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Dencatistat
Dencatistat
CAS 2377000-84-3
MFC24H27N7O5S MW 525.6 g/mol
4-[2-(cyclopropylsulfonylamino)pyrimidin-4-yl]-N-[5-(6-ethoxypyrazin-2-yl)-2-pyridinyl]oxane-4-carboxamide
4-[2-(cyclopropanesulfonamido)pyrimidin-4-yl]-N-[5-(6-ethoxypyrazin-2-yl)pyridin-2-yl]oxane-4-carboxamide
CTP synthase 1 inhibitor, antineoplastic, STP 938, CTPS1-IN-2, QG9C9SZZ3T
Dencatistat (formerly known as STP938) is a first-in-class, orally bioavailable cancer drug designed to target specific blood cancers and solid tumours
Dencatistat is an orally bioavailable, small molecule inhibitor of cytidine triphosphate synthase 1 (CTPS1), with potential antineoplastic activity. Upon oral administration, dencatistat targets, binds to and inhibits the activity of CTPS1, thereby decreasing the production of cytidine triphosphate (CTP), an essential building block of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). This may disrupt DNA and RNA synthesis and trigger apoptosis. CTPS1, an enzyme that catalyzes the rate-limiting step in pyrimidine synthesis, plays an important and nonredundant role in B-cell and T-cell proliferation. CTPS1 is required for rapid cell division in certain types of cancers that arise from blood cells.
Mechanism of Action
It works by inhibiting CTPS1 (Cytidine Triphosphate Synthase 1), a key enzyme that cancer cells “addicted” to for DNA synthesis.
- Targeted approach: It aims to kill cancer cells while leaving healthy cells unharmed by exploiting a “synthetic lethal” dependency in certain tumours.
- Precision medicine: It is particularly being tested in patients whose tumours lack CTPS2, a backup enzyme, which makes them highly vulnerable to dencatistat.
🏥 Clinical Status
Developed by Step Pharma, the drug is currently in several clinical trials:
- Lymphoma: Phase 1/2 trials for relapsed or refractory T-cell and B-cell lymphomas.
- Solid Tumours: Phase 1 studies for patients with solid tumours, specifically ovarian and endometrial cancers.
- Essential Thrombocythaemia: A Phase 1b trial for this blood disorder was initiated in 2025.
- Orphan Drug Status: Received FDA Orphan Drug Designation for T-cell lymphoma in May 2025.
- OriginatorStep Pharma
- ClassAnti-inflammatories; Antineoplastics; Antirheumatics; Antithrombotics; Small molecules
- Mechanism of ActionCTPS1 protein inhibitors
- Orphan Drug StatusYes – T-cell lymphoma
- Phase I/IIB-cell lymphoma; T-cell lymphoma
- Phase ISolid tumours; Thrombocytosis
- PreclinicalGraft-versus-host disease; Inflammation
- No development reportedRheumatoid arthritis
- 23 Feb 2026Step Pharma plans phase II trials for Gynaecological cancer
- 10 Feb 2026Preclinical development in Inflammation is till ongoing in France (PO) (Step Pharma pipeline, February 2026)
- 15 Oct 2025Adverse event data from a phase I/II trial in T-cell lymphoma/B-cell lymphoma released by Step Pharma
SYN
US20250177394, Compound CTPS1-IA
PAT
PAT
A. Preparation of Active Ingredient
20 Example A1 – Preparation of crude 4-(2-(cyclopropanesulfonamido)pyrimidin-4-yl)-N-(5- (6-ethoxypyrazin-2-yl)pyridin-2-yl)tetrahydro-2H-pyran-4-carboxamide
Step 4 – Preparation of crude 4-(2-(cyclopropanesulfonamido)pyrimidin-4-yl)-N-(5-(6- ethoxypyrazin-2-yl)pyridin-2-yl)tetrahydro-2H-pyran-4-carboxamide
4-(2-(cyclopropanesulfonamido)pyrimidin-4-yl)tetrahydro-2H-pyran-4-carboxylate (1.76 kg, 5.15 mol, 1.00 equiv.) and 5-(6-ethoxypyrazin-2-yl)pyridin-2-amine (1.22 kg, 5.65 mol, 1.10 equiv.) were suspended in a mixture of THF (27.1 L, 15.5 rel. vol.) and DMSO (2.63 L, 1.50 rel. vol.) and stirred until the solids were evenly dispersed. The mixture was concentrated by
STP-P3718PCT
102
distillation at atmospheric pressure and approximately 70 oC to a volume of 15 L. The temperature was adjusted to 20 ± 5 oC, potassium tert-butoxide (6.92 kg 20 wt% solution in THF, 12.3 mol, 2.40 equiv.) was added over 1 h and the reaction mixture stirred at 20 ± 5 oC for 70 minutes until completion. THF (880 mL, 0.500 rel vol.) was charged, followed by acetic acid (780 5 mL, 820 g, 13.6 mol, 2.64 equiv.) over 10 minutes, followed by methanol (4.40 L, 2.50 rel. vol.), followed by water (13.2 L, 7.50 rel. vol.) over 35 minutes. The mixture was stirred at 20 ± 5 oC for 15 minutes and then 16 h at 0 ± 5 oC. The resulting suspension was filtered and washed with water (2 × 8.80 L, 2 × 5.00 rel. vol.), followed by methanol (4.40 L, 2.50 rel. vol.) The filter cake was dried at 35 oC under a flow of nitrogen for 20 h to afford crude 4-(2-10 (cyclopropanesulfonamido)pyrimidin-4-yl)-N-(5-(6-ethoxypyrazin-2-yl)pyridin-2-yl)tetrahydro- 2H-pyran-4-carboxamide (“CTPS1-IA”).
PAT
- Aminopyrimidine derivatives as CTPS1 inhibitorsPublication Number: JP-7428692-B2Priority Date: 2018-03-23Grant Date: 2024-02-06
- Aminopyrimidine derivatives as ctps1 inhibitorsPublication Number: EP-3768674-A1Priority Date: 2018-03-23
- Aminopyrimidine derivative as a CTPS1 inhibitorPublication Number: JP-2021518436-APriority Date: 2018-03-23
- Aminopyrimidine derivatives as ctps1 inhibitorsPublication Number: EP-3768674-B1Priority Date: 2018-03-23Grant Date: 2024-01-03
- Aminopyrimidine derivatives as CTPS1 inhibitorsPublication Number: CN-111868051-APriority Date: 2018-03-23
- Aminopyrimidine derivatives as CTPS1 inhibitorsPublication Number: ES-2974445-T3Priority Date: 2018-03-23Grant Date: 2024-06-27
- CompoundsPublication Number: US-2021024507-A1Priority Date: 2018-03-23
- CompoundsPublication Number: US-2021387965-A1Priority Date: 2018-10-23
- CompoundsPublication Number: US-2023192673-A1Priority Date: 2018-06-04
- Aminopyrimidine derivatives as CTPS1 inhibitorsPublication Number: CN-111868051-BPriority Date: 2018-03-23Grant Date: 2024-04-09
- Aminopyrimidine derivatives as ctps1 inhibitorsPublication Number: WO-2019180244-A1Priority Date: 2018-03-23
- Aminopyrimidine derivatives as ctps1 inhibitorsPublication Number: WO-2019179652-A1Priority Date: 2018-03-23
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References
////////dencatistat, anax lab, CTP synthase 1 inhibitor, antineoplastic, STP 938, CTPS1-IN-2, QG9C9SZZ3T
Delocamten
Delocamten
CAS 2417411-02-8
MFC19H21F2N3O3 MW377.4 g/mol
(6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(oxan-4-yl)-5,6,7,8-tetrahydro-1H-pyrido[2,3-d]pyrimidine-2,4-dione
(6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(oxan-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4(1H,3H)-dione
cardiac myosin inhibitor, MYK-224; BMS-986435, MYK 224, BMS 986435, IE5886BN8T
Delocamten (development code MYK-224) is a small-molecule cardiac myosin inhibitor developed by Bristol Myers Squibb for hypertrophic cardiomyopathy.[1][2][3]
Delocamten is a small molecule drug. Delocamten is under investigation in clinical trial NCT06122779 (Study to Evaluate Safety, Tolerability and Drug Levels of BMS-986435/MYK-224 in Participants With Heart Failure With Preserved Ejection Fraction (HFpEF)). Delocamten has a monoisotopic molecular weight of 377.16 Da.
SYN
Example 1-3: Preparation of (6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(tetrahydro-2H-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2, 4 (1H, 3H)-dione (3)
Step 7. Synthesis of (6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(tetrahydro-2H-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2, 4 (1H, 3H)-dione (3). A mixture of crude 3G (1.0 g, 2.53 mmol) in CH 3CN (15 mL) was put into a microwave reactor with stirring at 120° C. for 30 min. Subsequently, the mixture was concentrated and the residue was purified by preparative HPLC (column: C18 silica gel; mobile phase: CH3CN:H 2O=20:80 (v v) increasing to CH3CN:H 2O=80:20 (v v) within 40 min; detector: UV 254 nm) to give compound 3 (302 mg, 32%), as a white solid, which was identified as Form 1 polymorph (see Example 2). LC-MS (ES, m/z): 378 [M+H] +; 1H NMR (300 MHz, d-DMSO): δ 10.20 (s, 1H), 7.38-7.05 (m, 3H), 6.45 (s, 1H), 5.11-4.81 (m, 3H), 3.89 (dd, J=10.8, 3.9 Hz, 2H), 3.34-3.27 (m, 3H), 2.76-2.48 (m, 4H), 2.28 (s, 3H), 1.39-1.36 (m, 2H); 19F NMR (376 MHz, d 6-DMSO): δ −123.51 (t, J=86.5 Hz), −191.57 (d, J=129.34 Hz).
PAT
Example 1-3: Preparation of (6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3- (tetrahydro-2H-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2, 4 (1H, 3H)-dione (3).
Scheme 3
[0165] Step 1. Synthesis of (R,E)-N-(2-fluoro-5-methylbenzylidene)-2-methylpropane-2-sulfinamide (3B). The reaction mixture was filtered and the filtrate was diluted with ether (150 mL). Subsequently, the resulting suspension was filtered. The filtrate was concentrated and the residue was dried in vacuo to give 3B (8.7 g, 97%) as a yellow oil. LC-MS (ES, m/z): 242 [M+H] + ; 1 H NMR (400 MHz, d 6 -DMSO): d 8.87 (s, 1H), 7.76 (m, 1H), 7.29 (m, 1H), 7.03 (m, 1H), 2.37 (d, J = 1.0 Hz, 3H), 1.27 (s, 9H).
[0166] Step 2. Synthesis of ethyl (2R,3S)-3-(((R)-tert-butylsulfinyl)amino)-2-fluoro-3-(2-fluoro-5-methylphenyl)propanoate (3C). To a solution of 3B (4 g, 16.6 mmol), ethyl 2- fluoroacetate (2.6 g, 24.6 mmol), and TMEDA (4.8 mL) in anhydrous THF (40 mL) was added LiHMDS (1 M in THF, 24.6 mL, 24.6 mmol) dropwise at -78 o C over 30 min under an atmosphere of Ar. After stirring at -78 o C for 1 h, the reaction was quenched by adding 1 N aq.
HCl (50 mL), while maintaining the inner temperature of the mixture at < -20 o C. Subsequently, the mixture was concentrated to remove most of the organic solvent and then extracted with EtOAc (100 mL x 3). The combined organic extracts were washed with brine (100 mL) and dried over anhydrous Na2SO4. The solvent was removed and the residue was dried in vacuo to give crude 3C (6.0 g) as a yellow oil, which was used for the next step without further purification. LC-MS (ES, m/z): 348 [M+H] + .
[0167] Step 3. Synthesis of (2R,3S)-3-(((R)-tert-butylsulfinyl)amino)-2-fluoro-3-(2-fluoro-5-methylphenyl)propanoic acid (3D). To a solution of 3C (6.0 g, 17.3 mmol) in THF (40 mL) was added 1N aq. NaOH (34.6 mL, 34.6 mmol) at rt. After stirring at rt for 1 h, the reaction mixture was added ice water (50 mL). The resulting mixture was extracted with EtOAc (100 mL x 2). The aqueous layer was adjusted to pH 5 with sat. aq. citric acid, followed by extraction with EtOAc (100 mL x 3). Subsequently, the combined organic extracts were washed with brine (100 mL) and dried over anhydrous Na 2 SO 4 . The solvent was removed and the residue was purified by preparative HPLC (Column: LC-MS (ES, m/z): 320 [M+H] + ; 1 H NMR (400 MHz, d 6 -DMSO): d 13.57 (br, 1H), 7.55 (dd, J = 7.5, 2.2 Hz, 1H), 7.23– 6.94 (m, 2H), 6.04 (d, J = 10.8 Hz, 1H), 5.37– 4.86 (m, 2H), 2.29 (s, 3H), 1.12 (s, 9H).
[0168] Step 4. Synthesis of (R)-N-((1S,2R)-2-fluoro-1-(2-fluoro-5-methylphenyl)-3-oxo-3- (2,4,6-trioxo-1-(tetrahydro-2H-pyran-4-yl)hexahydropyrimidin-5-yl)propyl)-2-methylpropane-2-sulfinamide (3E). A solution of 3D (700 mg, 2.19 mmol), 2-2 (698 mg, 3.29 mmol), and HATU (1.25 g, 3.29 mmol) in DMF (10 mL) was added DIEA (849 mg, 6.57 mmol) at 0 o C under an atmosphere of Ar. aq. sodium bicarbonate (30 mL) and the resulting solution was extracted with ethyl acetate (50 mL x3). The combined organic extracts were washed with brine (50 mL x 2) and dried over anhydrous Na 2 SO 4 . The solvent was removed and the residue was dried in vacuo to give crude 3E (1.3 g) as a white solid, which was used for the next step without further purification. LC-MS (ES, m/z): 514 [M+H] + ; 1 H NMR (400 MHz, d 6 -DMSO): d 12.16 (br, 1H), 7.66– 7.45 (m, 1H), 7.23– 6.98 (m, 2H), 6.37 (m, 1H), 6.13 (d, J = 10.7 Hz, 1H), 5.22 (m, 1H), 4.79 (m, 1H), 3.94 (m, 2H), 3.35 (t, J = 11.7 Hz, 2H), 2.52– 2.39 (m, 2H), 2.29 (s, 3H), 1.49 (d, J = 12.2 Hz, 2H), 1.04 (s, 9H).
[0169] Step 5. Synthesis of (R)-N-((1S,2S)-2-fluoro-1-(2-fluoro-5-methylphenyl)-3-(2,4,6- trioxo-1-(tetrahydro-2H-pyran-4-yl)hexahydropyrimidin-5-yl)propyl)-2-methylpropane-2-sulfinamide (3F). A solution of crude 3E (1.3 g, 2.53 mmol) in AcOH (10 mL) was added NaBH3CN (398 mg, 6.33 mmol) at 0 o C under an atmosphere of Ar. After stirring at rt for 1 h, the reaction mixture was added ice water (20 mL) and the resulting solution was extracted with EtOAc (50 mL x 3). Next, the combined organic extracts were washed with brine (50 mL) and
dried over anhydrous Na2SO4. The solvent was removed and the residue was dried in vacuo to give crude 3F (1.3 g) as a white solid, which was used for the next step without further purification. LC-MS (ES, m/z): 500 [M+H] + ; 1 H NMR (400 MHz, d 6 -DMSO): d 11.31 (d, J = 28.1 Hz, 1H), 7.41 (d, J = 7.4 Hz, 1H), 7.27– 6.84 (m, 2H), 6.11– 5.78 (m, 2H), 5.08– 4.43 (m, 3H), 3.87 (m, 3H), 2.29 (s, 6H), 1.99 (s, 1H), 1.53– 1.28 (m, 2H), 1.10 (d, J = 2.1 Hz, 10H).
[0170] Step 6. Synthesis of 5-((2S,3S)-3-amino-2-fluoro-3-(2-fluoro-5-methylphenyl)propyl)-1-(tetrahydro-2H-pyran-4-yl)pyrimidine-2, 4, 6 (1H, 3H, 5H)-trione (3G). A solution of crude 3F (1.3 g, 2.60 mmol) in ethanol (10 mL) was added thionyl chloride (334 mg) at 0 o C. After stirring at rt for 1 h, the reaction mixture was concentrated and the residue was dried in vacuo to give crude 3G (1.0 g) as a white solid, which was used for the next step without further purification. LC-MS (ES, m/z): 396 [M+H] + .
[0171] Step 7. Synthesis of (6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(tetrahydro-2H-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2, 4 (1H, 3H)-dione (3). A mixture of crude 3G (1.0 g, 2.53 mmol) in CH 3 CN (15 mL) was put into a microwave reactor with stirring at 120 o C for 30 min. Subsequently, the mixture was concentrated and the residue was purified by preparative HPLC (column: C18 silica gel; mobile phase: CH3CN:H2O = 20:80 (v/v) increasing to CH3CN:H2O = 80:20 (v/v) within 40 min; detector: UV 254 nm) to give compound 3 (302 mg, 32%), as a white solid, which was identified as Form 1 polymorph (see Example 2). LC-MS (ES, m/z): 378 [M+H] + ; 1 H NMR (300 MHz, d 6 -DMSO): d 10.20 (s, 1H), 7.38– 7.05 (m, 3H), 6.45 (s,1H), 5.11– 4.81 (m, 3H), 3.89 (dd, J = 10.8, 3.9 Hz, 2H), 3.34– 3.27 (m, 3H), 2.76–2.48 (m, 4H), 2.28 (s, 3H), 1.39–1.36 (m, 2H); 19 F NMR (376 MHz, d 6 -DMSO): d -123.51 (t, J = 86.5 Hz), -191.57 (d, J = 129.34 Hz).
PAT
- Tetrahydropyran (thp)-substituted bicyclic-pyrimidinedione compoundsPublication Number: EP-4464321-A2Priority Date: 2018-10-29
- Tetrahydropyran-substituted bicyclic pyrimidinedione compounds (THP)Publication Number: ES-2986923-T3Priority Date: 2018-10-29Grant Date: 2024-11-13
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-2024025894-A1Priority Date: 2018-10-29
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-12344607-B2Priority Date: 2018-10-29Grant Date: 2025-07-01
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-2025282779-A1Priority Date: 2018-10-29
- Tetrahydropyran (THP) Substituted Bicyclic Pyrimidinedione CompoundsPublication Number: CN-113056465-APriority Date: 2018-10-29
- Tetrahydropyrane (THP) -substituted bicyclic pyrimidinedione compoundsPublication Number: CN-119977963-APriority Date: 2018-10-29
- Tetrahydropyran (thp)-substituted bicyclic-pyrimidinedione compoundsPublication Number: EP-3873904-B1Priority Date: 2018-10-29Grant Date: 2024-07-10
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-11034693-B2Priority Date: 2018-10-29Grant Date: 2021-06-15
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-2022106314-A1Priority Date: 2018-10-29
- Tetrahydropyran (THP)-Substituted Bicyclic-Pyrimidinedione CompoundsPublication Number: JP-2024063091-APriority Date: 2018-10-29
- Tetrahydropyran (thp)-substituted bicyclic-pyrimidinedione compoundsPublication Number: TW-202426449-APriority Date: 2018-10-29
- Tetrahydropyrane (THP) -substituted bicyclic pyrimidinedione compoundsPublication Number: CN-113056465-BPriority Date: 2018-10-29Grant Date: 2025-01-28
- Tetrahydropyran (thp)-substituted bicyclic-pyrimidinedione compoundsPublication Number: US-2020165247-A1Priority Date: 2018-10-29
- BICYCLIC PYRIMIDINODIONA COMPOUNDS REPLACED WITH TETRAHYDROPYRAN, POLYMORPHIC FORM OF THE SAME AND THE USE OF THE SAME FOR THE TREATMENT OF HCMPublication Number: AR-116880-A1Priority Date: 2018-10-29
- Substituted 5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4-diones for treating cardiac diseasesPublication Number: US-2022340569-A1Priority Date: 2018-10-29
- Tetrahydropyran (thp)-substituted bicyclic-pyrimidinedione compoundsPublication Number: EP-3873904-A1Priority Date: 2018-10-29
- CRYSTALLINE FORMS OF (6S,7S)-6-FLUORO-7-(2-FLUORO-5-METHYLPHENYL)- 3-(TETRAHYDRO-2H-PYRAN-4-YL)-5,6,7,8-TETRAHYDROPYRIDO[2,3- d]PYRIMIDINE-2,4(1H,3H)-DIONEPublication Number: WO-2024026058-A8Priority Date: 2022-07-29
- Crystalline forms of (6s,7s)-6-fluoro-7-(2-fluoro-5-methylphenyl)- 3-(tetrahydro-2h-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3- d]pyrimidine-2,4(1h,3h)-dionePublication Number: EP-4561697-A1Priority Date: 2022-07-29
- Methods of Administering Myosin InhibitorsPublication Number: US-2023338378-A1Priority Date: 2022-04-26
- Methods of treatment with myosin modulatorPublication Number: US-2023158027-A1Priority Date: 2019-11-10
- tetrahydropyran-substituted bicyclic pyrimidinedione compounds (thp)Publication Number: BR-112021008077-A2Priority Date: 2018-10-29
- CRYSTALLINE FORMS OF (6S,7S)-6-FLUORO-7-(2-FLUORO-5-METHYLPHENYL)-3-(TETRAHYDRO-2H-PYRAN-4-YL)-5,6,7,8-TETRAHYDROPYRIDO[2,3-d]PYRIMIDINE-2,4(1H,3H)-DIONEPublication Number: US-2025034129-A1Priority Date: 2023-07-28
- CRYSTALLINE FORMS OF (6S,7S)-6-FLUORO-7-(2-FLUORO-5-METHYLPHENYL)-3-(TETRAHYDRO-2H-PYRANO-4-IL)-5,6,7,8-TETRAHYDROPYRIDE[2 ,3-D]PYRIMIDINE-2,4(1H,3H)-DIONEPublication Number: AR-130058-A1Priority Date: 2022-07-29
- Crystalline forms of (6s,7s)-6-fluoro-7-(2-fluoro-5-methylphenyl)- 3-(tetrahydro-2h-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3- d]pyrimidine-2,4(lh,3h)-dionePublication Number: WO-2024026058-A1Priority Date: 2022-07-29
- Crystalline form of (6S,7S)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(tetrahydro-2H-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4(1H,3H)-dionePublication Number: CN-119855816-APriority Date: 2022-07-29
- Crystalline forms of (6s,7s)-6-fluoro-7-(2-fluoro-5-methylphenyl)-3-(tetrahydro-2h-pyran-4-yl)-5,6,7,8-tetrahydropyrido[2,3-d]pyrimidine-2,4(1h,3h)-dionePublication Number: TW-202412788-APriority Date: 2022-07-29
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References
References
- Lehman, Sarah J.; Crocini, Claudia; Leinwand, Leslie A. (June 2022). “Targeting the sarcomere in inherited cardiomyopathies”. Nature Reviews Cardiology. 19 (6): 353–363. doi:10.1038/s41569-022-00682-0. ISSN 1759-5010. PMC 9119933. PMID 35304599.
- Sebastian, Sneha Annie; Padda, Inderbir; Lehr, Eric J.; Johal, Gurpreet (September 2023). “Aficamten: A Breakthrough Therapy for Symptomatic Obstructive Hypertrophic Cardiomyopathy”. American Journal of Cardiovascular Drugs. 23 (5): 519–532. doi:10.1007/s40256-023-00599-0. PMID 37526885. S2CID 260348901.
- Packard, Elizabeth; de Feria, Alejandro; Peshin, Supriya; Reza, Nosheen; Owens, Anjali Tiku (December 2022). “Contemporary Therapies and Future Directions in the Management of Hypertrophic Cardiomyopathy”. Cardiology and Therapy. 11 (4): 491–507. doi:10.1007/s40119-022-00283-5. PMC 9652179. PMID 36243823.
////////delocamten, ANAX LAB, cardiac myosin inhibitor, MYK-224; BMS-986435, MYK 224, BMS 986435, IE5886BN8T
Darlifarnib
Darlifarnib
CAS 2939824-30-1
MF C29H20N6O MW 468.51
14-amino-14-(3-methylimidazol-4-yl)-7-oxa-19-azapentacyclo[13.6.2.12,6.19,13.018,22]pentacosa-1(22),2(25),3,5,9,11,13(24),15(23),16,18,20-undecaene-10,20-dicarbonitrile
farnesyl transferase inhibitor, antineoplastic, KO-2806, KO 2806, T206317
Darlifarnib (KO-2806) is an investigational, orally active next-generation farnesyl transferase inhibitor (FTI) being developed by Kura Oncology to treat solid tumors, such as clear cell renal cell carcinoma (ccRCC). It inhibits the enzyme farnesyl transferase, blocking KRAS and mTORC1 signaling to induce tumor regression. It is often combined with other agents to overcome resistance.
Key Details About Darlifarnib
- Mechanism of Action: As a FTI, darlifarnib binds to and inhibits farnesyl transferase, which prevents the activation of RAS oncogenes and inhibits downstream mTORC1 signaling, leading to tumor cell death.
- Target Indications: Preclinical and early clinical data show potential in treating KRAS-mutant cancers, including non-small cell lung cancer (NSCLC), colorectal cancer (CRC), and clear cell renal cell carcinoma (ccRCC).
- Combination Therapy: Data from the Phase 1 FIT-001 trial (presented in April 2026) showed that combining darlifarnib with the TKI cabozantinib demonstrated robust activity in patients with pretreated, advanced ccRCC.
- Overcoming Resistance: Darlifarnib is designed to re-sensitize tumors that have become resistant to prior therapies, such as RAS inhibitors and tyrosine kinase inhibitors (TKIs).
- Status: It is an investigational drug and not yet FDA-approved.
- OriginatorKura Oncology
- ClassAntineoplastics; Small molecules
- Mechanism of ActionFarnesyltranstransferase inhibitors
- Phase IAdenocarcinoma; Colorectal cancer; Non-small cell lung cancer; Renal cell carcinoma; Solid tumours
- 12 Jan 2026Kura Oncology plans the one or more expansion cohorts of KO 2806 and cabozantinib in patients with advanced renal cell carcinoma in the first half of 2026
- 22 Oct 2025Pharmacodynamics data from a preclinical trial in Cancer presented at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics 2025 (AACR-NCI-EORTC-2025)
- 18 Oct 2025Adverse events and efficacy data from a phase I trial in Non-small cell lung cancer, Renal cell carcinoma, Adenocarcinoma released by Kura Oncology
PAT
PAT
Step A: Preparation of (058-1)
Step B: Preparation of (058-2)
Step C: Preparation of (rac)-3-amino-3-(1-methyl-1H-imidazol-5-yl)-6-oxa-2(4,6)-quinolina-1,4(1,3)-dibenzenacyclohexaphane-22,44-dicarbonitrile (rac-058)
Step D: Preparation of (S)-3-amino-3-(1-methyl-1H-imidazol-5-yl)-6-oxa-2(4,6)-quinolina-1,4(1,3)-dibenzenacyclohexaphane-22,44-dicarbonitrile ((S)-058)
PAT
- Macrocyclic compounds and compositions, and methods of preparing and using the samePublication Number: US-2023322711-A1Priority Date: 2021-11-30
- Macrocyclic compounds and compositions, and methods of preparing and using the samePublication Number: US-12018011-B2Priority Date: 2021-11-30Grant Date: 2024-06-25
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References
/////////////darlifarnib, ANAX LAB, farnesyl transferase inhibitor, antineoplastic, KO-2806, KO 2806, T206317
Daraxonrasib
Daraxonrasib
CAS 2765081-21-6
MFC44H58N8O5S MW811.0 g/mol
trans-(1S,2S)-N-[(7S,13S)-21-ethyl-20-[2-[(1S)-1-methoxyethyl]-5-(4-methylpiperazin-1-yl)-3-pyridinyl]-17,17-dimethyl-8,14-dioxo-15-oxa-4-thia-9,21,27,28-tetrazapentacyclo[17.5.2.12,5.19,13.022,26]octacosa-1(25),2,5(28),19,22(26),23-hexaen-7-yl]-2-methylcyclopropane-1-carboxamide
Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2,
Daraxonrasib (formerly RMC-6236) is an investigational, orally administered “molecular glue” RAS inhibitor developed by Revolution Medicines for treating advanced solid tumors with RAS mutations, particularly metastatic pancreatic cancer. April 2026 Phase 3 trials showed it significantly improves survival, demonstrating high potential as a first-line treatment.
Key Clinical Findings and Updates (as of April 2026):
- Mechanism: It acts as a RAS(ON) inhibitor, targeting mutated and wild-type RAS proteins (
) to disrupt cancer signaling.
- Breakthrough Results: Data from the RASolute 302 trial showed a substantial survival benefit in patients with previously treated metastatic pancreatic ductal adenocarcinoma (PDAC).
- High Response Rates: In trials, daraxonrasib combined with chemotherapy showed a 58% confirmed objective response rate (ORR) and 84% progression-free survival (PFS) at 6 months in untreated RAS-mutant metastatic pancreatic cancer.
- Safety Profile: Generally well-tolerated, with side effects including rash, diarrhea, stomatitis, and nausea.
- Recognition: Named the “2025 Molecule of the Year” by Drug Hunter for its, novel mechanism and clinical potential.
Daraxonrasib is currently being studied in the Phase 3 RASolute 303 trial for first-line treatment of pancreatic cancer.
Daraxonrasib (RMC-6236) is a RAS inhibitor drug. It is undergoing testing by Revolution Medicines to treat advanced solid tumors with RAS mutations, especially metastatic pancreatic ductal adenocarcinoma (PDAC) containing KRAS G12X mutations.[1] It received a breakthrough therapy designation from the U.S. Food and Drug Administration.[2]
Daraxonrasib is orally active and multi-selective RAS inhibitor. It uses a tri-complex mechanism to target the active, GTP-bound form of RAS proteins, including mutant and wild-type forms. Unlike conventional RAS inhibitors, it first binds to the chaperone-like protein cyclophilin A to form a complex, which then attaches to active RAS. This interaction blocks downstream effector binding and inhibits oncogenic signaling.[3]
In 2026, Daraxonrasib clinical trial completed a phase 3 clinical trial (RASolute 302) to assess efficacy compared to standard-of-care chemotherapy.[4] The trial met all primary and key secondary endpoints, including progression-free survival (PFS). The company reported median survival of 13.2 months with daraxonrasib vs. 6.7 months with standard chemotherapy. The hazard ratio for death was 0.40 (a 60% reduction in risk of death; p < 0.0001). Daraxonrasib was generally well tolerated with a manageable safety profile and no new safety signals.[5]
PAT
PAT
PATENT ATTORNEY DOCKET: 51432-038WO2 Part 4 – Purification of Compound A – (1S,2S)-N-[(7S,13S)-21-ethyl-20-{2-[(1S)-1- methoxyethyl]-5-(4-
1.0equiv) at 25°C. The resulting suspension was stirred until solids were completely dissolved. The resulting methanol solution was filtered through microporous filter and transferred to another reactor. Then the reactor temperature was maintained at 25°C and slowly water (2.41kg, 1.0 V) water was added over a period of 30 minutes. The resulting cloudy solution was stirred for another 30 minutes at 25°C. Then a solution of methanol and water (3.42kg, 1:2, v/v) slowly over 1 hour. The resulting suspension was stirred for 2 hours at 25°C. Again, to the suspension additional water (2.48kg) slowly added over 1 hour. The final, suspension was stirred for additional 1 hour. Water (9.29kg, 3.75 V) was added to the suspension slowly over 2 hours and the mixture was stirred for at least for 16 hours at 25°C. The resulting suspension was filtered and washed with mixed solvent water: MeOH (3:2, v/v) twice (2x 2.2 kg), followed by water (4.91kg) washing. The wet cake was dried under reduced pressure and controlled humidity (temperature: 25 ± 5 ˚C, vacuum ≥ -0.085 MPa, humidity: 10%~20%) for 37 hours to afford Compound A as a white solid (2.68 kg, 99.4% a/a purity, 93.0% w/w assay, KF: 6.7%, 3.07 mol, 92% yield, Table 27).
PAT
- Synthesis of ras inhibitorsPublication Number: WO-2024216017-A2Priority Date: 2023-04-14
- Macrocycle compounds useful as kras inhibitorsPublication Number: WO-2024008834-A1Priority Date: 2022-07-08
- Ras inhibitorsPublication Number: US-11690915-B2Priority Date: 2020-09-15Grant Date: 2023-07-04
- Ras inhibitorsPublication Number: US-2023226186-A1Priority Date: 2020-09-15
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References
References
- Cregg J, Edwards AV, Chang S, Lee BJ, Knox JE, Tomlinson AC, et al. (March 2025). “Discovery of Daraxonrasib (RMC-6236), a Potent and Orally Bioavailable RAS(ON) Multi-selective, Noncovalent Tri-complex Inhibitor for the Treatment of Patients with Multiple RAS-Addicted Cancers”. Journal of Medicinal Chemistry. 68 (6): 6064–6083. doi:10.1021/acs.jmedchem.4c02314. PMID 40056080.
- Sava J (July 1, 2025). “Daraxonrasib Earns FDA Breakthrough Status in Pancreatic Cancer”. Targeted Oncology. Retrieved October 12, 2025.
- Jiang J, Jiang L, Maldonato BJ, Wang Y, Holderfield M, Aronchik I, et al. (June 2024). “Translational and Therapeutic Evaluation of RAS-GTP Inhibition by RMC-6236 in RAS-Driven Cancers”. Cancer Discovery. 14 (6): 994–1017. doi:10.1158/2159-8290.CD-24-0027. PMC 11149917. PMID 38593348.
- Clinical trial number NCT05379985 at ClinicalTrials.gov
- Mast J (2026-04-13). “Revolution Medicines touts ‘unprecedented’ data for pancreatic cancer pill”. STAT. Retrieved 2026-04-13.
| Clinical data | |
|---|---|
| Other names | RMC-6236 |
| Identifiers | |
| IUPAC name | |
| CAS Number | 2765081-21-6 |
| PubChem CID | 164726578 |
| IUPHAR/BPS | 13368 |
| ChemSpider | 115275938 |
| UNII | B6T47Y2UAP |
| KEGG | D13265 |
| ChEBI | CHEBI:746946 |
| Chemical and physical data | |
| Formula | C44H58N8O5S |
| Molar mass | 811.06 g·mol−1 |
| 3D model (JSmol) | Interactive image |
| SMILES | |
| InChI | |
//////////daraxonrasib, anax labs, Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2,
Danifexor
Danifexor
CAS 2648738-68-3
MF C29H20Cl2N2O5 MW547.386
6-[6-[[5-cyclopropyl-3-(2,6-dichlorophenyl)-1,2-oxazol-4-yl]methoxy]naphthalen-2-yl]oxypyridine-3-carboxylic acid
| 3-Pyridinecarboxylic acid, 6-[[6-[[5-cyclopropyl-3-(2,6-dichlorophenyl)-4-isoxazolyl]methoxy]-2-naphthalenyl]oxy]- |
farnesoid X receptor agonist, TUU8G1CX9O, HEC 96719, ASC42
Danifexor is an investigational drug that acts as a potent and selective agonist for the farnesoid X receptor (FXR). It was primarily being developed for the treatment of liver diseases such as Primary Biliary Cholangitis (PBC). ProbeChem +1
However, recent reports from April 2024 indicate that development for Danifexor has been discontinued because it was deemed non-competitive against other emerging therapies for PBC.
Key Properties and Identifiers
Danifexor is a non-steroidal molecule with specific chemical markers used in laboratory research:
- Target: Farnesoid X receptor (FXR).
Therapeutic Context
The drug was designed to target the FXR pathway, which regulates bile acid, lipid, and glucose metabolism.
- Primary Goal: Treatment of Primary Biliary Cholangitis (PBC), a chronic liver disease.
- Mechanism: As an agonist, it binds to and activates FXR to help reduce the toxic buildup of bile acids in the liver.
SYN
Example 1
Preparation of 6-((6-((5-cyclopropyl-3-(2,6-dichlorophenyl)isoxazol-4-yl) methoxy)naphthalen-2-yl)oxy)nicotinic acid (Compound 1)
(a) Referring to the following reaction equation (Route A), Compound 1A-1 (1.0 g, 2.88 mmol, 1 eq.), Compound 1A-2 (0.46 g, 2.88 mmol, 1 eq.) and cesium carbonate (1.88 g, 5.76 mmol, 2 eq.) were dissolved in DMF (10 ml). The reaction was carried out at 65° C. for 2 h. After cooling, 10 ml water and 10 ml EA (ethyl acetate) were added for extraction, and the organic phase was washed with water and concentrated to dryness to give Compound 1A, 6-((5-cyclopropyl-3-(2,6-dichlorophenyl)isoxazol-4-yl)methoxy)naphthalen-2-ol, 0.8 g, yield: 65.0%. LCMS (ESI): calculated for C 23H 17C 12NO 3; [M+H] +: 426.1, found: 426.1.
b) Referring to the following reaction equation, Compound 1A (0.2 g, 0.47 mmol, 1 eq.), 6-bromonicotinic acid methyl ester (0.1 g, 0.47 mmol, 1 eq.) and cesium carbonate (0.306 g, 0.94 mmol, 2 eq.) were dissolved in DMF (10 ml). The reaction was carried out at 65° C. for 2 h. After cooling, 10 ml water and 10 ml EA were added for extraction, and the organic phase was washed with water and concentrated to dryness to give Compound 1B, methyl 6((6((5-cyclopropyl-3-(2,6-dichlorophenyl)isoxazol-4-yl)methoxy)naphthalene-2-yl)oxy)nicotinate, 0.21 g, yield: 80.0%. LCMS (ESI): calculated for C 30H 22C 12N 2O 5; [M+H] +: 561.1, found: 561.1.
PAT
PAT
- Use and pharmaceutical composition of phenylisoxazolyl methylene-naphthalene-ether derivativesPublication Number: WO-2021109713-A1Priority Date: 2019-12-03
- Compounds for modulating activity of fxr and uses thereofPublication Number: WO-2021109712-A1Priority Date: 2019-12-03
- Uses and pharmaceutical compositions of phenylisoxazolylmethylene-naphthalene-ether derivativesPublication Number: CN-112891348-APriority Date: 2019-12-03
- Compounds that modulate FXR activity and their applicationsPublication Number: CN-112898289-APriority Date: 2019-12-03
- Compounds that modulate FXR activity and their applicationsPublication Number: CN-112898289-BPriority Date: 2019-12-03Grant Date: 2022-11-04
- Uses and pharmaceutical compositions of phenylisoxazolyl methylene-naphthalene-ether derivativesPublication Number: KR-20220101697-APriority Date: 2019-12-03
- Compounds for modulating activity of fxr and uses thereofPublication Number: EP-4073070-A1Priority Date: 2019-12-03
- Use and pharmaceutical composition of phenylisoxazolyl methylene-naphthalene-ether derivativesPublication Number: EP-4073071-A1Priority Date: 2019-12-03
- Compounds for modulating activity of fxr and uses thereofPublication Number: WO-2021108974-A1Priority Date: 2019-12-03
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References
////////danifexor, ANAX LAB, farnesoid X receptor agonist, TUU8G1CX9O, HEC 96719, ASC42
Dabogratinib
Dabogratinib
CAS 2800223-30-5
MF C25H24Cl2N6O3S, 559.5 g/mol
5-[(1R)-1-(3,5-dichloro-4-pyridinyl)ethoxy]-3-[6-(2-methylsulfonyl-2,6-diazaspiro[3.3]heptan-6-yl)-3-pyridinyl]-1H-indazole
(R)-5-(1-(3,5-Dichloropyridin-4-yl)ethoxy)-3-(6-(6-(methylsulfonyl)-2,6-diazaspiro[3.3]heptan-2-yl)pyridin-3-yl)-1H-indazole
[6-(5-{5-[(1R)-1-(3,5-dichloropyridin-4-yl)ethoxy]-1H-indazol-3-yl}pyridin-2-yl)-2,6-diazaspiro[3.3]heptan-2-yl](methyl)-λ6sulfanedioneTYRA-300
fibroblast growth factor receptor inhibitor, antineoplastic, TYRA-300, TYRA 300, A1AV2, FH245S2JZJ
Dabogratinib (TYRA-300) is an orally active, highly selective inhibitor of fibroblast growth factor receptor 3 (FGFR3), designed to treat cancers with FGFR3 alterations and genetic diseases like achondroplasia. It shows potent tumor growth inhibition in preclinical studies and early phase I/II (SURF301) clinical activity against advanced bladder cancer and metastatic urothelial carcinoma.
Key Aspects of Dabogratinib (TYRA-300)
- Mechanism: It acts as a selective inhibitor of FGFR3 with a high selectivity over other isoforms (FGFR1/2/4), which helps minimize toxicity.
- Target Indications: It is being developed for FGFR3-mutant cancers, including non-muscle invasive bladder cancer (NMIBC) and metastatic urothelial carcinoma, as well as pediatric achondroplasia.
- Preclinical Performance: Studies showed that it reduces tumor growth and drives tumor regression, especially in xenograft models with FGFR3-activating mutations (e.g., S249C).
- Clinical Trials:
- SURF301 (Phase I/II): Ongoing study, Tyra Biosciences reported early efficacy in patients with advanced metastatic urothelial carcinoma (mUC) harboring FGFR3 mutations/fusions.
- SURF302 (Phase II): Evaluating the drug in patients with FGFR3-altered, low-grade, intermediate-risk non–muscle invasive bladder cancer (NMIBC).
- BEACH301 (Phase II): Studying the drug in children with achondroplasia, as it is designed to increase long-bone growth.
- Properties: It is an orally bioavailable molecule with an IC50 of
for FGFR3.
Dabogratinib is an orally bioavailable, selective inhibitor of human fibroblast growth factor receptor 3 (FGFR3), with potential antineoplastic activity. Upon oral administration, dabogratinib specifically targets and binds to certain FGFR3 activating gene alterations, and specifically the gatekeeper mutants V555L/M. This blocks FGFR3-mediated signaling and leads to an inhibition of tumor cell proliferation in FGFR3-overexpressing cells. FGFR3, a receptor tyrosine kinase, is involved in angiogenesis and in the proliferation, differentiation, and survival of tumor cells. FGFR3 expression is associated with poor prognosis. It is overexpressed by certain tumor cell types.
- Efficacy and Safety of TYRA-300 in Participants With FGFR3 Altered Low Grade, Intermediate Risk Non-Muscle Invasive Bladder CancerCTID: NCT06995677Phase: Phase 2Status: RecruitingDate: 2026-04-09
- A Study of TYRA-300 in Children With Achondroplasia: BEACH301CTID: NCT06842355Phase: Phase 2Status: RecruitingDate: 2026-03-06
- Safety and Preliminary Anti-Tumor Activity of TYRA-300 in Advanced Urothelial Carcinoma and Other Solid Tumors With FGFR3 Gene AlterationsCTID: NCT05544552Phase: Phase 1/Phase 2Status: Active, not recruitingDate: 2026-01-12
PAT
Example 46. 5-[(1R)-1-(3,5-dichloro-4-pyridyl)ethoxy]-3-[6-(2-methylsulfonyl-2,6-diazaspiro[3.3]heptan-6-yl)-3-pyridyl]-1H-indazole
(5-[(1R)-1-(3,5-dichloro-4-pyridyl)ethoxy]-3-[6-(2-methylsulfonyl-2,6-diazaspiro[3.3]heptan-6-yl)-3-pyridyl]-1H-indazole. Triethylamine (20.5 uL, 0.148 mmol, 1.2 equiv) and methylsulfonyl chloride (9.5 uL, 0.123 mmol, 1.0 equiv) were sequentially added at room temperature to a solution of example 45 (59.0 mg, 0.123 mmol, 1 equiv) in anhydrous THE (3 mL). After stirring for 2 hours, the reaction mixture was concentrated under reduced pressure and diluted with saturated brine (30 mL) and dichloromethane (30 mL). The layers were separated. The organic layer was dried over sodium sulfate, filtered and concentrated under reduced pressure on to Celite (1 g). The product was purified on an Interchim automated chromatography system (RediSep Rf Gold HP C18, 15.5 g cartridge), eluting with a gradient of 0 to 100% acetonitrile in water. The fractions containing product were collected and lyophilized to give a white solid (45.0 mg, 65% yield). Analysis: LCMS: m/z=559.2 (M+H); 1H NMR (400 MHz, DMSO-d6) δ 13.02 (br s, 1H), 8.59 (s, 2H), 8.52 (dd, J=0.6, 2.2 Hz, 1H), 7.87 (dd, J=2.4, 8.6 Hz, 1H), 7.46 (d, J=8.9 Hz, 1H), 7.16 (d, J=2.1 Hz, 1H), 7.09 (dd, J=2.3, 9.0 Hz, 1H), 6.54 (dd, J=0.4, 8.6 Hz, 1H), 6.10 (q, J=6.6 Hz, 1H), 4.17 (s, 4H), 4.12 (s, 4H), 3.03 (s, 3H), 1.76 (d, J=6.6 Hz, 3H).
PAT
- Indazole compoundsPublication Number: TW-202241906-APriority Date: 2020-12-30
- Indazole compounds as kinase inhibitorsPublication Number: EP-4271673-A1Priority Date: 2020-12-30
- Indazole compounds as kinase inhibitorsPublication Number: WO-2022147246-A1Priority Date: 2020-12-30
- Indazole compounds as kinase inhibitorsPublication Number: US-12264149-B2Priority Date: 2020-12-30Grant Date: 2025-04-01
- Polymorphic compounds and uses thereofPublication Number: EP-4547670-A1Priority Date: 2022-06-29
- Indazole compounds as kinase inhibitorsPublication Number: US-12071428-B2Priority Date: 2020-12-30Grant Date: 2024-08-27
- Indazole Compounds as Kinase InhibitorsPublication Number: KR-20230152654-APriority Date: 2020-12-30
- Indazole compounds as kinase inhibitorsPublication Number: US-2024109865-A1Priority Date: 2020-12-30
- Indazole compounds as kinase inhibitorsPublication Number: US-2024208941-A1Priority Date: 2020-12-30
- Tyra-300 (5-[(1r)-1-(3,5-dichloro-4-pyridyl)ethoxy]-3-[6-(2-methylsulfonyl-2,6-diazaspiro[3.3]heptan-6-yl)-3-pyridyl]-1h-indazole ) in combination with a pd-1 or pd-l1 antagonist for use in the treatment of cancerPublication Number: WO-2025064744-A1Priority Date: 2023-09-22
- Fgfr inhibitors and methods of use thereofPublication Number: WO-2025061029-A1Priority Date: 2023-09-18
- Polymorphic compounds and uses thereofPublication Number: AU-2023300357-A1Priority Date: 2022-06-29
- Polymorphic compounds and uses thereofPublication Number: WO-2024006883-A1Priority Date: 2022-06-29
- Polymorphic compounds and uses thereofPublication Number: TW-202408493-APriority Date: 2022-06-29
ADVT
ANAX LABORATORIES
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References
Publication Name: Journal of Medicinal Chemistry
Publication Date: 2024-09-11
PMID: 39258897
DOI: 10.1021/acs.jmedchem.4c01531
////////dabogratinib, anax lab, fibroblast growth factor receptor inhibitor, antineoplastic, TYRA-300, TYRA 300, A1AV2, FH245S2JZJ
Colfosceril miristate
Colfosceril miristate
CAS 18194-24-6
MF C36H72NO8P MW677.9325
1,2 Dimyristoyl glycero 3 phosphorylcholine
(2R)-2,3-bis(tetradecanoyloxy)propyl 2-(trimethylazaniumyl)ethyl phosphate
surfactant replacement, DIMYRISTOYL LECITHIN, Dimyristoyllecithin, DMCP, DMPC
Colfosceril miristate (1,2-dimyristoyl-sn-glycero-3-phosphocholine or DMPC) is a synthetic phospholipid commonly used in research to study lipid bilayers, liposomes, and drug delivery systems. It serves as a model membrane system due to its phase transition properties and has shown potential in enhancing nanoparticle uptake and acting as a drug stabilizer.
Key Aspects of Colfosceril Miristate (DMPC):
- Scientific Application: Primarily used in laboratory research for studying lipid monolayers and bilayers.
- Drug Delivery: Employed in the creation of liposomes for drug delivery applications.
- Biological Activity: Exhibits antiproliferative effects on various tumor cell lines and can increase the cellular uptake of nanoparticles.
- Characteristics: It is a synthetic phospholipid, frequently studied for its phase transition temperature (approx.
).
- Storage: Should be stored at
or
to maintain stability.
Important Distinction:
It is crucial not to confuse Colfosceril miristate (DMPC) with Colfosceril palmitate (DPPC). Colfosceril palmitate is a different synthetic surfactant historically used in medicine to treat neonatal respiratory distress syndrome
1,2-DIMYRISTOYL-SN-GLYCERO-3-PHOSPHOCHOLINE (dimyristoyl phosphatidylcholine, DMPC) is a synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes. DMPC is a frequently studied artificial lipid because it undergoes a phase transition at a convenient temperature. Upon cooling below 23.6°C it undergoes a transition from the liquid crystalline phase to the solid rippled phase, characterized by periodic corrugations of the bilayer.
Dimyristoylphosphatidylcholine is a phosphatidylcholine, a kind of phospholipid. Along with other lipids, it can be used to prepare liposomes.[1]
PAT
PAT
Compositions of Phosphorylated Tau Peptides and Uses Thereof
Publication Number: US-2025326806-A1
- Antigen Binding Polypeptides, Polypeptide Complexes and Methods of Use ThereofPublication Number: US-2025326823-A1
- Variant rna-guided cas12f4 nucleases and dna binding proteinsPublication Number: US-2025327095-A1
- Modulation of novel immune checkpoint targetsPublication Number: US-12447213-B2Grant Date: 2025-10-21
- Therapeutic peptidesPublication Number: US-12448425-B2Grant Date: 2025-10-21
- Cytokine conjugates for the treatment of proliferative and infectious diseasesPublication Number: US-2025325632-A1
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| Names | |
|---|---|
| Systematic IUPAC name(2R)-2,3-Bis(tetradecanoyloxy)propyl 2-(trimethylazaniumyl)ethyl phosphate | |
| Other names1,2-dimyristoylphosphatidylcholine, 1,2-dimyristoyl-sn-glycero-3-phosphocholine, 1,2-ditetradecanoyl-sn-glycero-3-phosphocholine, DMPC, 14:0 PC | |
| Identifiers | |
| CAS Number | 18194-24-6 |
| 3D model (JSmol) | Interactive image |
| ChEBI | CHEBI:45240 |
| ChEMBL | ChEMBL1235508 |
| ChemSpider | 4573168 |
| ECHA InfoCard | 100.038.245 |
| EC Number | 242-085-9 |
| PubChem CID | 5459377 |
| UNII | 52QK2NZ2T0 |
| CompTox Dashboard (EPA) | DTXSID00860227 |
| InChI | |
| SMILES | |
| Properties | |
| Chemical formula | C36H72NO8P |
| Molar mass | 677.945 g·mol−1 |
| Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).Infobox references | |
References
- Liposomal drug delivery system from laboratory to clinic, N. A. Kshirsagar, S. K. Pandya, G. B. Kirodian, S. Sanath, Journal of Postgraduate Medicine, 51 (#5) (2005), pp. 5-15, PMID 16519249.
//////////colfosceril miristate, ANAX LAB, surfactant replacement, DIMYRISTOYL LECITHIN, Dimyristoyllecithin, DMCP, DMPC
Claturafenib
Claturafenib
CAS 2754408-94-9
MF C18H15Cl2F2N5O3S MW490.3 g/mol
N-[2-chloro-3-[(5-chloro-3-methyl-4-oxoquinazolin-6-yl)amino]-4-fluorophenyl]-3-fluoroazetidine-1-sulfonamide
N-{2-chloro-3-[(5-chloro-3-methyl-4-oxo-3,4-dihydroquinazolin-6-yl)amino]-4-fluorophenyl}-3-fluoroazetidine-1-sulfonamide
B-Raf (BRAF) inhibitor, antineoplastic, PF-07799933, PF 07799933, ARRY440, ARRY 440, PC35M52J8T
Claturafenib (development code PF-07799933) is an investigational cancer drug currently being developed by Pfizer. It is a selective, orally active pan-mutant BRAF inhibitor designed to treat advanced solid tumours with specific genetic alterations
Mechanism of Action
Claturafenib belongs to a class of drugs that target the MAPK/ERK signaling pathway, which is often hijacked by cancer cells to promote uncontrolled growth.
- Pan-Mutant Inhibition: Unlike first-generation BRAF inhibitors, claturafenib inhibits multiple classes of BRAF mutations, including Class 1 (V600), Class 2, and Class 3 alterations.
- Brain-Penetrant: It is designed to cross the blood-brain barrier, allowing it to potentially treat brain metastases or primary brain tumours.
- Dimer Disruption: It works by disrupting the formation of BRAF-containing dimers, which are responsible for signaling in many resistant or non-V600 mutant cancers.
- Selectivity: It is highly selective for mutant BRAF, significantly sparing normal (wild-type) cells to reduce off-target side effects.
🏥 Clinical Status
As of April 2026, claturafenib is in Phase 1 clinical trials.
- Target Indications: Advanced solid malignancies, including melanoma, colorectal cancer (CRC), and non-small cell lung cancer (NSCLC).
- Combination Therapy: It is being studied both as a single agent (monotherapy) and in combination with other drugs like binimetinib (a MEK inhibitor) or cetuximab (an EGFR inhibitor).
- Ongoing Study: Clinical trial NCT05355701 is currently evaluating its safety, dosage, and efficacy in patients whose disease has progressed on other treatments.
- A Study to Learn About the Study Medicine Called PF-07799933 in People With Advanced Solid Tumors With BRAF Alterations.CTID: NCT05355701Phase: Phase 1Status: RecruitingDate: 2026-03-27
- A Study to Learn About the Study Medicine Called PF-07799544 as Monotherapy or in Combination in People With Advanced Solid TumorsCTID: NCT05538130Phase: Phase 1Status: RecruitingDate: 2026-03-27
Claturafenib is an orally bioavailable class 1 and 2 inhibitor of the serine/threonine-protein kinase B-raf (BRAF) protein, with potential antineoplastic activity. Upon oral administration, claturafenib selectively binds to and inhibits the activity of class 1 and 2 BRAF alterations. This inhibits the proliferation of tumor cells which express these BRAF alterations. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) signaling pathways, which may be constitutively activated due to BRAF gene mutations. Mutated forms and fusions of BRAF are associated with a number of neoplastic diseases.
| Property | Value |
|---|---|
| Molecular Formula |        |
| Molecular Weight | 490.31 g/mol |
| CAS Number | 2754408-94-9 |
| Other Names | ARRY-440, PF07799933 |
📍 Note: Claturafenib is an investigational compound and has not yet been approved by the FDA or other regulatory agencies for general use
SYN
SYN
Example 126
N-(2-chloro-3-((5-chloro-3-methyl-4-oxo-3,4-dihydroquinazolin-6-yl)amino)-4-fluorophenyl)-3-fluoroazetidine-1-sulfonamide
PAT
- 4-oxo-3,4-dihydroquinazolinon compounds for the treatment of braf-associated diseases and disordersPublication Number: CA-3186343-A1Priority Date: 2020-06-09
- Compounds for the treatment of BRAF-associated diseases and disordersPublication Number: US-12303509-B2Priority Date: 2020-06-09Grant Date: 2025-05-20
- 3,4-dihydro-2,7-naphthyridine-1,6(2H,7H)-dione compound as MEK inhibitorPublication Number: CN-117561255-APriority Date: 2021-03-31
- 4-oxo-3,4-dihydroquinazolinone compounds for the treatment of BRAF-related diseases and disordersPublication Number: KR-20230019944-APriority Date: 2020-06-09
- Compounds for the treatment of braf-associated diseases and disordersPublication Number: US-2022288074-A1Priority Date: 2020-06-09
- 4-oxo-3, 4-dihydroquinazolinone compounds for the treatment of BRAF related diseases and disordersPublication Number: CN-116096710-APriority Date: 2020-06-09
- 4-oxo-3,4-dihydroquinazolinon compounds for the treatment of braf-associated diseases and disordersPublication Number: EP-4161907-A1Priority Date: 2020-06-09
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References
////////claturafenib, ANAX, B-Raf (BRAF) inhibitor, antineoplastic, PF-07799933, PF 07799933, ARRY440, ARRY 440, PC35M52J8T
Cirtociclib
Cirtociclib
CAS 2888704-84-3
MF C15H17F2N7O2 MW365.34 g/mol
N-[3-(difluoromethoxy)-1H-pyrazol-5-yl]-1-(oxan-4-ylmethyl)pyrazolo[3,4-b]pyrazin-6-amine
N-[5-(difluoromethoxy)-1H-pyrazol-3-yl]-1-[(oxan-4-yl)methyl]-1H-pyrazolo[3,4-b]pyrazin-6-amine
cyclin-dependent kinase inhibitor, antineoplastic, BLU-222, BLU 222, BLU 170298, U93X72ED47, CDK2 Inhibitor BLU-222
Cirtociclib (also known as BLU-222) is an investigational drug that acts as a highly selective inhibitor of cyclin-dependent kinase 2 (CDK2). It is being developed by Blueprint Therapeutics for the treatment of advanced solid tumours, particularly those with genetic drivers like CCNE1 amplification, which are common in certain ovarian and breast cancers
Certociclib is a small molecule drug. Certociclib is under investigation in clinical trial NCT05252416 ((VELA) Study of BLU-222 in Advanced Solid Tumors). Certociclib has a monoisotopic molecular weight of 365.14 Da.
Certociclib is an orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon administration, certociclib selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDK2, a serine/threonine kinase that plays an important role in the regulation of cell cycle progression and cellular proliferation, is overexpressed in certain tumor cells.
How It Works
- Targeting CDK2: It binds to CDK2, a protein that regulates the cell cycle.
- Cell Cycle Arrest: By inhibiting CDK2, the drug causes G1 arrest, preventing cancer cells from replicating.
- Selectivity: It is designed to be “best-in-class” for its high selectivity for CDK2 over other kinases like CDK1, CDK4, or CDK6.
Therapeutic Potential
- Ovarian Cancer: Specifically targets high-grade serous ovarian cancer where CCNE1 is amplified.
- Breast Cancer: Shows promise in treating hormone receptor-positive/HER2-negative (HR+/HER2-) breast cancer, especially when the cancer has become resistant to existing CDK4/6 inhibitors.
- Combination Therapy: Researchers are testing it alongside other drugs, such as palbociclib, ribociclib, or chemotherapy agents like carboplatin, to enhance efficacy.
Current Status
- Clinical Trials: It is currently being evaluated in a Phase 1/2 clinical trial known as the VELA study (NCT05252416) for patients with advanced solid tumours.
- Research Status: It is not yet approved for general medical use and is primarily available for research and clinical trial participants.
(VELA) Study of BLU-222 in Advanced Solid Tumors
CTID: NCT05252416
Phase: Phase 1
Status: Terminated
Date: 2025-11-28
🌟 Key Point: Cirtociclib represents a new generation of precision medicine aimed at overcoming resistance to standard cancer therapies by specifically targeting the CDK2 pathway
PAT
The structure of one CDK2 inhibitor, referred to herein as “a compound of formula (I)” or N-(5-(difluoromethoxy)-lH-pyrazol-3-yl)-l-((tetrahydro-2H-pyran-4-yl)methyl)-lH-pyrazolo[3,4-b]pyrazin-6-amine is shown below:
PAT
Example 2
N-(5-(difluoromethoxy)-1H-pyrazol-3-yl)-1-((tetrahydro-2H-pyran-4-yl)methyl)-1H-pyrazolo[3,4-b]pyrazin-6-amine
A mixture of 6-chloro-1-((tetrahydro-2H-pyran-4-yl)methyl)-1H-pyrazolo[3,4-b]pyrazine (Preparation 87, 780 mg, 3.09 mmol), 5-(difluoromethoxy)-1H-pyrazol-3-amine (554 mg, 3.72 mmol), tBuXphos Pd G3 (150 mg, 0.19 mmol) and KOAc (892 mg, 9.08 mmol) in dioxane (15 mL) was stirred at 90° C. for 6 h under N 2. The reaction mixture was evaporated to dryness in vacuo and the residue was purified by prep-HPLC-4 to afford the title compound as a white solid (361.4 mg, 32%). LCMS m/z=366 [M+H] +; 1H NMR (400 MHz, DMSO-d 6) δ: 12.21 (s, 1H), 10.82 (s, 1H), 8.19 (s, 1H), 8.17 (s, 1H), 7.32 (t, 1H), 5.98 (d, 1H), 4.40 (d, 2H), 3.87-3.75 (m, 2H), 3.29-3.16 (m, 2H), 2.24-2.11 (m, 1H), 1.46-1.29 (m, 4H).
PAT
- The cdk2 inhibitor blu-222 for treatment of cancerPublication Number: WO-2024168298-A1Priority Date: 2023-02-10
- Solid forms of a cdk2 inhibitorPublication Number: WO-2024148083-A1Priority Date: 2023-01-04
- Cdk2 inhibitorsPublication Number: US-2023322791-A1Priority Date: 2021-06-28
- Cdk2 inhibitorsPublication Number: US-2023159535-A1Priority Date: 2021-06-28
- CDK2 inhibitorsPublication Number: US-11970498-B2Priority Date: 2021-06-28Grant Date: 2024-04-30
- Cdk2 inhibitorsPublication Number: US-2024383902-A1Priority Date: 2021-06-28
- CDK2 inhibitorsPublication Number: US-11932648-B2Priority Date: 2021-06-28Grant Date: 2024-03-19
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References
/////////cirtociclib, cyclin-dependent kinase inhibitor, antineoplastic, BLU-222, BLU 222, BLU 170298, U93X72ED47, CDK2 Inhibitor BLU-222
Ceperognastat
Ceperognastat
CAS 2241514-56-5
MF C16H22FN5O3S MW383.4 g/mol
Acetamide, N-(4-fluoro-5-(((2S,4S)-2-methyl-4-((5-methyl-1,2,4-oxadiazol-3-yl)methoxy)-1-piperidinyl)methyl)-2-thiazolyl)-
N-[4-fluoro-5-({(2S,4S)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]piperidin-1-yl}methyl)-1,3-thiazol-2-yl]acetamide
O-GlcNAcase (OGA) enzyme inhibitor, LY3372689, LY3372689, U0SGP6ZX2V
Ceperognastat (LY3372689) is a drug candidate molecule under investigation to treat Alzheimer’s disease. It targets the enzyme O-GlcNAcase.[2][3] Its result is to reduce formation of tau protein tangles.
A molecule containing radioactive fluorine was used with a PET scan to show that ceperognastat binds in the human brain.[4]
Ceperognastat was discovered via a high-throughput screening campaign followed by further optimization.[5]
Eli Lilly and Company is recruiting subjects for a clinical trial.[6] Some hospitals in Australia: St Vincent’s Hospital, Sydney Hornsby Ku-Ring-Gai Hospital, The Prince Charles Hospital, The Queen Elizabeth Hospital, Adelaide, Box Hill Hospital, and Delmont Private Hospital are involved.[7] Results of the trial were expected by June 2024.[8] Primary completion of the study occurred on 9th July 2024, with full completion expected in August 2024. In an investor call, it was disclosed that ceperognastat missed the primary endpoint of improvement on the Integrated Alzheimer’s Disease Rating Scale. The detailed results of this study are expected to be disclosed at a conference in late 2024.[9]
Chemical
The molecule contains three rings: thiazole, piperidine and oxadiazole. Other functional groups included are an ether, acetamide, and a fluoride.[10]
- A Study of LY3372689 to Assess the Safety, Tolerability, and Efficacy in Participants With Alzheimer’s DiseaseCTID: NCT05063539Phase: Phase 2Status: CompletedDate: 2025-07-28
- A Study of the Effects of Multiple Doses of LY3372689 on the Brain in Healthy ParticipantsCTID: NCT04392271Phase: Phase 1Status: CompletedDate: 2020-11-04
- A Safety Study of LY3372689 in Healthy ParticipantsCTID: NCT04106206Phase: Phase 1Status: CompletedDate: 2020-04-24
- A Study of the Effects of LY3372689 on the Brain in Healthy ParticipantsCTID: NCT03944031Phase: Phase 1Status: CompletedDate: 2020-04-22
- A Safety Study of LY3372689 Given By Mouth to Healthy ParticipantsCTID: NCT03819270Phase: Phase 1Status: CompletedDate: 2019-07-05
REF
- Discovery and clinical translation of ceperognastat, an O‐GlcNAcase (OGA) inhibitor, for the treatment of Alzheimer’s diseasePublication Name: Alzheimer’s & Dementia: Translational Research & Clinical InterventionsPublication Date: 2024-10PMCID: PMC11694536PMID: 39748851DOI: 10.1002/trc2.70020
- Discovery of 4-(Arylethynyl)piperidine Derivatives as Potent Nonsaccharide O-GlcNAcase Inhibitors for the Treatment of Alzheimer’s DiseasePublication Name: Journal of Medicinal ChemistryPublication Date: 2024-08-07PMID: 39109492DOI: 10.1021/acs.jmedchem.4c01132
SYN
EXAMPLE 1
Synthesis of N-[4-fluoro-5-[[(2S,5S)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]-1-piperidyl]methyl]thiazol-2-yl]acetamide
PAT
- N-[4-fluoro-5-[[(2s,4s)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]-1-piperidyl]methyl]thiazol-2-yl]acetamide as oga inhibitorPublication Number: EP-3573983-B1Priority Date: 2017-01-27Grant Date: 2021-04-21
- N-[4-fluoro-5-[[(2s,4s)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]-1-piperidyl]methyl]thiazol-2-yl]acetamide as oga inhibitorPublication Number: NZ-754849-APriority Date: 2017-01-27
- N- [4-Fluoro-5-[[(2S, 4S) -2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl) methoxy] as OGA inhibitor -1-piperidyl] methyl] thiazol-2-yl] acetamidePublication Number: JP-2020504142-APriority Date: 2017-01-27
- N-[4-fluoro-5-[[(2S,4S)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]-1-piperidyl]methyl] Thiazol-2-yl]acetamide as an inhibitor of OGAPublication Number: IL-267693-APriority Date: 2017-01-27
- Acetamide N-[4-fluor-5-]](4S,2S)-2-methyl-4-](5-methyl-1,2,4-oxadiazole-3-yl)methoxy[-1-piperdyl[methyl] [Thiazole-2-yl] as an OGA inhibitorPublication Number: JO-P20190182-A1Priority Date: 2017-01-27
- N-[4-FLUORO-5-[[(2S,4S)-2-METHYL-4-[(5-METHYL-1,2,4-OXADIAZOLE-3-IL)METHOXI]-1-PIPERIDIL]METHYL]THIAZOLE-2-IL] ACETAMIDE AS AN OGA INHIBITOR.Publication Number: MX-387166-BPriority Date: 2017-01-27
- N-[4-fluoro-5-[[(2s,4s)-2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]-1-piperidyl]methyl]thiazol-2-yl]acetamide as oga inhibitorPublication Number: MY-197494-APriority Date: 2017-01-27
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References
References
- “Data Sheet LY3372689” (PDF). 26 December 2024. Retrieved 4 February 2025.
- “LY3372689”. http://www.alzforum.org.
- Cheng, Steven S.; Mody, Alison C.; Woo, Christina M. (2024-11-07). “Opportunities for Therapeutic Modulation of O-GlcNAc”. Chemical Reviews. 124 (22): 12918–13019. doi:10.1021/acs.chemrev.4c00417. ISSN 0009-2665. PMID 39509538.
- Shcherbinin, Sergey; Kielbasa, William; Dubois, Susan; Lowe, Stephen L; Phipps, Krista M; Tseng, James; Kevin, Donnelly B; Natanegara, Fanni; Warner, Susan; Dreyfus, Nicolas; Lindsay-Scott, Peter; Hawk, Mai Khanh; McDonald, Nicholas; Zhang, Xiaoyu; Gilmore, Julie A; Biglan, Kevin; Mergott, Dustin J; Russell, David; Gunn, Roger N; Constantinescu, Cristian; Nuthall, Hugh Norman; Collins, Emily C (December 2020). “Brain target occupancy of LY3372689, an inhibitor of the O-GlcNAcase (OGA) enzyme: Translation from rat to human: Neuroimaging / evaluating treatments”. Alzheimer’s & Dementia. 16 (S4). doi:10.1002/alz.040558. S2CID 227501893.
- Kielbasa, William; Goldsmith, Paul; Donnelly, Kevin B.; Nuthall, Hugh N.; Shcherbinin, Sergey; Fleisher, Adam S.; Hendle, Jörg; DuBois, Susan L.; Lowe, Stephen L.; Zhang, Feiyu Fred; Woerly, Eric M.; Dreyfus, Nicolas J.-F.; Evans, David; Gilmore, Jeremy; Mancini, Michele (October 2024). “Discovery and clinical translation of ceperognastat, an O-GlcNAcase (OGA) inhibitor, for the treatment of Alzheimer’s disease”. Alzheimer’s & Dementia: Translational Research & Clinical Interventions. 10 (4) e70020. doi:10.1002/trc2.70020. ISSN 2352-8737. PMC 11694536. PMID 39748851.
- “Assessment of Safety, Tolerability, and Efficacy of LY3372689 in Early Symptomatic Alzheimer’s Disease”. clinicaltrials.gov. 22 March 2022. Retrieved 31 March 2022.
- “A Study of LY3372689 to Assess the Safety, Tolerability, and Efficacy in Participants With Alzheimer’s Disease”. Retrieved 31 March 2022.
- Krietsch Boerner, Leigh (25 March 2022). “Hybrid meeting divulges structures of drug candidates”. Chemical & Engineering News. ISSN 0009-2347.
- edge.media-server.com https://edge.media-server.com/mmc/p/3kqnwjy6/. Retrieved 2024-10-06.
{{cite web}}: Missing or empty|title=(help) - Dreyfus, Nicolas Jacques Francois; Lindsay-Scott, Peter James (2 August 2018). “N-[4-Fluoro-5-[[(2S,4S)-2-Methyl-4-[(5-Methyl-1,2,4-Oxadiazol-3-Yl)methoxy]-1-Piperidyl]methyl]thiazol-2-Yl]acetamide as Oga Inhibitor”. Retrieved 31 March 2022.
| Names | |
|---|---|
| IUPAC nameN-[4-fluoro-5-[[2-methyl-4-[(5-methyl-1,2,4-oxadiazol-3-yl)methoxy]piperidin-1-yl]methyl]-1,3-thiazol-2-yl]acetamide | |
| Identifiers | |
| CAS Number | 2241514-56-5 [1] |
| 3D model (JSmol) | Interactive image |
| ChemSpider | 129432852 |
| PubChem CID | 135271363 |
| InChI | |
| SMILES | |
| Properties | |
| Chemical formula | C16H22FN5O3S |
| Molar mass | 383.44 g·mol−1 |
| Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).Infobox references | |
/////////ceperognastat, O-GlcNAcase (OGA) enzyme inhibitor, LY3372689, LY3372689, U0SGP6ZX2V
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