5 g/mol

(1R,11R)-5-[2-(1-aminocyclobutyl)pyrimidin-5-yl]-18-(difluoromethoxy)-12-methyl-2,9,12-triazapentacyclo[9.8.1.02,10.03,8.014,19]icosa-3(8),4,6,9,14(19),15,17-heptaen-13-one

(7R,14R)-11-[2-(1-AMINOCYCLOBUTYL)-5-PYRIMIDINYL]-1-(DIFLUOROMETHOXY)-6,7-DIHYDRO-6-METHYL-7,14-METHANOBENZIMIDAZO[1,2-B][2,5]BENZODIAZOCIN-5(14H)-ONE

(7R,14R)-11-[2-(1-Aminocyclobutyl)pyrimidin-5-yl]-1-(difluoromethoxy)-6-methyl-6,7-dihydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one

(7R,14R)-11-[2-(1-aminocyclobutyl)pyrimidin-5-yl]-1-(difluoromethoxy)-6-methyl-6,7-dihydro-7,14-methano[1,3]benzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one
tumor necrosis factor (TNF) signaling inhibitor, SAR441566, SAR 441566, PLY98MAN4C

  • OriginatorSanofi
  • ClassAmines; Anti-inflammatories; Antipsoriatics; Antirheumatics; Azabicyclo compounds; Benzimidazoles; Cyclobutanes; Fluorinated hydrocarbons; Heterocyclic compounds with 4 or more rings; Ketones; Phenyl ethers; Pyrimidines; Small molecules
  • Mechanism of ActionTumour necrosis factor alpha inhibitors
  • Phase IICrohn’s disease; Psoriasis; Rheumatoid arthritis; Ulcerative colitis
  • No development reportedInflammation
  • 09 Dec 2025Sanofi plans a phase-I trial (In volunteers) in December 2025 (PO, Tablet), (NCT07272629)
  • 29 Oct 2025Sanofi plans a phase II SPECIFI-IBD-LTS trial for Crohn’s Disease or Ulcerative Colitis ( Treatment-experienced) in unknown location (PO, Tablet) in December 2025 (NCT07222189)
  • 16 Sep 2025Chemical structure information added.
  • You need to be a logged in or subscribed to view this c

Balinatunfib (SAR441566) is an experimental drug which acts as a potent small molecule inhibitor of TNF. Rather than blocking TNF receptors, balinatunfib inactivates TNF directly by stabilising an inactive form of the TNF trimer which fails to bind to its target receptors. It is in early stage clinical trials for rheumatoid arthritis and other chronic autoimmune diseases.[1][2]

SYN

https://www.chemical.ai/blog/humanai-synergy-in-retrosynthetic-analysis-and-route-optimization-of-balinatunfib

PAT

 (WO 2016/050975,

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2016050975&_cid=P22-MK3F7M-67505-1

Intermediate 40 

(1R,3R)-1-[2-bromo-6-(difluoromethoxy)phenyl]-7-chloro-2,3-dihydro-1H-pyrrolo[1,2-a]benzimidazol-3-amine

Intermediate 38 (5 g, 11.64 mmol) was suspended in toluene (22 mL) and cooled to 0°C before addition of diphenylphosphoryl azide (3.4 mL, 15 mmol) and 1,8-diazabicyclo[5.4.0]undec-7-ene (2.5 mL, 16 mmol). The mixture was allowed to warm up to r.t and stirred for 2 hours and subsequently at 45°C overnight. The reaction mixture was diluted with EtOAc (150 mL) and the organic phase washed with a saturated aqueous solution of ammonium chloride (50 mL) then a saturated solution of aqueous sodium bicarbonate (50 mL), and concentrated in vacuo. The crude residue thus obtained was solubilized in THF (100 mL) and water (10 mL), trimethylphosphine (17.46 mL, 17.46 mmol) was added and the reaction mixture stirred overnight. The mixture was concentrated in vacuo, partitioned between EtOAc (200 mL) and water (150 mL). The organic layer was extracted with 0.2M HCl aq (3 x 200 mL). The combined acid layer was stirred in an ice bath, whilst 10% NaOH solution was added with stirring until pH increased to 10. The stirred was continued for further 15 minutes to complete precipitation. The precipitate was filtered, rinsed with water (20 mL), then dried under suction for 10 minutes before drying under high vacuum overnight to afford 3.92 g (78%) of the title compound as an off white solid. LCMS basic: RT 1.96 min. (ES+) 428/430 (M+H)+

EXAMPLE 11

(7R, 14R)-11-chloro-1-(difluoromethoxy)-6,7-dihydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one

Intermediate 40 (3.7 g, 8.6 mmol), activated molecular sieve 4A powder (1.2 g), potassium carbonate (1.5 equiv., 13 mmol) followed by dichloro[9,9-dimethyl-4,5-bis(diphenylphosphino)xanthene]palladium(II) (0.04 equiv., 0.35 mmol) were poured into the center of the 100 mL Glass Parr reaction vessel. 3 cycles of vacuum (~20 mmHg) followed by Argon were applied to the closed reactor.

Anhydrous dimethyl sulfoxide (35 mL) was added, followed by phenol 5M in DMSO (1.1 equiv., 9.5 mmol). The solution was degassed by 3 vacuum (~20 mmHg) / argon cycles followed by 3 cycles of vacuum / CO resulting in a final CO pressure of 1 bar.

The mixture was stirred and heated overnight at 100 °C under the CO atmosphere . The reaction was cooled to 30°C, the reactor vessel was opened and EtOAc (40 mL) was added. The resulting mixture was filtered on a pad of Celite, evaporated in vacuo to yield a green oil.

The residue thus obtained was taken up in EtOAc (100 mL) and the organic layer was washed with water, K2CO3 (saturated aqueous solution) and brine (saturated aqueous solution). The aqueous layer was then re-extracted with EtOAc (1 x 50 mL). The combined organic layers were dried over MgSO4, filtered and evaporated to dryness. The obtained green solid (3.65 g), was taken up in EtOAc, the insoluble material was filtered and rinsed with Et2O to afford 1.06 g (33.1%) of the title compound as a grey solid.

The filtrate can be purified by flash chromatography to provide additional product if required:

LCMS basic: MH+ m/z = 376, RT 1.90 minutes.

1H NMR (300 MHz, DMSO) δ 9.12 (d, 1 H, J = 6.7 Hz), 8.23 (dd, 1 H, J = 7.0, 2.4 Hz), 7.60 (m, 5 H), 7.20 (dd, 1 H, J = 8.7, 2.1 Hz), 6.29 (d, 1 H, J = 7.1 Hz), 4.87 (dd, 1 H, J = 6.7 Hz, 6.7 Hz), 3.46 (m, 1 H), 2.72 (d, 1 H, J = 13.4 Hz).

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US283322316&_cid=P22-MK3EWF-57090-1

Intermediate 3

(7R,14R)-11-Chloro-1-(difluoromethoxy)-6-methyl-6,7-dihydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one

      To a solution of (7R,14R)-11-chloro-1-(difluoromethoxy)-6,7-dihydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one (WO 2016/050975, Example 11) (10 g, 26.6 mmol) in dry THF (135 mL), cooled to −78° C. under nitrogen, was added potassium bis(trimethylsilyl)amide (1M in THF, 30 mL, 30 mmol) dropwise over 15 minutes. The resulting mixture was stirred at −78° C. for 1 h prior to the addition of iodomethane (2.5 mL, 40 mmol) dropwise over 5 minutes. The reaction mixture was stirred at −78° C. for 1 h, then allowed to warm slowly to ambient temperature overnight. The reaction mixture was poured into saturated aqueous ammonium chloride solution (600 mL) and extracted with EtOAc (2×800 mL). The organic extracts were dried (Na 2SO 4), filtered and concentrated in vacuo. Purification by flash chromatography on silica (elution with 5% MeOH/DCM) afforded the title compound (9.12 g, 88%) as a beige solid. δ H (300 MHz, DMSO-d 6) 8.33-8.21 (m, 1H), 7.87-7.33 (m, 5H), 7.22 (dd, J 8.7, 2.1 Hz, 1H), 6.23 (d, J 7.1 Hz, 1H), 5.22 (d, J 7.1 Hz, 1H), 3.55-3.41 (m, 1H), 3.33 (s, 3H), 2.81 (d, J 13.8 Hz, 1H). LCMS (ES+) [M+H] + 390.0, RT 1.10 minutes (Method 3).

Intermediate 17

tert-Butyl (1-{5-[(7R,14R)-1-(difluoromethoxy)-6-methyl-5-oxo-5,6,7,14-tetrahydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-11-yl]pyrimidin-2-yl}cyclobutyl)-carbamate

      A flame-dried flask under nitrogen equipped with a reflux condenser was charged with Intermediate 3 (13.3 g, 34.0 mmol), tris(dibenzylideneacetone)dipalladium(0) (1.61 g, 1.71 mmol), XPhos (1.63 g, 3.43 mmol), bis(pinacolato)diboron (9.85 g, 38.8 mmol) and potassium acetate (8.5 g, 87 mmol), then 1,4-dioxane (136 mL) was added. The resulting mixture was stirred at 100° C. for 22 h before Intermediate 16 (12.3 g, 37.4 mmol) and aqueous tribasic potassium phosphate solution (1.27 mol/L, 40 mL, 50.8 mmol) were added. The reaction mixture was heated under reflux for 3 h before being charged with additional tris(dibenzylideneacetone)dipalladium(0) (500 mg, 0.53 mmol), XPhos (510 mg, 1.07 mmol) and aqueous tribasic potassium phosphate solution (1.27 mol/L, 20 mL, 25.4 mmol). The mixture was stirred for 1 h, then cooled to room temperature, diluted with DCM (600 mL) and washed with brine (400 mL). The aqueous phase was extracted with DCM (500 mL), then the combined organic extracts were passed through a phase separator and concentrated in vacuo. Purification by flash chromatography on silica (elution with 0-5% MeOH/DCM) afforded the title compound (18.0 g, 88%) as an off-white solid. δ H (400 MHz, CDCl 3) 8.93 (s, 2H), 8.49 (dd, J8.2, 1.3 Hz, 1H), 7.84 (dd, J8.5, 0.7 Hz, 1H), 7.74-7.63 (m, 1H), 7.48-7.38 (m, 2H), 7.34-7.29 (m, 1H), 6.84 (t, J72.8 Hz, 1H), 6.31 (d, J7.2 Hz, 1H), 5.92 (s, 1H), 5.01 (d, J7.1 Hz, 1H), 3.53 (s, 3H), 3.51-3.43 (m, 1H), 2.90 (d, J 13.6 Hz, 1H), 2.84-2.57 (m, 3H), 2.22-2.07 (m, 3H), 1.43 (s, 9H). LCMS (ES+) [M+H] + 603.2, RT 1.25 minutes (Method 3).

EXAMPLE 6

(7R,14R)-11-[2-(1-Aminocyclobutyl)pyrimidin-5-yl]-1-(difluoromethoxy)-6-methyl-6,7-dihydro-7,14-methanobenzimidazo[1,2-b][2,5]benzodiazocin-5(14H)-one

To a solution of Intermediate 17 (18.0 g, 29.9 mmol) in 1,4-dioxane (25 mL) was added 4M hydrochloric acid in 1,4-dioxane (40 mL). The resulting mixture was stirred at room temperature for 1 h, then concentrated in vacuo. The residue was dissolved in water (500 mL) and washed with EtOAc (2×300 mL). The aqueous layer was basified to pH 9 with 2N aqueous sodium hydroxide solution, which resulted in precipitation of a solid. EtOAc (500 mL) was added and the mixture was stirred until all solids had dissolved. The residue was partitioned, then the aqueous layer was further extracted with EtOAc (500 mL). The combined organic layers were dried over Na 2SO 4 and filtered, then concentrated in vacuo and dried overnight under high vacuum. The foamy residue was suspended in a mixture of diethyl ether and hexane (150 mL), then stirred and shaken vigorously, before being concentrated in vacuo, to afford the title compound (12.4 g, 83%) as a white amorphous solid. δ H (400 MHz, DMSO-d 6) 9.05 (s, 2H), 8.32-8.22 (m, 1H), 7.91-7.66 (m, 3H), 7.62 (dd, J8.5, 1.8 Hz, 1H), 7.53-7.46 (m, 2H), 6.31 (d, J7.1 Hz, 1H), 5.26 (d, J 7.2 Hz, 1H), 3.52 (dt, J 14.2, 7.3 Hz, 1H), 3.36 (s, 3H), 2.84 (d, J 13.8 Hz, 1H), 2.63 (dtd, J11.5, 5.6, 2.5 Hz, 2H), 2.38 (s, 2H), 2.16-2.05 (m, 2H), 2.04-1.91 (m, 1H), 1.87-1.73 (m, 1H). LCMS (ES+APCI) [M-NH 2] − 486.0, RT 1.66 minutes (Method 2). LCMS (ES+) [M+H] + 503.0, RT 1.71 minutes (Method 1).

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2025008402&_cid=P22-MK3EWF-57090-1

 (7R,14R)-1 l-[2-(l-aminocyclobutyl)pyrimidin-5-yl]-l-(difhroromethoxy)-6-methyl-6,7-dihydro-7, 14-methanobenzimidazo[l,2-b][2,5]benzodiazocin-5(14H)-one.

PAT

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References

  1.  Vugler A, O’Connell J, Nguyen MA, Weitz D, Leeuw T, Hickford E, et al. (2022). “An orally available small molecule that targets soluble TNF to deliver anti-TNF biologic-like efficacy in rheumatoid arthritis”. Frontiers in Pharmacology. 13 1037983. doi:10.3389/fphar.2022.1037983. PMC 9709720. PMID 36467083.
  2.  Li Y, Ye R, Dai H, Lin J, Cheng Y, Zhou Y, et al. (January 2025). “Exploring TNFR1: from discovery to targeted therapy development”. Journal of Translational Medicine. 23 (1): 71. doi:10.1186/s12967-025-06122-0. PMC 11734553. PMID 39815286.
Identifiers
IUPAC name
CAS Number2248726-53-4
PubChem CID132042903
IUPHAR/BPS13583
ChemSpider129738176
Chemical and physical data
FormulaC27H24F2N6O2
Molar mass502.526 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

//////////Balinatunfib, tumor necrosis factor (TNF) signaling inhibitor, SAR441566, SAR 441566, PLY98MAN4C

Amogammadex

January 2, 2026 2:51 am / Leave a comment


Amogammadex

CAS 1309580-40-2

MF C88H136N8O56S8 MW2458.56

(2R)-2-acetamido-3-[[(1S,3S,5S,6S,8S,10S,11S,13S,15S,16S,18S,20S,21S,23S,25S,26S,28S,30S,31S,33S,35S,36S,38S,40S,41R,42R,43R,44R,45R,46R,47R,48R,49R,50R,51R,52R,53R,54R,55R,56R)-10,15,20,25,30,35,40-heptakis[[(2R)-2-acetamido-2-carboxyethyl]sulfanylmethyl]-41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56-hexadecahydroxy-2,4,7,9,12,14,17,19,22,24,27,29,32,34,37,39-hexadecaoxanonacyclo[36.2.2.23,6.28,11.213,16.218,21.223,26.228,31.233,36]hexapentacontan-5-yl]methylsulfanyl]propanoic acid

L-CYSTEINE, S,S’,S”,S”’,S””,S”””,S”””,S”””’-(6A,6B,6C,6D,6E,6F,6G,6H-OCTADEOXY-.GAMMA.-CYCLODEXTRIN-6A,6B,6C,6D,6E,6F,6G,6H-OCTAYL)OCTAKIS(N-ACETYL-
AMOGAMMADEX [INN]
CYCLOOCTAKIS-(1->4)-(6-S-((2R)-2-ACETAMIDO-2-CARBOXYETHYL)-6-THIO-.ALPHA.-D-GLUCOPYRANOSYL)

cyclooctakis-(1→4)-{6-S-[(2R)-2-acetamido-2-carboxyethyl]-6-thio-α-Dglucopyranosyl}
rocuronium and vecuronium reversal agent, L-CYSTEINE, S,S’,S”,S”’,S””,S”””,S”””,S”””’-(6A,6B,6C,6D,6E,6F,6G,6H-OCTADEOXY-.GAMMA.-CYCLODEXTRIN-6A,6B,6C,6D,6E,6F,6G,6H-OCTAYL)OCTAKIS(N-ACETYL-
AMOGAMMADEX [INN]
CYCLOOCTAKIS-(1->4)-(6-S-((2R)-2-ACETAMIDO-2-CARBOXYETHYL)-6-THIO-.ALPHA.-D-GLUCOPYRANOSYL)

Pat

WO2012068981

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2012068981&_cid=P21-MJW9RG-10499-1

CD-8

Weigh 23.7 g (0.088 mol) of N-acetylcysteine ​​and measure 160 ml of dry DMF. Add both to a dry three-necked flask and stir until completely dissolved. Cool the reaction solution to approximately -10°C in a constant temperature bath. Slowly add 8.81 g of sodium hydride (60%) in portions under argon protection and mechanical stirring, maintaining the temperature below -5°C. After the addition is complete, continue stirring until no more bubbles emerge, then transfer the solution to approximately 5°C and react until no more bubbles emerge (approximately 2-3 hours).

With the temperature controlled at approximately 5°C in an ice bath, add 8.38 g (3.85 mmol) of DMF solution of 6-per-deoxy-6-per-iodo-γ-cyclodextrin to the reaction solution of the fully reacted N-acetylcysteine ​​sodium salt. Under argon protection, mechanically stir to ensure homogeneity and continue stirring for 30 min. Gradually raise the temperature of the reaction solution to 70°C and react for 12 h. Then cool the reaction solution to room temperature, filter, wash the filter cake twice with DMF, and then wash with acetone until triphenylphosphine and triphenyloxyphosphine are removed. Dry under reduced pressure to obtain crude sodium salt. Dissolve the crude sodium salt in glacial acetic acid, and then pass dry hydrogen chloride gas into the solution under ice bath cooling. A white solid precipitates after 20 min. Filter after no more white solid precipitates (approximately 1 h). Dry acetone was gradually added to the filtrate, and a solid precipitated out. The mixture was filtered, and the filter cake was washed with acetone until there was no sour taste. The cake was dried under reduced pressure to obtain 6-per-deoxy-6-per-(N-acetylglycine methyl)thioether-γ-cyclodextrin (CD-8) with a yield of 48%.

Ή NMR spectra of CD-8 in heavy water (D2O ) : 52.02 (CH3,m,3H), 2.69,2.44 (CH2,m,2H), 3.02 (CH,m,H), 3.06,2.81 (CH2,m,2H), 3.73 (2CH,m,2H), 4.19 (CH,m,H), 4.74 (CH,m,H), 5.03 (CH,s,H) ppm.

PAT

CN102060941 

https://patentscope.wipo.int/search/en/detail.jsf?docId=CN84636898&_cid=P21-MJW9XY-15988-1

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Aleniglipron

December 30, 2025 2:42 am / Leave a comment


Aleniglipron

CAS 2685823-26-9

MF C49H55FN9O6P MW916.0 g/mol

3-[(1S,2S)-1-[2-[(4S)-3-[3-[4-diethylphosphoryl-3-(methylamino)phenyl]-2-oxoimidazol-1-yl]-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-6,7-dihydro-4H-pyrazolo[4,3-c]pyridine-5-carbonyl]-5-(oxan-4-yl)indol-1-yl]-2-methylcyclopropyl]-4H-1,2,4-oxadiazol-5-one

glucagon-like peptide 1 (GLP-1) receptor agonist, GSBR-1290, GSBR 1290, Z6XCL6R9SX

Aleniglipron (development code GSBR-1290) is a small-molecule GLP-1 agonist developed by Structure Therapeutics.[1] It is delivered orally and is in a Phase II trial as of 2023.[2][3][4] In June 2024, Structure Therapeutics reported positive topline data from a Phase 2a obesity study in which GSBR-1290 demonstrated clinically meaningful and statistically significant placebo-adjusted mean weight loss and generally favorable safety and tolerability results.[5]

  • Aleniglipron Phase 2 Body Composition StudyCTID: NCT07169942Phase: Phase 2Status: Active, not recruitingDate: 2025-10-31
  • A Dose-Range Study of Aleniglipron (GSBR-1290) in Participants Living With Obesity or Overweight With at Least One Weight-related ComorbidityCTID: NCT06703021Phase: Phase 2Status: Active, not recruitingDate: 2025-09-15
  • A Phase 2b, Dose-range Finding Study of the Efficacy and Safety of Multiple Doses of Aleniglipron (GSBR-1290) in Participants Living With Obesity or Overweight With at Least One Weight-related ComorbidityCTID: NCT06693843Phase: Phase 2Status: Active, not recruitingDate: 2025-08-26

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=US367934715&_cid=P10-MJRZ0C-74156-1

Example 2: Synthesis of

3-((1S,2S)-1-(2-((S)-3-(3-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridine-5-carbonyl)-5-(tetrahydro-2H-pyran-4-yl)-1H-indol-1-yl)-2-methylcyclopropyl)-1,2,4-oxadiazol-5(4H)-one (Compound 121a)

Step A: (4-bromo-2-fluorophenyl)diethylphosphine oxide

      The mixture of 4-bromo-2-fluoro-1-iodobenzene (2.00 g, 6.60 mmol), diethylphosphine oxide (775 mg, 7.30 mmol), Pd 2(dba) 3 (302 mg, 0.330 mmol) and XantPhos (382 mg, 0.660 mmol) in 40 mL of 1,4-dioxane was sparged with argon. Then triethylamine (1.30 g, 13.2 mmol) was added. The mixture was heated at 60° C. for 12 h under an atmosphere of argon. LCMS showed the reaction was completed. The mixture was concentrated, and the residue was diluted with ethyl acetate (100 mL) and washed with water (50 mL). The organic layer was dried and concentrated. The residue was purified with silica gel column chromatography (PE/EA/methanol=1:2:0.1) to provide (4-bromo-2-fluorophenyl)diethylphosphine oxide (1.50 g, 5.37 mmol, 80.6% yield) as a pale white solid.
      LCMS: m/z=279.0, 281.0 (M+H) +.
       1H NMR (400 MHz, DMSO-d 6) δ 7.63-7.73 (m, 3H), 1.95-2.08 (m, 2H), 1.80-1.92 (m, 2H), 0.80-1.10 (m, 6H).

Step B: (4-bromo-2-(methylamino)phenyl)diethylphosphine oxide

      To a mixture of (4-bromo-2-fluorophenyl)diethylphosphine oxide (360 mg, 1.29 mmol) in 2 mL of methanol was added methylamine (9.8 M in methanol, 4 mL, 39.2 mmol). The mixture was heated at 80° C. for 3 h in a microwave reactor. LCMS showed most of the starting material was consumed. The mixture was concentrated, diluted with ethyl acetate (50 mL), and washed with water (30 mL). The organic layer was dried and concentrated. The resulting residue was purified with silica gel column chromatography (PE/EA/methanol=1:2:0.1) to provide (4-bromo-2-(methylamino)phenyl)diethylphosphine oxide (179 mg, 0.617 mmol, 47.9% yield) as a white solid.
      LCMS: m/z=290.0, 292.0 (M+H) +.
       1H NMR (600 MHz, DMSO-d 6) δ 7.75-7.76 (m, 1H), 7.11 (dd, J=13.2, 8.4 Hz, 1H), 6.63-6.80 (m, 2H), 2.71 (d, J=5.4 Hz, 3H), 1.88-1.94 (m, 4H), 0.90-1.05 (m, 6H).

Step C: tert-butyl (S)-3-(3-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-2,4,6,7-tetrahydro-5H-pyrazolo[4,3-c]pyridine-5-carboxylate

      The mixture of (4-bromo-2-(methylamino)phenyl)diethylphosphine oxide (310 mg, 1.07 mmol), tert-butyl (S)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-3-(2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2,4,6,7-tetrahydro-5H-pyrazolo[4,3-c]pyridine-5-carboxylate (428 mg, 0.970 mmol), CuI (278 mg, 1.46 mmol), potassium carbonate (268 mg, 1.94 mmol), and (1S,2S)—N 1,N 2-dimethylcyclohexane-1,2-diamine (208 mg, 1.46 mmol) in NMP (25 mL) was heated at 130° C. for 3 h under an atmosphere of argon. LCMS showed the reaction was completed. The mixture was added ethyl acetate (100 mL) and washed with water (50 mL*3). The organic layer was dried and concentrated. The residue was purified with silica gel column chromatography (PE/EA/methanol=1:4:0.3) to provide tert-butyl (5)-3-(3-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-2,4,6,7-tetrahydro-5H-pyrazolo[4,3-c]pyridine-5-carboxylate (530 mg, 0.810 mmol, 84.0% yield) as a pale yellow solid. LCMS: m/z=651.3 (M+H) +.
       1H NMR (600 MHz, DMSO-d 6) δ 7.73 (q, J=4.8 Hz, 1H), 7.35 (d, J=3.0 Hz, 1H), 7.26 (dd, J=13.2, 8.4 Hz, 1H), 7.11 (d, J=6.6 Hz, 2H), 6.98 (s, 1H), 6.89 (d, J=7.8 Hz, 1H), 6.86 (s, 1H), 5.12 (br. s, 1H), 4.13-4.34 (m, 1H), 3.02-3.19 (m, 1H), 2.69-2.74 (m, 4H), 2.61-2.69 (m, 1H), 2.19 (s, 6H), 1.89-1.95 (m, 4H), 1.43 (s, 9H), 1.17-1.18 (m, 3H), 0.95-1.05 (m, 6H).

Step D: (5)-1-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-3-(2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridin-3-yl)-1,3-dihydro-2H-imidazol-2-one hydrochloride

      To a mixture of tert-butyl (S)-3-(3-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-2,4,6,7-tetrahydro-5H-pyrazolo[4,3-c]pyridine-5-carboxylate (520 mg, 0.800 mmol) in 1,4-dioxane (6 mL) was added hydrogen chloride (4 M in 1,4-dioxane, 12 mL, 48.0 mmol).
      The mixture was stirred at room temperature for 3 h. LCMS showed the reaction was completed. The mixture was concentrated, and the residue was dispersed in 40 mL of ethyl ether. The resulting solid was collected and dried in vacuo to provide (S)-1-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-3-(2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridin-3-yl)-1,3-dihydro-2H-imidazol-2-one hydrochloride (430 mg, 0.730 mmol, 91.7% yield) as a pale yellow solid.
      LCMS: m/z=551.2 (M+H) +.
       1H NMR (400 MHz, DMSO-d 6) δ 10.14 (s, 1H), 9.46-9.53 (m, 1H), 7.39 (d, J=3.2 Hz, 1H), 7.27 (dd, J=12.8, 8.4 Hz, 1H), 7.13 (d, J=6.4 Hz, 2H), 6.93 (d, J=3.2 Hz, 1H), 6.90 (dt, J=8.4, 2.0 Hz, 1H), 6.86-6.87 (m, 1H), 4.55-4.59 (m, 2H), 3.58-3.62 (m, 1H), 3.28-3.33 (m, 1H), 3.03-3.10 (m, 1H), 2.90-3.05 (m, 1H), 2.73 (s, 3H), 2.20 (d, J=2.0 Hz, 6H), 1.88-1.97 (m, 4H), 1.36 (d, J=6.8 Hz, 3H), 0.90-1.05 (m, 6H).

Step E: 3-((1S,2S)-1-(2-((S)-3-(3-(4-(diethylphosphoryl)-3-(methylamino) phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridine-5-carbonyl)-5-(tetrahydro-2H-pyran-4-yl)-1H-indol-1-yl)-2-methylcyclopropyl)-1,2,4-oxadiazol-5(4H)-one

      To a mixture of 1-((1S,2S)-2-methyl-1-(5-oxo-4,5-dihydro-1,2,4-oxadiazol-3-yl)cyclopropyl)-5-(tetrahydro-2H-pyran-4-yl)-1H-indole-2-carboxylic acid (272 mg, 0.710 mmol) and DMF (7 mL) in a 50 mL flask (flask A) were added HATU (810 mg, 2.13 mmol) and triethylamine (1.45 g, 14.3 mmol). The mixture was stirred at room temperature for 10 mins. In another 50 mL flask (flask B), (5)-1-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-3-(2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridin-3-yl)-1,3-dihydro-2H-imidazol-2-one hydrochloride (420 mg, 0.710 mmol) and triethylamine (2.90 g, 28.7 mmol) in 7 mL of DMF was stirred at room temperature for 10 mins. Then the mixture in flask B was added into flask A dropwise. The resulting mixture was stirred at room temperature for 12 h. LCMS showed most of the starting material was consumed. The mixture was diluted with DCM (100 mL) and washed with water (50 mL*3). The organic layer was dried and concentrated. The residue was purified with Prep-HPLC (0.01% hydrochloric acid in water and acetonitrile) to provide 3-((1S,2S)-1-(2-((S)-3-(3-(4-(diethylphosphoryl)-3-(methylamino)phenyl)-2-oxo-2,3-dihydro-1H-imidazol-1-yl)-2-(4-fluoro-3,5-dimethylphenyl)-4-methyl-4,5,6,7-tetrahydro-2H-pyrazolo[4,3-c]pyridine-5-carbonyl)-5-(tetrahydro-2H-pyran-4-yl)-1H-indol-1-yl)-2-methylcyclopropyl)-1,2,4-oxadiazol-5 (4H)-one (290 mg) as a white solid.
      LCMS: m/z=916.4 (M+H) +.
       1H NMR (400 MHz, DMSO-d 6, 80° C.) δ 11.58 (br. s, 1H), 7.66 (br. s, 1H), 7.52 (s, 1H), 7.42 (d, J=8.4 Hz, 1H), 7.05-7.30 (m, 5H), 6.70-6.95 (m, 4H), 5.56 (br. s, 1H), 4.45 (br. s, 1H), 3.95-3.99 (m, 2H), 3.40-3.70 (m, 3H), 2.83-2.90 (m, 3H), 2.60-2.80 (m, 3H), 2.22 (d, J=1.6 Hz, 6H), 1.88-1.96 (m, 4H), 1.58-1.80 (m, 7H), 1.43 (br. s, 3H), 1.17 (br. s, 3H), 0.95-1.10 (m, 6H).

PAT

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References

  1.  Mao, Ting; Meng, Qinghua; Zhang, Haizhen; Zhang, Jinqiang J.; Shi, Songting; Guan, Zhibo; Jiang, Xinglong; Zhang, Fang; Lei, Hui; Lin, Xichen (20 June 2023). “760-P: Discovery of GSBR-1290, a Highly Potent, Orally Available, Novel Small Molecule GLP-1 Receptor Agonist”. Diabetes. 72 (Supplement_1) 760-P. doi:10.2337/db23-760-P. S2CID 259430363.
  2.  “Structure Therapeutics Initiates Phase 2a Study of Oral GLP-1 agonist GSBR-1290 for the Treatment of Type 2 Diabetes and Obesity”. BioSpace. 25 May 2023. Retrieved 4 November 2023.
  3.  “Structure announces positive results from oral GLP-1 receptor agonist gsbr-1290”. Bariatric News. 2 October 2023. Retrieved 4 November 2023.
  4.  Satija, Bhanvi (29 September 2023). “Structure Therapeutics surges as early data from obesity pill tops expectations”. Reuters. Retrieved 4 November 2023.
  5.  “Structure Therapeutics Reports Positive Topline Data from its Phase 2a Obesity Study and Capsule to Tablet PK Study for its Oral Non-Peptide Small Molecule GLP-1 Receptor Agonist GSBR-1290”. BioSpace. 2024-06-03. Retrieved 2024-10-24.
Legal status
Legal statusInvestigational
Identifiers
IUPAC name
CAS Number2685823-26-9
PubChem CID164809721
DrugBankDB18551
UNIIZ6XCL6R9SX
Chemical and physical data
FormulaC49H55FN9O6P
Molar mass916.008 g·mol−1
InChI

//////////Aleniglipron, glucagon-like peptide 1 (GLP-1) receptor agonist, GSBR-1290, GSBR 1290, Z6XCL6R9SX

Zoracopan

December 24, 2025 2:52 am / Leave a comment


Zoracopan

CAS 2243483-63-6

MF C31H31BrN6O3 MW 615.52

2-Azabicyclo[3.1.0]hexane-3-carboxamide, 2-[2-[3-acetyl-7-methyl-5-(2-methyl-5-pyrimidinyl)-1H-indol-1-yl]acetyl]-N-(6-bromo-3-methyl-2-pyridinyl)-5-methyl-, (1R,3S,5R)-

(1R,3S,5R)-2-{[3-acetyl-7-methyl-5-(2-methylpyrimidin5-yl)-1H-indol-1-yl]acetyl}-N-(6-bromo-3-methylpyridin2-yl)-5-methyl-2-azabicyclo[3.1.0]hexane-3-carboxamide
complement factor D inhibitor, ALXN-2080, ALXN 2080, E7799Y8LXY

Zoracopan is a selective complement factor D (CFD) inhibitor. When administered systemically (orally or intravenously), Zoracopan accumulates and is sustained-released in ocular tissues, primarily in the choroid-retinal pigment epithelium (C-RPE) and/or iridociliary body (I-CB).

Zoracopan is a small molecule drug. The usage of the INN stem ‘-copan’ in the name indicates that Zoracopan is a complement receptor antagonist/complement inhibitor. Zoracopan is under investigation in clinical trial NCT06173596 (A Study to Evaluate Potential Drug Interactions Between ALXN2080 and Itraconazole, Fluconazole & Carbamazepine in Healthy Adults). Zoracopan has a monoisotopic molecular weight of 614.16 Da.

  • Safety and Tolerability, PK, and PD Study of Single and Multiple ALXN2080 Doses in Healthy ParticipantsCTID: NCT05428696Phase: Phase 1Status: CompletedDate: 2024-06-07
  • A Study to Evaluate Potential Drug Interactions Between ALXN2080 and Itraconazole, Fluconazole & Carbamazepine in Healthy AdultsCTID: NCT06173596Phase: Phase 1Status: CompletedDate: 2024-06-20
  • A Study to Investigate the Potential Drug Interactions Between ALXN2080 and Rosuvastatin and Metformin in Healthy Adult ParticipantsCTID: NCT06160414Phase: Phase 1Status: CompletedDate: 2025-04-24

WO2024259085

WO2024137329

SYN

US11084800,

426

https://patentscope.wipo.int/search/en/detail.jsf?docId=US289331902&_cid=P10-MJJEYB-31207-1

SYN

WO2021183555

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2018160889&_cid=P10-MJJEK1-12570-1

PAT

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[1]. Ocular drug depot for complement-mediated disorders. WO2021183555A1 – Ocular drug depot for complement-mediated disorders – Google Patents.

////zoracopan, complement factor D inhibitor, ALXN-2080, ALXN 2080, E7799Y8LXY

Zerencotrep

December 21, 2025 2:44 am / Leave a comment


Zerencotrep

CAS 1628287-16-0

MF C23H20ClF3N4O5, MW 524.88

7-[(4-chlorophenyl)methyl]-1-(3-hydroxypropyl)-3-methyl-8-[3-(trifluoromethoxy)phenoxy]purine-2,6-dione

7-[(4-chlorophenyl)methyl]-1-(3-hydroxypropyl)-3-
methyl-8-[3-(trifluoromethoxy)phenoxy]-3,7-dihydro1H-purine-2,6-dione
transient receptor potential channel 4 and 5 (TRPC4, TRPC5) inhibitor, Pico 145, HC 608, HMIMSYLCWQ

Pico145 (HC-608) is a remarkable inhibitor of TRPC1/4/5 channels, inhibits (-)-englerin A-activated TRPC4/TRPC5 channels, with IC50s of 0.349 and 1.3 nM in cells, and shows no effect on TRPC3, TRPC6, TRPV1, TRPV4, TRPA1, TRPM2, TRPM8.


Zerencotrep is a small molecule drug. The usage of the INN stem ‘-cotrep’ in the name indicates that Zerencotrep is a transient receptor potential canonical channel 5 (TRPC5) antagonist. Zerencotrep has a monoisotopic molecular weight of 524.11 Da.

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014143799&_cid=P22-MJF454-30876-1

The following examples 7a through 7k were prepared using the method of example 6, step 1.

Example 7a 7-(4-chlorobenzyl)-l -(3-hydroxypropyl)-3-methyl-8-(3-(trifluoromethoxy)phenoxy)-l -purine-2,6(3H,7H)-dione

The title compound was prepared using the method of example 6, step 1 and purified

preparative HPLC to give 7-(4-chlorobenzyl)-l -(3-hydroxypropyl)-3-methyl-8-(3-

(trifluoromethoxy)phenoxy)-lH-purine-2,6(3H,7H)-dione (10 mg, 17.3% yield) as white solid. lH-NMR (CD3OD) δ 7.57-7.53(t, IH), 7.46-7.44(d, 2H), 7.37-7.33(m, 4H), 7.26-7.24(d, IH), 5.49(s, 2H), 4.13-4.09(t, IH), 3.64-3.60(t, 2H), 3.42(s, 3H), 1.89-1.86(m, 2H). LCMS retention time 3.059 min; LCMS MH+ 525.

PAT

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///////////zerencotrep, Pico 145, HC 608, HMIMSYLCWQ

Zemprocitinib

December 20, 2025 2:54 am / Leave a comment


Zemprocitinib

CAS 2417414-44-7

MF C16H19N5O2S MW 345.4 g/mol

N-[3-(3,5,8,10-tetrazatricyclo[7.3.0.02,6]dodeca-1,4,6,8,11-pentaen-3-yl)-1-bicyclo[1.1.1]pentanyl]propane-1-sulfonamide

N-[3-(imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl]propane-1-sulfonamide
Janus kinase inhibitor, anti-inflammatory, LNK 01001, LG6MM3RP86

Zemprocitinib (also known as LNK01001) is a selective Janus kinase (JAK) 1 inhibitor, a type of small molecule drug being developed for inflammatory and autoimmune conditions like rheumatoid arthritis, atopic dermatitis, and ankylosing spondylitis. It works by blocking the JAK1 enzyme, reducing the inflammatory signals that cause these diseases, and has shown promising results in clinical trials, with development reaching Phase 3. 

Key Aspects:

  • Drug Class: JAK1 Inhibitor.
  • Mechanism: Blocks Janus Kinase 1, a key enzyme in inflammatory pathways.
  • Developer: Initially Lynk Pharmaceuticals.
  • Potential Uses: Rheumatoid Arthritis, Atopic Dermatitis, Ankylosing Spondylitis, Psoriasis, Alopecia Areata.
  • Development Stage: Reached Phase 3 clinical trials for several indications.
  • Chemical Info: CAS: 2417414-44-7; Formula: C16H19N5O2S. 

In Summary:

Zemprocitinib is an investigational drug targeting inflammation by inhibiting JAK1, with potential to treat various autoimmune disorders, showing strong efficacy in early clinical trials for conditions like rheumatoid arthritis. 

SYN

US20220009927

https://patentscope.wipo.int/search/en/detail.jsf?docId=US347660217&_cid=P21-MJDP3D-82397-1

Example 1

Step 1. 4-Chloro-1-tosyl-1H-pyrrolo[2,3-b]pyridine (1b)

      Compound 1a (30 g, 0.2 mol) and TsCl (45 g, 0.24 mol) were dissolved in a mixture of acetone and water (600 mL, V:V=5:1) followed by the addition of NaOH (11.8 g, 0.29 mmol) at 0° C. After stirring at RT for 1 h, the mixture was concentrated to 100 mL of solvent and cooled with ice-water. The formed solid was filtered and dried to afford title product as a white solid (52 g, 86% yield). 1H NMR (400 MHz, CDCl 3) δ 8.30 (d, J=5.6 Hz, 1H), 8.05 (d, J=8.4 Hz, 2H), 7.76 (d, J=4.0 Hz, 1H), 7.27 (d, J=8.4 Hz, 2H), 7.18 (d, J=5.2 Hz, 1H), 6.69 (d, J=4.0 Hz, 1H), 2.37 (s, 3H).

Step 2. 4-Chloro-5-nitro-1-tosyl-1H-pyrrolo[2,3-b]pyridine (1c)

      To a mixture of compound 1b (5.0 g, 16.3 mmol) and 75 mL of DCM was added tetrabutylammonium nitrate (2.9 g, 21.3 mmol) portion-wise at 0° C. followed by trifluoroacetic anhydride (3.14 mL, 22.2 mmol) slowly. After stirring for 16 hrs at RT, another portion of tetrabutylammonium nitrate (0.58 g, 4.23 mmol) and trifluoroacetic anhydride (0.8 mL, 5.7 mmol) were added at 0° C. After warmed up to room temperature, the reaction mixture was stirred for 4 hrs at RT. The reaction mixture was diluted with DCM (150 mL), washed with water (30 mL×2) and then concentrated to dryness. The residue was triturated in MeOH to afford title product as a white solid (3.15 g, 55% yield). LC-MS (Method 2): t R=1.76 min, m/z (M+H) +=351.8.

Step 3. Tert-butyl 3-((5-nitro-1-tosyl-1H-pyrrolo[2,3-b]pyridin-4-yl)amino)bicyclo[1.1.1]pentane-1-carboxylate (Id)

      Compound 1c (500 mg, 1.42 mmol), tert-butyl 3-aminobicyclo[1.1.1]pentane-1-carboxylate (313 mg, 1.71 mmol) and DIPEA (276 mg, 2.13 mmol) were dissolved in isopropanol (5 mL). The above solution was stirred at 120° C. for 2 hrs. After cooling, the formed solid was collected by filtering and dried to afford the title product as a brown solid (612 mg, 86% yield). 1H NMR (400 MHz, CDCl 3) δ 9.28 (s, 1H), 9.11 (s, 1H), 8.07 (d, J=8.0 Hz, 2H), 7.64 (d, J=5.6 Hz, 1H), 7.30 (d, J=8.0 Hz, 2H), 6.96 (d, J=5.6 Hz, 1H), 2.48 (s, 6H), 2.40 (s, 3H), 1.47 (s, 9H).

Step 4. Tert-butyl 3-((5-amino-1-tosyl-1H-pyrrolo[2,3-b]pyridin-4-yl)amino)bicyclo[1.1.1]pentane-1-carboxylate (le)

      Compound 1d (600 mg, 1.22 mmol) was dissolved in MeOH (6 mL) followed by the addition of Pd/C (48 mg, 10% wt) in one portion. The mixture was hydrogenated (1 atm) at RT for 16 hrs. The mixture was filtered and the filtrate was concentrated. The residue was purified by prep. TLC (PE:EtOAc=1:1) to afford the title product as a white solid (258 mg, 46% yield). LC-MS (Method 2): t R=1.64 min, m/z (M+H) +=469.0.

Step 5. Tert-butyl 3-(6-tosylimidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentane-1-carboxylate (1f)

      Compound 1e (258 mg, 0.55 mmol), triethyl orthoformate (204 mg, 1.37 mmol) and p-toluenesulfonic acid (10 mg, 0.05 mmol) were dissolved in toluene (6 mL). The mixture was stirred for 16 hrs at 120° C. After cooling, the mixture was concentrated to dryness. The residue was purified by chromatography on silica gel (elute: PE:EtOAc=1:1) to afford the title product as a brown solid (191 mg, 73% yield). 1H NMR (400 MHz, CDCl 3) δ 8.91 (s, 1H), 8.10 (d, J=8.0 Hz, 2H), 7.82 (d, J=8.0 Hz, 2H), 7.27-7.25 (m, 2H), 6.83 (d, J=4.4 Hz, 1H), 2.71 (s, 6H), 2.35 (s, 3H), 1.51 (s, 9H).

Step 6. 3-(6-Tosylimidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6LF)-yl)bicyclo[1.1.1]pentane-1-carboxylic acid (1g)

      To a solution of compound 1f (191 mg, 0.40 mmol) in DCM (2 mL) was added TFA (1 mL). After stirring for 16 hrs at RT, the mixture was concentrated to dryness to afford crude title product as a brown solid (170 mg, 100% yield). LC-MS (Method 2): t R=1.47 min, m/z (M+H) +=423.0

Step 7. Tert-butyl (3-(6-tosylimidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6LF)-yl)bicyclo[1.1.1]pentan-1-yl)carbamate (1h)

      To a mixture of compound 1g (153 mg, 0.36 mmol) in tert-butanol (7.2 mL) was added DPPA (130 mg, 0.47 mmol) and TEA (73 mg, 0.72 mmol) under N 2. The mixture was stirred at RT for 30 minutes and then raised to 90° C. and stirred for another 16 hrs. After cooling, the mixture was concentrated to dryness. The residue was purified by chromatography on silica gel (elute: DCM:MeOH=50:1) to afford the title product as a brown solid (160 mg, 89% yield). LC-MS (Method 2): t R=1.71 min, m/z (M+H) +=494.0.

Step 8. Tert-butyl (3-(imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl)carbamate (1i)

      To a solution of compound 1h (160 mg, 0.32 mmol) in MeOH (3 mL) and water (3 mL) was added NaOH (300 mg, 7.5 mmol). After stirring for 4 hrs at RT, the mixture was concentrated. The residue was diluted with water (20 mL) and extracted with EtOAc (30 mL*2). The combined organic layers were concentrated to dryness and the residue was purified by chromatography on silica gel (elute: DCM:MeOH=20:1) to afford the title product as a white solid (60 mg, 55% yield). 1H NMR (400 MHz, CDCl 3) δ 9.99 (s, 1H), 9.81 (s, 1H), 7.80 (s, 1H), 7.39 (d, J=4.4 Hz, 1H), 6.36 (d, J=4.4 Hz, 1H), 5.30 (br s, 1H), 2.80 (s, 6H), 1.50 (s, 9H).

Step 9. 3-(Imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-amine 2,2,2-trifluoroacetate (1j)

      To a solution of compound 1i (60 mg, 0.18 mmol) in DCM (2 mL) was added TFA (0.5 mL). After stirring for 1 hour at RT, the mixture was concentrated to dryness to afford crude title product as a brown solid (100 mg, 100% yield). LC-MS (Method 2): t R=0.309 min, m/z (M+H) +=240.0

Step 10. N-(3-(Imidazo[4,5-d]pyrrolo[2,3-b]pyridin-1(6H)-yl)bicyclo[1.1.1]pentan-1-yl)propane-1-sulfonamide (1)

      To a solution of compound 1j (40 mg, 0.16 mmol) and TEA (51 mg, 50 mmol) in DMF (1 mL) was added propane-1-sulfonyl chloride (28 mg, 0.5 mmol) at 0° C. After stirring for 3 hrs at RT, the mixture was diluted with water (20 mL) and extracted with EtOAc (20 mL*3). The combined organic layers were concentrated to dryness. The residue was purified prep. HPLC (Method A) to afford the title product as a white solid (10 mg, 18% yield). LC-MS (Method 1): t R=2.71 min, m/z (M+H) +=346.0. 1H NMR (400 MHz, DMSO-d 6) δ 11.94 (s, 1H), 8.59 (d, J=1.6 Hz, 1H), 8.40 (s, 1H), 8.13 (s, 1H), 7.51 (s, 1H), 6.70 (d, J=1.6 Hz, 1H), 3.08 (d, J=8.8 Hz, 2H), 2.70 (s, 6H), 1.74-1.72 (m, 2H), 1.73 (d, J=6.0 Hz, 3H).

PAT

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///////////Zemprocitinib, Janus kinase inhibitor, anti-inflammatory, LNK 01001, LG6MM3RP86

Zavolosotine

December 17, 2025 2:29 am / Leave a comment


Zavolosotine

CAS 2604416-66-0

MF C20H18F5N5O MW439.38

4-[(3S)-3-aminopyrrolidin-1-yl]-6-cyano-5-(3,5-difluorophenyl)-N-[(2S)-1,1,1-trifluoropropan-2-yl]pyridine-3-carboxamide

4-[(3S)-3-aminopyrrolidin-1-yl]-6-cyano-5-(3,5-difluorophenyl)-N-[(2S)-1,1,1-trifluoropropan-2-yl]pyridine-3-carboxamide

4-[(3S)-3-aminopyrrolidin-1-yl]-6-cyano-5-(3,5-difluorophenyl)- N-[(2S)-1,1,1-trifluoropropan-2-yl]pyridine3-carboxamide
somatostatin receptor agonist, 275EAX4XXX

Zavolosotine (Compound 1) is an orally active agonist for somatostatin receptor type 5 (SST5) with EC50 <1 nM. Zavolosotine inhibits insulin and glucagon secretion, increases levels of glucagon in blood in rat model.

SYN

WO2022177988

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2022177988&_cid=P20-MJ9E0I-92373-1

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=US318018214&_cid=P20-MJ9DV5-88499-1

Example 4. 4-[(3S)-3-aminopyrrolidin-1-yl]-6-cyano-5-(3,5-difluorophenyl)-N-[(2S)-1,1,1-trifluoropropan-2-yl]pyridine-3-carboxamide (Compound 1-71)

Step 4-1, preparation of tert-butyl (S)-(1-(2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate: to a DMF (70 mL) solution was added 4,6-dichloronicotinaldehyde (6.8 g, 1.0 Eq, 39 mmol), tert-butyl (S)-pyrrolidin-3-ylcarbamate (7.6 g, 1.1 Eq, 41 mmol) and TEA (16 mL, 3.1 Eq, 120 mmol). The resulting mixture was stirred at 50° C. for 4 hours. The reaction crude was quenched with water (100 mL) and extracted with ethyl acetate (3×40 mL). The organic layers were combined, washed with brine, dried and concentrated under vacuum. The remaining residue was purified by silica gel chromatography eluting with ethyl acetate/petroleum ether (1/3) to afford tert-butyl (S)-(1-(2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (5.3 g, 42%) as a yellow solid. MS (M+H) +=326.2.
      Step 4-2, preparation of tert-butyl (S)-(1-(3-bromo-2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate: to an AcOH (60 mL) solution of tert-butyl (S)-(1-(2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (5.3 g, 1.0 Eq, 16 mmol) was added NBS (3.1 g, 1.1 Eq, 17 mmol) at 10° C. The resulting mixture was stirred at the same temperature for 1 hour. The reaction mixture was quenched with saturated NaHCO 4 and extracted with ethyl acetate (3×40 mL). The organic layers were combined, washed with brine, dried and concentrated under vacuum. The remaining residue was purified by silica gel chromatography eluting with ethyl acetate/petroleum ether (1/4) to afford tert-butyl (S)-(1-(3-bromo-2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (3.5 g, 53%) as a yellow solid. MS (M+H) +=404.1, 406.1.
      Step 4-3, preparation of tert-butyl (S)-(1-(2-chloro-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate: to a mixture of tert-butyl (S)-(1-(3-bromo-2-chloro-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (3.5 g, 1.0 Eq, 8.6 mmol), (3,5-difluorophenyl)boronic acid (0.88 Eq, 7.6 mmol, 1.2 g), Pd(DtBPF)Cl 2 (300 mg, 0.05 Eq, 0.46 mmol) and potassium phosphate (5.4 g, 2.9 Eq, 25 mmol) was added Toluene (140 mL) and water (14 mL) under atmospheric nitrogen. The resulting mixture was stirred at 40° C. for 2 hours. The reaction crude was concentrated under reduced pressure and the remaining residue was purified by silica gel column chromatography eluting with petroleum ether/EtOAc (3:1) to afford tert-butyl (S)-(1-(2-chloro-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (2.7 g, 71%) as a yellow solid. MS (M+H) +=438.0, 440.0.
      Step 4-4, preparation of tert-butyl (S)-(1-(2-cyano-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate: to a mixture of tert-butyl (S)-(1-(2-chloro-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (2.7 g, 1.0 Eq, 6.2 mmol), Pd 2(dba) 3.CHCl 3 (310 mg, 0.05 Eq, 0.31 mmol), Zn(CN) 2 (1.4 g, 1.9 Eq, 12 mmol) and (9,9-dimethyl-9H-xanthene-4,5-diyl)bis(diphenylphosphane) (720 mg, 0.20 Eq, 1.24 mmol) was added DMF (30 mL) under atmospheric nitrogen. The resulting mixture was heated under microwave radiation conditions at 135° C. for 1 hour. The reaction crude was quenched with water (100 mL) and extracted with EtOAc (3×40 mL). Organic layers were combined, washed with brine, dried over anhydrous Na 2SO 4, filtered and concentrated under vacuum. The remaining residue was purified by silica gel chromatography eluting with petroleum ether/EtOAc (1:1) to afford tert-butyl (S)-(1-(2-cyano-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (2.2 g, 83%) as a yellow solid. MS (M+H) +=429.2.
      Step 4-5, preparation of (S)-4-(3-((tert-butoxycarbonyl)amino)pyrrolidin-1-yl)-6-cyano-5-(3,5-difluorophenyl)nicotinic acid: to a tert-butyl alcohol solution (20 mL) of (S)-(1-(2-cyano-3-(3,5-difluorophenyl)-5-formylpyridin-4-yl)pyrrolidin-3-yl)carbamate (2.4 g, 1.0 Eq, 5.1 mmol) was added sodium dihydrogen phosphate (2.4 g, 3.0 Eq, 15 mmol) 2-methylbut-2-ene (11.0 g, 31 Eq, 157 mmol), sodium chlorite (1.0 g, 2.2 Eq, 11 mmol) and water (6.6 mL). The resulting mixture was stirred at ambient temperature for 1 hour. The reaction mixture was quenched with saturated NaHSO 4 (50 mL) and extracted with ethyl acetate (3×40 mL). The organic layers were combined, washed with brine, dried and concentrated under vacuum to afford (S)-4-(3-((tert-butoxycarbonyl)amino)pyrrolidin-1-yl)-6-cyano-5-(3,5-difluorophenyl)nicotinic acid (2.0 g, 88%) as a yellow solid. This material was used for next step without purification. MS (M+H) +=445.2.
      Step 4-6, preparation of tert-butyl ((S)-1-(2-cyano-3-(3,5-difluorophenyl)-5-(((S)-1,1,1-trifluoropropan-2-yl)carbamoyl)pyridin-4-yl)pyrrolidin-3-yl)carbamate: to a DMF solution (2.0 mL) of (S)-4-(3-((tert-butoxycarbonyl)amino)pyrrolidin-1-yl)-6-cyano-5-(3,5-difluorophenyl)nicotinic acid (70 mg, 1.0 Eq, 0.16 mmol) was added (S)-1,1,1-trifluoropropan-2-amine hydrochloride (35 mg, 1.5 Eq, 0.23 mmol), N-ethyl-N-isopropylpropan-2-amine (4.4 Eq, 0.70 mmol, 0.12 mL) and HATU (60 mg, 1.0 Eq, 0.16 mmol). The resulting mixture was stirred at ambient temperature for 2 hours. The reaction crude was purified by Prep-HPLC using the following conditions: SunFire Prep C18 OBD Column, 19*150 mm 5 μm; mobile phase, Water (0.1% FA) and ACN (24.0% ACN up to 46.0% in 7 min); Total flow rate, 20 mL/min; Detector, UV 220 nm. This resulted in tert-butyl ((S)-1-(2-cyano-3-(3,5-difluorophenyl)-5-(((S)-1,1,1-trifluoropropan-2-yl)carbamoyl)pyridin-4-yl)pyrrolidin-3-yl)carbamate (45 mg, 53%) as a light yellow solid. MS (M+H) +=540.3.
      Step 4-7, preparation of 4-((S)-3-aminopyrrolidin-1-yl)-6-cyano-5-(3,5-difluorophenyl)-N—((S)-1,1,1-trifluoropropan-2-yl)nicotinamide: to a DCM solution (2.0 mL) of tert-butyl ((S)-1-(2-cyano-3-(3,5-difluorophenyl)-5-(((S)-1,1,1-trifluoropropan-2-yl)carbamoyl)pyridin-4-yl)pyrrolidin-3-yl)carbamate (45 mg, 1.0 Eq, 0.083 mmol) was added TFA (1.0 mL). The resulting mixture was stirred at ambient temperature for 2 hours. The reaction solution was concentrated and freeze-dried under vacuum to afford the TFA salt of 4-((S)-3-aminopyrrolidin-1-yl)-6-cyano-5-(3,5-difluorophenyl)-N—((S)-1,1,1-trifluoropropan-2-yl)nicotinamide bis(2,2,2-trifluoroacetate) (40.2 mg, 72%) as a light yellow solid. MS (M+H) +=440.2.

PAT

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[1]. FERRARA-COOK C, et al., Somatostatin receptor type 5 agonist for the treatment of hyperinsulinism. WO2022177988 .

///////////zavolosotine, somatostatin receptor agonist, 275EAX4XXX

Vicadrostat

December 13, 2025 6:30 am / Leave a comment


Vicadrostat

CAS 1868065-21-7

MF C15H12ClN3O3 MW 317.73

2-chloro-4-[(6R)-6-(hydroxymethyl)-6-methyl-4-oxo-6,7-dihydropyrano[3,4-d]imidazol-3(4H)-yl]benzonitrile
aldosterone synthase inhibitor, BI 690517, AF4VW4GA3H

Vicadrostat is an aldosterone synthase inhibitor (IC50=48 nM). Vicadrostat can be used for research in kidney diseases and cardiovascular diseases

Vicadrostat (BI 690517) is an investigational drug by Boehringer Ingelheim that selectively blocks aldosterone synthase, reducing excess aldosterone linked to kidney, heart, and metabolic diseases like chronic kidney disease (CKD) and heart failure. Currently in Phase III trials (EASi-KIDNEY and EASi-HF), it’s being tested alone and with empagliflozin (an SGLT2 inhibitor) to reduce proteinuria and improve heart/kidney health, showing promise in reducing albuminuria. 

What it is

  • Type: A highly selective Aldosterone Synthase Inhibitor (ASI).
  • Mechanism: Blocks the enzyme that makes aldosterone, a hormone that causes fluid retention and damage in heart/kidney conditions. 

What it’s for

  • Conditions: Investigated for Chronic Kidney Disease (CKD) and Heart Failure with Preserved Ejection Fraction (HFpEF).
  • Goal: To reduce high aldosterone levels, organ damage, and slow disease progression, particularly in interconnected cardiovascular and renal conditions. 

How it’s being studied

  • Combination Therapy: Key trials combine vicadrostat with empagliflozin (Jardiance).
  • Promising Results: A Phase II trial showed significant reduction in urine protein (albuminuria) when combined with empagliflozin.
  • Clinical Trials: Undergoing large Phase III trials (EASi-KIDNEY and EASi-HF) to confirm its efficacy and safety. 

Key benefit

  • Offers a potential new treatment by targeting aldosterone, addressing multiple interconnected organ systems (heart, kidney, metabolism) simultaneously. 
  • OriginatorBoehringer Ingelheim
  • Class2 ring heterocyclic compounds; Alcohols; Benzonitrile; Chlorinated hydrocarbons; Imidazoles; Pyrones; Small molecules; Urologics
  • Mechanism of ActionCytochrome P-450 CYP11B2 inhibitors
  • Phase IIICardiovascular disorders; Heart failure; Hypertension; Renal failure; Type 2 diabetes mellitus
  • No development reportedDiabetic nephropathies
  • 28 Oct 2025No recent reports of development identified for phase-I development in Renal-failure(In volunteers) in Netherlands (IV)
  • 28 Oct 2025No recent reports of development identified for phase-I development in Renal-failure(In volunteers) in Netherlands (PO)
  • 08 Sep 2025Boehringer Ingelheim initiates a phase I trial (In volunteers, Combination therapy) in Germany (NCT07133399)
  • A Study to Test Whether Vicadrostat in Combination With Empagliflozin Helps People With Chronic Kidney DiseaseCTID: NCT06926660Phase: Phase 2Status: RecruitingDate: 2025-11-28
  • A Study to Test Whether Vicadrostat (BI 690517) in Combination With Empagliflozin Helps People With Heart Failure and a Weak Pumping Function of the Left Side of the HeartCTID: NCT06935370Phase: Phase 3Status: RecruitingDate: 2025-11-26
  • A Study to Test Whether Vicadrostat in Combination With Empagliflozin Helps People With Heart FailureCTID: NCT06424288Phase: Phase 3Status: RecruitingDate: 2025-11-26
  • A Study to Test Vicadrostat (BI 690517) Taken Together With Empagliflozin in People With Type 2 Diabetes, High Blood Pressure, and Cardiovascular DiseaseCTID: NCT07064473Phase: Phase 3Status: RecruitingDate: 2025-11-26
  • A Study in Healthy Men to Compare the Amount of Vicadrostat and Empagliflozin in the Blood When Taken Separately and TogetherCTID: NCT07035457Phase: Phase 1Status: CompletedDate: 2025-08-20

SYN

compound 29 A [WO2016014736A1]

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2016014736&_cid=P12-MJ3WOZ-69028-1

Example 8: Synthesis of 2-chloro-4-[(6R)-6-(hydroxymethyl)-6-methyl-4-oxo-3H,4H,6H,7H-pyrano[3,4-d]imidazol-3-yl]benzonitrile (29 enantiomer A) and 2-chloro-4-[(6S)-6-(hydroxymethyl)-6-methyl-4-oxo-3H,4H,6H,7H-pyrano[3,4-d]imidazol-3-yl]benzonitrile (29 enantiomer B)

29 enan

A mixture of 0.50 g (1.7 mmol) of I-07e and 0.56 g (2.5 mmol) of 77% m-CPBA (m-chloroperoxybenzoic acid) in 10 mL of CH2CI2 is stirred fori 6 h. EtOAc (200 mL) and 20 mL of 10% Na2S03 are added. The mixture is washed twice with 50 mL of NaHC03 and the washes are extracted with 50 mL of CH2C12. The organic extracts are combined, dried with MgS04, filtered and concentrated to give 507 mg of racemic 29 as a pale yellow solid. Chiral

chromatography of 507 mg (LUX 5u Cellulose 4, 28% EtOH:C02, 80 g/min, 120 bar, 40 °C) delivers 238 mg of 29 enantiomer A and 230 mg of 29 enantiomer B. The absolute

stereochemistry for compounds 29 A and 29 B were determined by high resolution single crystal X-ray crystallography structure determination and careful examination of the Flack parameter on the refined structures (H.D. Flack and G. Bernardinelli, 2008, Chirality, 20, 681-690).

The following compounds are prepared from the appropriate olefin I-07c and n in the same manner as 29 enantiomers A & B.

3- (3,4-dichlorophenyl)-6-(hydroxymethyl)-6-methyl-3H,4H,6H,7H-pyrano[3,4- d]imidazol-4-one (30 enantiomers A & B) from I-07c.(RegisPack, 25% (EtOH + 1% iPrNH2):C02, 80 mL/min, 100 bar, 25 °C)

4- [6-(hydroxymethyl)-6-methyl-4-oxo-3H,4H,6H,7H-pyrano[3,4-d]imidazol-3-yl]-3- methylbenzonitrile (31 enantiomers A & B) from I-07n. (LUX 5u Cellulose 4, 25% EtOH:C02, 90 g/min, 120 bar, 40 °C)

SYN

https://patentscope.wipo.int/search/en/detail.jsf;jsessionid=9D1B049BBF0DDAFA23D2F0BE26189EE7.wapp1nC?docId=WO2025190858&_cid=P12-MJ3WMH-67572-1

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2025174790&_cid=P12-MJ3WOZ-69028-1

PAT

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[1]. Jennifer Burke, et al. Aldosterone synthase inhibitors.WO2016014736.2018-09-07

//////////vicadrostat, aldosterone synthase inhibitor, BI 690517, AF4VW4GA3H

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