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ORGANIC SPECTROSCOPY

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DR ANTHONY MELVIN CRASTO Ph.D

DR ANTHONY MELVIN CRASTO Ph.D

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

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Enzomenib


Enzomenib

CAS 2412555-70-3

MF C33H43FN6O3 MW 590.7 g/mol

5-fluoro-2-[4-[7-[(1S,3S,4R)-5-methylidene-2-azabicyclo[2.2.2]octane-3-carbonyl]-2,7-diazaspiro[3.5]nonan-2-yl]pyrimidin-5-yl]oxy-N,N-di(propan-2-yl)benzamide

5-fluoro-2-[(4-{7-[(1S,3S,4R)-5-methylidene-2-azabicyclo[2.2.2]octane-3-carbonyl]-2,7-
diazaspiro[3.5]nonan-2-yl}pyrimidin-5-yl)oxy]-N,Ndi(propan-2-yl)benzamide
menin-MLL (mixed-lineage leukemia) protein, interaction inhibitor, antineoplastic, DSP-5336, Fast Track,  Orphan Drug designations

Enzomenib is an investigational new drug that is being evaluated for the treatment of acute leukemia.[1] It is a small molecule inhibitor that targets the interaction between menin and mixed-lineage leukemia (MLL) proteins.[2] Enzomenib particularly in patients with KMT2A (MLL) rearrangements or NPM1 mutations.[3]

The U.S. Food and Drug Administration (FDA) has granted both Fast Track and Orphan Drug designations to Enzomenib.[4]

Enzomenib is an orally bioavailable, small molecule inhibitor of menin, with potential antineoplastic activity. Upon oral administration, enzomenib targets and binds to the nuclear protein menin, thereby preventing the interaction between the two proteins menin and menin-mixed lineage leukemia (MLL; myeloid/lymphoid leukemia; KMT2A) and the formation of the menin-MLL complex. This reduces the expression of downstream target genes and results in an inhibition of the proliferation of MLL-rearranged leukemic cells. The menin-MLL complex plays a key role in the survival, growth, transformation and proliferation of certain kinds of leukemia cells.

PAT

US10815241, Example 6

https://patentscope.wipo.int/search/en/detail.jsf?docId=US295244745&_cid=P21-MGISYZ-31333-1

Example 3 to 19

      The following compounds of Examples 3 to 19 were prepared according to a similar method to Example 1 by using each corresponding starting compound.
      

PAT

Optically active azabicyclo derivatives

Publication Number: JP-7614262-B2

Priority Date: 2018-08-27

Grant Date: 2025-01-15

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References

  1.  “Enzomenib – Sumitomo Pharma”. AdisInsight. Springer Nature Switzerland AG.
  2.  Dempke WC, Desole M, Chiusolo P, Sica S, Schmidt-Hieber M (September 2023). “Targeting the undruggable: menin inhibitors ante portas”. Journal of Cancer Research and Clinical Oncology. 149 (11): 9451–9459. doi:10.1007/s00432-023-04752-9. PMC 11798168. PMID 37103568.
  3.  “Sumitomo Pharma Presents New Clinical Data on DSP-5336 at the European Hematology Association 2024 Congress”. Sumitomo Pharma Co., Ltd. 14 June 2024.
  4.  Flaherty C (15 July 2024). “FDA Grants Fast Track Designation to DSP-5336 in KMT2A/NMP1+ AML”. OncLive.
Clinical data
Other namesDSP-5336
Identifiers
IUPAC name
CAS Number2412555-70-3
PubChem CID146430058
DrugBankDB18514
ChemSpider129534736
UNIIVW83Y2JLZ5
ChEMBLChEMBL5314915
Chemical and physical data
FormulaC33H43FN6O3
Molar mass590.744 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

//////////enzomenib, Interaction inhibitor, antineoplastic, DSP 5336, Fast Track,  Orphan Drug designations

Dapolsertib


Dapolsertib

CAS 1616359-00-2

MF C15H18Br2N4O MW 446.14 g/mol

5,6-dibromo-4-nitro-2-piperidin-4-yl-1-propan-2-ylbenzimidazole

5,6-dibromo-4-nitro-2-(piperidin-4-yl)-1-(propan-2-yl)-1H-1,3-benzimidazole
serine/ threonine kinase inhibitor, antineoplastic

Ryvu Therapeutics SA, MEN1703, SEL24-B489

  • SEL24-B489
  • SEL-24 free base
  • 9M7X64VTLI
  • SEL-24

Dapolsertib is an investigational new drug that is being evaluated for the treatment of cancer. It is dual inhibitor of PIM family of serine/threonine protein kinases and mutant forms of FMS-related tyrosine kinase 3 (FLT3) that is being developed by Ryvu Therapeutics SA.[1]

Dapolsertib is an orally available inhibitor of PIM family serine/threonine protein kinases and mutant forms of FMS-related tyrosine kinase 3 (FLT3; STK1) with potential antineoplastic activity. Upon oral administration, dapolsertib binds to and inhibits the kinase activities of PIM-1, -2 and -3, and mutant forms of FLT3, which may result in the interruption of the G1/S phase cell cycle transition, an inhibition of cell proliferation, and an induction of apoptosis in tumor cells that overexpress PIMs or express mutant forms of FLT3. FLT3, a tyrosine kinase receptor that is overexpressed or mutated in various cancers, plays a role in signaling pathways that regulate hematopoietic progenitor cell proliferation, and in leukemic cell proliferation and survival. PIM kinases, downstream effectors of many cytokine and growth factor signaling pathways, including the FLT3 signaling pathway, play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.

  • MEN1703 (SEL24) in Participants With Acute Myeloid LeukemiaCTID: NCT03008187Phase: Phase 1/Phase 2Status: CompletedDate: 2025-04-29
  • MEN1703 (SEL24) to Treat Relapsed or Refractory Aggressive B-cell Non-Hodgkin Lymphoma (JASPIS-01)CTID: NCT06534437Phase: Phase 2Status: RecruitingDate: 2025-04-11

PAT

WO2014096388

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014096388&_cid=P12-MG5YKY-59978-1

3.9. Compounds of Example 26:

3.9. Compounds of Example 26:

5,6-dibromo-4-nitro-2-(piperidin-4-yl)-1-(propan-2-yl)-1H-1,3-benzodiazole (Example 26A):

4,5-dibromo-1-N-(propan-2-yl)benzene-1,2-diamine (2,8g, 9,lmmol) and

isonipeconic acid (1,17g, 9,lmmol) were taken up in phosphoric acid (17,82g, 0,18mol). The resulting mixture was stirred at 180°C for 3,5 hours. The mixture was allowed to cool to RT and diluted with water to 200ml. The solution was basified to pH 14.0 using solid NaOH. The resulting precipitate was then filtered off and washed repeatedly with MeOH. The filtrate was concentrated in-vacuo. The product was purified on Al2O3 (basic) using DCM/MeOH/NH3 sat. in MEOH (25: 15: 1). The obtained product (8,7mmol, 3,9g) was dissolved in cone. H2SO4 (30ml). Next KNO3 (8,7mmol, 0,89g) was added in one portion at 0° C. The resulting mixture was stirred at 0°C for 3h and at RT overnight. Then the mixture was poured onto ice. The product was filtered and washed with water.The product was purified on on Al2O3 (basic) using DCM/MeOH/NH3 sat. in MEOH (25: 15: 1) to afford 5,6-dibromo-4- nitro-2-(piperidin-4-yl)-1-(propan-2-yl)-1H-1,3-benzodiazole (1,9g). 1H NMR (600 MHz, DMSO) δ 8.74 (bs, 1H), 8.48 (s, 1H), 8.35 (bs, 1H), 4.94 (hept, J = 6.8 Hz, 1H), 3.52 – 3.46 (m, 1H), 3.42 – 3.37 (m, 2H), 3.08 (bs, 2H), 2.07 – 1.96 (m, 4H), 1.60 (d, J = 6.9 Hz, 6H). m/z 446,8; rt 2,7min.

5,6-dibromo-4-nitro-2-(piperidin-4-yl)-1-(propan-2-yl)-1H-1,3-benzodiazole (Example 26A):

4,5-dibromo-1-N-(propan-2-yl)benzene-1,2-diamine (2,8g, 9,lmmol) and

isonipeconic acid (1,17g, 9,lmmol) were taken up in phosphoric acid (17,82g, 0,18mol). The resulting mixture was stirred at 180°C for 3,5 hours. The mixture was allowed to cool to RT and diluted with water to 200ml. The solution was basified to pH 14.0 using solid NaOH. The resulting precipitate was then filtered off and washed repeatedly with MeOH. The filtrate was concentrated in-vacuo. The product was purified on Al2O3 (basic) using DCM/MeOH/NH3 sat. in MEOH (25: 15: 1). The obtained product (8,7mmol, 3,9g) was dissolved in cone. H2SO4 (30ml). Next KNO3 (8,7mmol, 0,89g) was added in one portion at 0° C. The resulting mixture was stirred at 0°C for 3h and at RT overnight. Then the mixture was poured onto ice. The product was filtered and washed with water.The product was purified on on Al2O3 (basic) using DCM/MeOH/NH3 sat. in MEOH (25: 15: 1) to afford 5,6-dibromo-4- nitro-2-(piperidin-4-yl)-1-(propan-2-yl)-1H-1,3-benzodiazole (1,9g). 1H NMR (600 MHz, DMSO) δ 8.74 (bs, 1H), 8.48 (s, 1H), 8.35 (bs, 1H), 4.94 (hept, J = 6.8 Hz, 1H), 3.52 – 3.46 (m, 1H), 3.42 – 3.37 (m, 2H), 3.08 (bs, 2H), 2.07 – 1.96 (m, 4H), 1.60 (d, J = 6.9 Hz, 6H). m/z 446,8; rt 2,7min.

PAT

Novel benzimidazole derivatives as kinase inhibitors

Publication Number: WO-2014096388-A2

Priority Date: 2012-12-21

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Clinical data
Other namesMEN1703, SEL24-B489
Identifiers
IUPAC name
CAS Number1616359-00-2
PubChem CID76286825
IUPHAR/BPS13204
ChemSpider81367232
UNII9M7X64VTLI
ChEMBLChEMBL4467168
Chemical and physical data
FormulaC15H18Br2N4O2
Molar mass446.143 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

References

  1.  Wu M, Li C, Zhu X (December 2018). “FLT3 inhibitors in acute myeloid leukemia”. Journal of Hematology & Oncology. 11 (1) 133. doi:10.1186/s13045-018-0675-4. PMC 6280371. PMID 30514344.

//////////Dapolsertib, antineoplastic, MEN1703, SEL24-B489, MEN 1703, SEL24 B489, Ryvu Therapeutics SA

Crelosidenib


Crelosidenib

CAS 2230263-60-0

7-{[(1S)-1-(4-{(1S)-1-[4-(prop-2-enoyl)piperazin-1-yl]-2-cyclopropylethyl}phenyl)ethyl]amino}-1-ethyl-1,4-dihydro-2Hpyrimido[4,5-d][1,3]oxazin-2-one
isocitrate dehydrogenase 1 (IDH1) inhibitor, antineoplastic

MF C28H36N6O3 MW 504.6 g/mol

  • LY3410738
  • 7-[[(1S)-1-[4-[(1S)-2-cyclopropyl-1-(4-prop-2-enoylpiperazin-1-yl)ethyl]phenyl]ethyl]amino]-1-ethyl-4H-pyrimido[4,5-d][1,3]oxazin-2-one
  • 7-(((1S)-1-(4-((1S)-2-cyclopropyl-1-(4-prop-2-enoylpiperazin-1-yl)ethyl)phenyl)ethyl)amino)-1-ethyl-4H-pyrimido(4,5-d)(1,3)oxazin-2-one

Crelosidenib is an investigational new drug that is being evaluated for the treatment of cancer. It acts as a selective inhibitor of isocitrate dehydrogenase 1 (IDH1), an enzyme that plays a crucial role in cellular metabolism and is frequently mutated in various cancers, including cholangiocarcinoma.[1][2]

Crelosidenib is an orally available inhibitor of mutant form of the isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble), including the substitution mutation at arginine (R) in position 132, IDH1(R132), with potential antineoplastic activity. Upon oral administration, crelosidenib specifically and covalently binds to and modifies a single cysteine (Cys269) in the allosteric binding pocket of mutant forms of IDH1, thereby inactivating IDH1. This inhibits the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This depletes 2-HG levels, prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing mutant forms of IDH1. In addition, crelosidenib has the ability to cross the blood-brain barrier (BBB). IDH1 mutations, including IDH1(R132) mutations, are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.

Syn

example 2 [US11001596B2]

https://patentscope.wipo.int/search/en/detail.jsf?docId=US289829390&_cid=P12-MG4UBU-88518-1

PAT

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Clinical data
Other namesLY3410738
Identifiers
IUPAC name
CAS Number2230263-60-0
PubChem CID135125140
IUPHAR/BPS12340
ChemSpider115009279
UNIIA4DU555RMD
KEGGD12708
Chemical and physical data
FormulaC28H36N6O3
Molar mass504.635 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

References

  1.  Zarei M, Hue JJ, Hajihassani O, Graor HJ, Katayama ES, Loftus AW, et al. (February 2022). “Clinical development of IDH1 inhibitors for cancer therapy”. Cancer Treatment Reviews. 103 102334. doi:10.1016/j.ctrv.2021.102334. PMID 34974243.
  2.  Demir T, Moloney C, Mahalingam D (July 2024). “Emerging targeted therapies and strategies to overcome resistance in biliary tract cancers”. Critical Reviews in Oncology/Hematology. 199 104388. doi:10.1016/j.critrevonc.2024.104388. PMID 38754771.

.///////////Crelosidenib, Antineoplastic, cholangiocarcinoma, LY3410738, LY 3410738

Camibirstat


Camibirstat

CAS 2671128-05-3

N-{(2S)-1-[(4-{6-[(2R,6S)-2,6-dimethylmorpholin-4-yl]pyridin-2-yl}-1,3-thiazol-2-yl)amino]-3-methoxy-1-oxopropan-2-yl}-1-(methanesulfonyl)-1H-pyrrole-3-carboxamide
ATPase inhibitor, antineoplastic

MW C24H30N6O6S2 MF 562.7 g/mol

  • 1H-Pyrrole-3-carboxamide, N-((1S)-2-((4-(6-((2R,6S)-2,6-dimethyl-4-morpholinyl)-2-pyridinyl)-2-thiazolyl)amino)-1-(methoxymethyl)-2-oxoethyl)-1-(methylsulfonyl)-
  • N-[(2S)-1-[[4-[6-[(2S,6R)-2,6-dimethylmorpholin-4-yl]pyridin-2-yl]-1,3-thiazol-2-yl]amino]-3-methoxy-1-oxopropan-2-yl]-1-methylsulfonylpyrrole-3-carboxamide
  • FHD 286

Camibirstat is an investigational new drug that is being evaluated for the treatment of cancer. It is a small molecule that acts as a selective inhibitor of SMARCA2 and SMARCA4, which are key components of the SWI/SNF chromatin remodeling complex.[1]

It is being developed by Foghorn Therapeutics.[2]

Camibirstat is an orally bioavailable, allosteric, small molecule inhibitor of transcription activator BRG1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 4; SMARCA4) and BRM (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2; SMARCA2), with potential antineoplastic activity. Upon oral administration, camibirstat targets, binds to, and inhibits the activity of BRG1 and/or BRM, the primary ATPase components and mutually exclusive subunits of the BRG1/BRM-associated factor (BAF) complexes. This may lead to the inhibition of the SWI/SNF chromatin remodeling complex, disrupt chromatin remodeling and gene expression, and result in the downregulation of oncogenic pathways and the inhibition of tumor cell proliferation. BAF is an important regulator of transcriptional programs and gene expression. Mutations in BAF or its transcription factor partners are found in certain diseases including cancers.

PAT

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US331910582&_cid=P11-MG1TKU-39131-1

Example 1. Preparation of N—((S)-1-((4-(6-(cis-2,6-dimethylmorpholino)pyridin-2-yl)thiazol-2-yl)amino)-3-methoxy-1-oxopropan-2-yl)-1-(methylsulfonyl)-1H-pyrrole-3-carboxamide

      N—((S)-1-((4-(6-(cis-2,6-dimethylmorpholino)pyridin-2-yl)thiazol-2-yl)amino)-3-methoxy-1-oxopropan-2-yl)-1-(methylsulfonyl)-1H-pyrrole-3-carboxamide was synthesized as shown in Scheme 1 below.

Step 7: Preparation of N—((S)-1-((4-(6-(cis-2,6-dimethylmorpholino)pyridin-2-yl)thiazol-2-yl)amino)-3-methoxy-1-oxopropan-2-O-1-(methylsulfonyl)-1H-pyrrole-3-carboxamide

   To a solution of 1-methylsulfonylpyrrole-3-carboxylic acid (Intermediate K) (2.43 g, 12.9 mmol), EDCI (2.69 g, 14.0 mmol), HOBt (1.89 g, 14.0 mmol), and DIPEA (10.2 mL, 58.4 mmol) in dichloromethane (50 mL) was added Intermediate J (5.00 g, 11.7 mmol). After stirring at room temperature for 4 h, the reaction mixture was concentrated under reduced pressure. The residue was diluted with water and extracted three times with ethyl acetate. The combined organic layers were washed three times with saturated aqueous NH 4Cl, once with brine, dried over Na 2SO 4, filtered, and concentrated under reduced pressure to give a residue. The residue was purified by silica gel column chromatography (petroleum ether:ethyl acetate=1:1 to 1:2). The residue was triturated with methyl tert-butyl ether. After 0.5 h, the suspension was filtered, the filter cake was washed with methyl tert-butyl ether, and dried in vacuo. The solid was dissolved in dimethyl sulfoxide (12 mL) and added dropwise to water (800 mL). The suspension was filtered to give wet filter cake. The filter cake was suspended in water and stirred at room temperature. After 1 hour, the solid was collected by filtration, washed three times with water and dried in vacuo to give N—((S)-1-((4-(6-(cis-2,6-dimethylmorpholino)pyridin-2-yl)thiazol-2-yl)amino)-3-methoxy-1-oxopropan-2-yl)-1-(methylsulfonyl)-1H-pyrrole-3-carboxamide (3.9 g, 6.93 mmol, 59.3% yield) as a white solid.
      LCMS (ESI) m/z: [M+H] +=563.1.
       1H NMR (400 MHz, DMSO-d6) δ 12.49 (br s, 1H), 8.51 (d, J=7.2 Hz, 1H), 7.98-7.97 (m, 1H), 7.78 (s, 1H), 7.67-7.57 (m, 1H), 7.29-7.27 (m, 1H), 7.26 (d, J=7.2 Hz, 1H), 6.88-6.74 (m, 2H), 4.94-4.91 (m, 1H), 4.25 (d, J=11.6 Hz, 2H), 3.77-3.67 (m, 2H), 3.63-3.62 (m, 2H), 3.57 (s, 3H), 3.31 (s, 3H), 2.44-2.38 (m, 2H), 1.18 (d, J=6.0 Hz, 6H).

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Clinical data
Other namesFHD286
Identifiers
IUPAC name
CAS Number2671128-05-3
PubChem CID156818030
ChemSpider115010237
UNIIQHA5XLA4SA
ChEMBLChEMBL5095181
Chemical and physical data
FormulaC24H30N6O6S2
Molar mass562.66 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

References

  1.  Yu L, Wu D (July 2024). “SMARCA2 and SMARCA4 Participate in DNA Damage Repair”. Frontiers in Bioscience (Landmark Edition). 29 (7): 262. doi:10.31083/j.fbl2907262. PMID 39082357.
  2.  “Camibirstat”. PatSnap.

/////////////Camibirstat, ATPase inhibitor, antineoplastic, Foghorn Therapeutics, FHD 286

Brimarafenib


Brimarafenib

CAS 1643326-82-2

MF C24H17F3N4O4 MW482.4 g/mol

N-{(1S,1aS,6bS)-5-[(7-oxo-5,6,7,8-tetrahydro-1,8-naphthyridin-4-yl)oxy]-1a,6b-dihydro-1H-cyclopropa[b]benzofuran-1-yl}-N′-(2,4,5-trifluorophenyl)urea
rapidly accelerated fibrosarcoma (Raf) kinase inhibitor,

  • 1-((1S,1aS,6bS)-5-((7-oxo-6,8-dihydro-5H-1,8-naphthyridin-4-yl)oxy)-1a,6b-dihydro-1H-cyclopropa(b)(1)benzofuran-1-yl)-3-(2,4,5-trifluorophenyl)urea
  • 1-[(1S,1aS,6bS)-5-[(7-oxo-6,8-dihydro-5H-1,8-naphthyridin-4-yl)oxy]-1a,6b-dihydro-1H-cyclopropa[b][1]benzofuran-1-yl]-3-(2,4,5-trifluorophenyl)urea

Antineoplastic, MapKure, LLC, SpringWorks Therapeutics, BeiGene, BGB-3245, BGB 3245, GXS33OY2CB

Brimarafenib is an investigational new drug that is being evaluated for the treatment of cancer. It targets the proto-oncogene BRAF with activating mutations BRAF mutations (such as V600E), non-V600 BRAF mutations, and RAF fusions.[1][2]

It is being developed by MapKure, LLC, a joint venture between SpringWorks Therapeutics and BeiGene.[1]

Brimarafenib is an orally available inhibitor of both monomer and dimer forms of activating mutations of the serine/threonine-protein kinase BRAF (B-raf) protein, including V600 BRAF mutations, non-V600 BRAF mutations, and RAF fusions, with potential antineoplastic activity. Upon administration, brimarafenib targets and binds to both monomeric and dimeric forms of activating BRAF mutations and fusions. This may result in the inhibition of BRAF-mediated signaling and inhibit proliferation in tumor cells expressing BRAF mutations and fusions. BRAF belongs to the RAF family of serine/threonine protein kinases and plays a role in regulating the mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. BRAF mutations and fusions have been identified in a number of solid tumors and are drivers of cancer growth.

PAT

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014206343&_cid=P22-MG0802-32937-1

PAT

Fused tricyclic urea compounds as raf kinase and/or raf kinase dimer inhibitors

Publication Number: WO-2014206343-A1

Priority Date: 2013-06-28

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Clinical data
Other namesBGB-3245
Identifiers
IUPAC name
CAS Number1643326-82-2
PubChem CID117807031
IUPHAR/BPS13203
ChemSpider129144353
UNIIGXS33OY2CB
Chemical and physical data
FormulaC24H17F3N4O4
Molar mass482.419 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

References

  1.  “Brimarafenib”.
  2.  Tellenbach FL, Seiler LL, Johnson M, Rehrauer H, Schukla P, Martinez-Gomez J, et al. “Combination of the Novel Raf Dimer Inhibitor Brimarafenib with the Mek Inhibitor Mirdametinib is Effective Against Nras Mutant Melanoma”. SSRN: 4934723. doi:10.2139/ssrn.4934723.

///////Brimarafenib, Antineoplastic, MapKure, LLC, SpringWorks Therapeutics, BeiGene, BGB-3245, BGB 3245, GXS33OY2CB

Ateganosine


Ateganosine

CAS 789-61-7

MF C10H13N5O3S MW 283.31 g/mol

2′-deoxy-6-thioguanosine
nucleoside analogue, antineoplastic

  • 6-THIO-2′-DEOXYGUANOSINE
  • 2′-Deoxythioguanosine
  • TGdR
  • Thioguanine deoxyriboside
  • KR0RFB46DF
  • NSC-71261

Ateganosine is a telomerase inhibitor[1] and apoptosis inducer currently under investigation for the treatment of various cancers, including non-small cell lung cancer (NSCLC).[2]

Beta-Thioguanine Deoxyriboside is a thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication. This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo. Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells. (NCI04)

  • THIO Sequenced With Cemiplimab in Advanced NSCLCCTID: NCT05208944Phase: Phase 2Status: RecruitingDate: 2025-05-31
  • A Phase III Study With THIO + Cemiplimab vs Chemotherapy as 3rd Line Treatment in Advanced/Metastatic NSCLCCTID: NCT06908304Phase: Phase 3Status: Not yet recruitingDate: 2025-04-08

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References

  1.  Eglenen-Polat B, Kowash RR, Huang HC, Siteni S, Zhu M, Chen K, et al. (January 2024). “A telomere-targeting drug depletes cancer initiating cells and promotes anti-tumor immunity in small cell lung cancer”. Nature Communications. 15 (1) 672. Bibcode:2024NatCo..15..672E. doi:10.1038/s41467-024-44861-8. PMC 10803750. PMID 38253555.
  2.  “Ateganosine”. PatSnap.
Clinical data
Other names2′-Deoxythioguanosine
Identifiers
IUPAC name
CAS Number789-61-7
PubChem CID3000603
DrugBankDB18117
ChemSpider2272164
UNIIKR0RFB46DF
KEGGD13071
ChEMBLChEMBL3250476
CompTox Dashboard (EPA)DTXSID4021345 
Chemical and physical data
FormulaC10H13N5O3S
Molar mass283.31 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

////////Ateganosine, nucleoside analogue, antineoplastic, 6-THIO-2′-DEOXYGUANOSINE, 2′-Deoxythioguanosine, TGdR, Thioguanine deoxyriboside, KR0RFB46DF, fast track designation, NSC-71261, NSC 71261

Asandeutertinib


Asandeutertinib, Osimertinib-d3

CAS 1638281-46-5

  • 9EKD2E8BM5
  • N-(2-(2-(dimethylamino)ethyl-methylamino)-4-methoxy-5-((4-(1-(trideuteriomethyl)indol-3-yl)pyrimidin-2-yl)amino)phenyl)prop-2-enamide
  • N-[2-[2-(dimethylamino)ethyl-methylamino]-4-methoxy-5-[[4-[1-(trideuteriomethyl)indol-3-yl]pyrimidin-2-yl]amino]phenyl]prop-2-enamide

N-[2-{2-(dimethylamino)ethylamino}-4-methoxy-5-({4-[1-(2H3)methyl-1H-indol-3-yl]pyrimidin-2-
yl}amino)phenyl]prop-2-enamide
epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, antineoplastic

MF C28H30. 2H3. N7O2, C28H30D3N7O2 MW 502.6 g/mol

Asandeutertinib is an investigational new drug that is being evaluated for the treatment of cancer. It is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) with antineoplastic properties.[1][2] Developed by TYK Medicines, this small molecule drug is currently being investigated for the treatment of non-small cell lung cancer (NSCLC), particularly in patients with EGFR mutations.[1][3]

PAT

SYN

[US10414756]

https://patentscope.wipo.int/search/en/detail.jsf?docId=US210080627&_cid=P21-MFT3HT-86141-1

Embodiment 3A

N-(2-{2-dimethylaminoethyl-methylamino}-4-methoxy-5-{[4-(1-(D3-methyl)indol-3-yl)pyrimidin-2-yl]amino}phenyl)-2-acrylamide

Under ice bath condition, to N 1-(2-dimethylaminoethyl)-5-methoxy-N 1-methyl-N 4-[4-(1-[D 3-methylindol]-3-yl)pyrimidin-2-yl]phenyl-1,2,4-triamine (intermediate 3, 20 g) in THF (200 mL) and water (20 mL), was added 6.9 g NaOH. Acryloyl chloride 4.05 g was added while stirring, the reaction mixture was stirred for 30 min at room temperature, then stirred for 1 h at room temperature. After the result of TLC showed that the reaction was complete, 200 mL water and 20 mL aqueous ammonia were added into the reaction mixture, the solid was precipitated and filtered out. The solid was collected and washed with water, dried for 8 h at 50° C. to deliver the title compound (yield 87%).
       1H-NMR: 2.70 (3H, s), 2.88 (6H, d), 3.35 (4H, s), 3.92 (3H, s), 5.77 (1H, d), 6.27 (1H, d), 6.67 (1H, dd), 7.04-7.25 (2H, m), 7.28 (1H, t), 7.46 (1H, d), 7.59 (1H, d), 8.23 (2H, s), 8.85 (1H, s), 9.45 (1H, s), 9.55 (1H, s).
      ESI+: [M+H +] 503.29.

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References

  1.  “Asandeutertinib”. PatSnap.
  2.  “Asandeutertinib”. IUPHAR/BPS Guide to PHARMACOLOGY.
  3.  Han B, Zhang W, Wu L, Chen B, Zhao Y, Liu J, et al. (October 2024). “P1. 12A. 07 A Phase 1 Study of TY-9591 in Advanced Non-Small Cell Lung Cancer (NSCLC) Patients with EGFR Positive Mutation”. Journal of Thoracic Oncology. 19 (10): S195. doi:10.1016/j.jtho.2024.09.353.
Clinical data
Other namesRunnor-9591, TY 9591
Identifiers
IUPAC name
CAS Number1638281-46-5
PubChem CID87056175
IUPHAR/BPS13201
ChemSpider129431787
UNII9EKD2E8BM5
Chemical and physical data
FormulaC28H30D3N7O2
Molar mass502.636 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

////////////Asandeutertinib, antineoplastic, 9EKD2E8BM5, Osimertinib-d3

Amcenestrant (SAR 439859)


Amcenestrant Chemical Structure
Amcenestrant.png

Amcenestrant  (SAR 439859)

アムセネストラント

Molecular Weight554.48
FormulaC31H30Cl2FNO3
CAS No.2114339-57-8

6-(2,4-dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid

Amcenestrant

8-(2,4-dichlorophenyl)-9-(4-{[(3 S )-1-(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro – 5H- Benzo[7]annulene-3-carboxylic acid

8-(2,4-Dichlorophenyl)-9-(4-{[(3 S )-1-(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5 H -benzo [7]annulene-3-carboxylic acid

C31H30Cl2FNO3  : 554.48 [ 2114339-57-8 ] _ _ _ _ _ _

EfficacyAntineoplastic, Selective estrogen receptor downregulator
CommentSelective estrogen receptor downregulator (SERD)
Treatment of breast cancer

SAR439859 (compound 43d) is an orally active, nonsteroidal and selective estrogen receptor degrader (SERD). SAR439859 is a potent ER antagonist and has ER degrading activity with an EC50 of 0.2 nM for ERα degradation. SAR439859 demonstrates robust antitumor efficacy and limited cross-resistance in ER+ breast cancer.

Amcenestrant is an orally available, nonsteroidal selective estrogen receptor degrader/downregulator (SERD), with potential antineoplastic activity. Upon oral administration, amcenestrant specifically targets and binds to the estrogen receptor (ER) and induces a conformational change that promotes ER degradation. This prevents ER-mediated signaling and inhibits both the growth and survival of ER-expressing cancer cells.

Amcenestrant is reported to be a selective estrogen receptor degrader (SERD) which has estrogen receptor antagonist properties and accelerates the proteasomal degradation of the estrogen receptor. Amcenestrant is under clinical investigation as an anticancer agent, in particular for treatment of breast cancer.

The compound and processes for preparation thereof are described in International Publication No. WO 2017/140669.

Crystalline forms are described in International Publication No. WO 2021/116074.

PAPER

Journal of Medicinal Chemistry (2020), 63(2), 512-52

https://pubs.acs.org/doi/10.1021/acs.jmedchem.9b01293

6-(2,4-Dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3- yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic Acid (43d).

To a solution of 6-(2,4-dichloro-phenyl)-5-[4-[1-(3-fluoropropyl)-pyrrolidin-3-yloxy]-phenyl]-8,9-dihydro-7H-benzocycloheptene-2-carboxylic acid methyl ester (42d) (80 mg, 140.72 μmol) in methanol (5 mL) was added 5 N NaOH (562.88 μL), the reaction mixture was heated to 60 °C for 5 h, and the solvent was removed under reduced pressure. The residue was taken up in water (10 mL), and aqueous HCl (5 M) was added to pH 7. The slurry was extracted with dichloromethane, dried over magnesium sulfate, filtered, and concentrated under reduced pressure. The solid was purified by column chromatography eluting with a mixture of dichloromethane, acetonitrile, and methanol (90/5/5 v/v/v) to give 60 mg (77%) of 6- (2,4-dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]- oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid (43d). 1 H NMR (400 MHz, DMSO-d6): 1.68 (m, 1H), 1.79 (dm, J = 25.3 Hz, 2 H), 2.07 to 2.23 (m, 5H), 2.38 (m, 1H), 2.46 (t, J = 7.2 Hz, 2H), 2.52 (m, 1H), 2.62 (m, 1H), 2.55 to 2.89 (m, 3H), 4.47 (td, J = 6.2 and 47.6 Hz, 2H), 4.72 (m, 1H), 6.63 (d, J = 8.9 Hz, 2H), 6.71 (m, 3H), 7.18 (d, J = 8.4 Hz, 1H), 8.26 (dd, J = 2.0 and 8.4 Hz, 1H), 7.58 (d, J = 2.0 Hz, 1H), 7.63 (d, J = 8.4 Hz, 1H), 7.79 (s, 1H), 12.3 (m, 1H). LCMS: 554 (M + H)+ . 

PATENT

Amcenestrant can be prepared according to methods known from the literature, for example U.S. Patent No. 9,714,221.

Example 1: Preparation of amorphous Amcenestrant

[00164] Amcenestrant (20 mg, prepared according to U.S. Patent No. 9,714,221) was dissolved in ethyl acetate (0.2 mL) at room temperature (25°C). Solution was left in opened flask at RT for 16 days, until all the solvent evaporated. Obtained solid was analyzed by XRPD.

PATENT

U.S. Patent No. 9,714,221

https://patents.google.com/patent/US9714221B1/en

PATENT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2017140669

Example 51. 6-(2,4-dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid

Methode B:

Step 1 : 6-(2,4-dichloro-phenyl)-5-{4-[1-(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}-8,9-dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester.

To a solution of methyl 8-bromo-9-(4-{[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate hydrobromide (D5) (150 mg, 298.56 μιηοΙ), in dioxane (12 ml) and water (2 ml), was added 2,4-dichlorophenyl-boronic acid (62.67 mg, 328.41 μηηοΙ), Cs2C03 (204.48 mg, 626.97 μηιοΙ), and Pd(dppf)CI2 (14.63 mg, 17.91 μιηοΙ). The reaction mixture was heated at 90°C for 3 hours, and partitioned between AcOEt and water. The phases were separated and the organic phase washed with brine, dried over MgS04 and concentrated under reduced pressure. The residue was purified by column chromatography eluting with a mixture of DCM, acetonitrile and MeOH (96/2/2; V/V/V) to give 80 mg (47%) of 6-(2,4-dichloro-phenyl)-5-{4-[1-(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}-8,9-dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester.

LC/MS (m/z, MH+): 568

Step 2 : 6-(2,4-dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid

To a solution of 6-(2,4-dichloro-phenyl)-5-{4-[1-(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}-8,9-dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester (80 mg, 140.72μιηο!) in MeOH (5 ml) was added a solution of NaOH (562.88 μΙ, 5 M) and the reaction mixture was heated at 60°C for 5 hours and the solvent removed under reduced pressure. The residue was taken up in water (10 ml) and aqueous HCI (5 M) added to pH

7. The slurry was extracted with DCM, dried over MgS04 and concentrated under reduced pressure. The solid was purified by column chromatography eluting with a mixture of DCM, acetonitrile and MeOH (90/5/5; V/V/V) to give 60 mg (77%) of 6-(2,4-dichlorophenyl)-5-[4-[(3S)-1-(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid.

PATENT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2019020559

Intermediate (c). Tert-butyl (3S)-3-[4-(4,4!5!5-tetramethyl-1 !3,2-dioxaborolan-2yl)phenoxy]pyrrolidine-1 -carboxylate

To a solution of commercially available 4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenol (a) (82.7 g, 364.51 mmol) in THF (2 L) was added under argon (R)-1 -N-Boc-3-hydroxypyrrolidine (b) (84.43 g, 437.41 mmol) followed by Ν,Ν,Ν’,Ν’-tetramethylazodicarboxamide (99.1 g, 546.77 mmol). The clear reaction mixture turned orange and triphenylphosphine (143.41 g, 546.77 mmol) was added. The reaction mixture was stirred at room temperature for 24 hours, meanwhile a precipitate of triphenylphosphine oxide formed (Ph3P=0). The reaction mixture was poured in water (1 .5 L) and extracted with ethyl acetate (AcOEt) (3×1 .5 L). Gathered organic phases were dried over magnesium sulfate (MgS04), filtered and concentrated under reduced pressure. The residue was taken up into diisopropylether (1 .5 L) and the solid formed (Ph3P=0) was filtered. The solvent was concentrated under reduced pressure and the residue purified by column chromatography eluting with a mixture of heptane with AcOEt (90/10; v/v) to give 145 g (100%) of tert-butyl (3S)-3-[4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy]pyrrolidine-1 -carboxylate (c) as a colorless oil.

1H NMR (400 MHz, DMSO-d6, δ ppm): 1 .27 (s : 12H); 1 .39 (s : 9H); 2.05 (m : 1 H); 2.14 (m : 1 H); 3.37 (3H); 3.55 (m : 1 H); 5.05 (s : 1 H); 6.94 (d, J = 8.4 Hz : 2H); 7.61 (d, J = 8.4 Hz : 2H)

Intermediate (d). (3S)-3-[4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2yl)phenoxy]pyrrolidine, hydrochloride

To a solution of (S)-tert-butyl 3-(4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy)pyrrolidine-1 -carboxylate (c) (80 g, 195.23 mmol) in MeOH (450 ml) was added slowly HCI 4N in dioxane (250 ml).

After 1 .5 hours, the reaction mixture was concentrated under reduced pressure and the residue was taken up into Et20 with stirring to give a solid which then was filtered and dried under vacuum to give 61.8 g (95%) of (3S)-3-[4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2yl)phenoxy]pyrrolidine, hydrochloride (d) as a white powder.

1H NMR (400 MHz, DMSO-d6, δ ppm): 1.28 (s : 12H); 2.10 (m : 1 H); 2.21 (m : 1 H); 3.31 (3H); 3.48 (m : 1 H); 5.19 (m : 1 H); 6.97 (d, J = 8.4 Hz : 2H); 7.63 (d, J = 8.4 Hz : 2H); 9.48 (s : 1 H); 9.71 (s : 1 H).

LC/MS (m/z, MH+): 290

Intermediate (e). (3S)-1 -(3-fluoropropyl)-3-[4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy]pyrrolidine

To a suspension of (S)-3-(4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy)pyrrolidine hydrochloride (d) (20 g, 61.42 mmol) in acetonitrile (100 ml), was added K2C03 (21 .22 g, 153.54 mmol) and 1 -iodo-3-fluoropropane (12.15 g, 61.42 mmol), under argon. The reaction

mixture was stirred at 40°C for 24 hours. After cooling to room temperature, the reaction mixture was filtered and washed with acetonitrile. The filtrate was concentrated under reduced pressure and the residue was taken up in DCM and the solid formed was filtered and washed with DCM. The filtrate was concentrated to give 21.5 g (100%) of (3S)-1 -(3-fluoropropyl)-3-[4-(4,4,5,5-tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy]pyrrolidine (e) as a yellow foam.

1H NMR (400 MHz, DMSO-d6, δ ppm): 1.27 (s : 12H); 1 .77 (m : 2H); 1 .84 (m : 1 H); 2.27 (m : 1 H); 2.41 (m : 1 H); 2.49 (2H); 2.62 (dd, J = 2.6 and 10.4Hz : 1 H); 2.69 (m : 1 H); 2.83 (dd, J = 6.2 and 10.4Hz : 1 H); 4.47 (td, J = 6.2 and 47Hz : 2H) ; 4.99 (m : 1 H); 6.77 (d , J = 8.4 Hz : 2H); 7.58 (d, J = 8.4 Hz : 2H).

LC/MS (m/z, MH+): 350

Intermediate (B). 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yl 2,2-dimethylpropanoate

To a solution of 2-hydroxy-6,7,8,9-tetrahydro-5H-benzo[7]annulen-5-one (A) (1 .52 g, 8.63 mmol), in acetone (60 ml), was added K2C03 (1 .19 g, 8.63 mmol) and pivaloyl chloride (1.06 ml, 8.63 mmol). The reaction mixture was stirred at room temperature for 16 hours, filtered and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of heptane in AcOEt (100/0 to 85/15, v/v) to give 1.55 g (69%) of 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yl 2,2-dimethylpropanoate (B) as a colorless oil.

1H NMR (400 MHz, DMSO-d6, δ ppm): 7.65 (d, 1 H); 7.10-7.04 (m, 2H); 2.95 (t, 2H); 2.68 (t, 2H); 1 .85-1 .65 (m, 4H).

LC/MS (m/z, MH+): 261

Intermediate (C). 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulen-3-yl 2,2-dimethylpropanoate

To a solution of 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yl 2,2-dimethylpropanoate (B) (15 g, 57.62 mmol) in DCM (500 ml) was added dropwise under argon pyridine (7.28 ml, 86.43 mmol) and trifluoromethanesulfonic anhydride (19.58 ml, 1 15.24 mmol). The reaction mixture was stirred at room temperature for 2 hours and ice (200 g) was added. The phases were separated, the aqueous phase was washed with DCM and the gathered organic phases were dried over MgS04, filtered and evaporated under reduced pressure to give 22 g (97%) of 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulen-3-yl 2,2-dimethylpropanoate (C) as a white solid.

LC/MS (m/z, MH-): 391

Intermediate (D). 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl-2,2-dimeth lpropanoate

To a solution of 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulen-3-yl-2,2-dimethylpropanoate (C) (22 g, 56.07 mmol) and (3S)-1 -(3-fluoropropyl)-3-[4-(tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy]pyrrolidine (e) (20.56 g, 58.87 mmol) in dioxane (420 ml) and water (120 ml) was added under argon Pd(dppf)CI2 (2.75 g, 3.36 mmol) and Cs2C03 (36.57 g, 1 12.13 mmol). The reaction mixture was stirred for 1 hour at room temperature and was partitioned between water and DCM. The aqueous phase was washed with DCM and the gathered organic phases dried over MgS04, filtered and concentrated under reduced pressure. The residue was purified by column chromatography eluting with a gradient of MeOH in DCM (0 to 5%; V/V) to give 31 g (100 %) of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl-2,2-dimethylpropanoate (D).

LC/MS (m/z, MH+): 466

Intermediate (E). 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-ol

To a solution under argon of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl-2,2-dimethylpropanoate (D) (24.8 g, 53.26 mmol) in MeOH (300 ml), was added NaOH 5M (23 ml, 1 15.00 mmol). The reaction mixture was stirred for 2 hours at room temperature. pH was then adjusted to 7 by addition of 6N aqueous HCI solution. The MeOH was concentrated under reduced pressure, then DCM was added. The organic phase was dried over MgS04, and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of DCM/ MeOH from 100/0 to 95/05 to give 18.8 g (93%) of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-ol (E) as a beige solid.

LC/MS (m/z, MH+): 382

Intermediate (F). 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl trifluoromethanesulfonate

To a solution of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-ol (E) (20.6 g, 54.00 mmol) in DCM (200 ml) and pyridine (6.55 ml, 81 .00 mmol), cooled to 5°C (ice bath), was added dropwise trifluoromethanesulfonic anhydride (18.93 ml, 108.00 mmol) under argon, and the reaction temperature was maintained <15°C. The ice bath was removed, and the brown suspension was stirred at room temperature for 2 hours. Ice (200 g) and DCM (200 ml) were added and the phases separated. The organic phase was dried over MgS04, and concentrated under reduced pressure. The residue was

purified by flash chromatography eluting with a gradient of DCM/MeOH from 100/0 to 95/05 to give 24.7 g (89.1 %) of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl trifluoromethanesulfonate (F) as a brown oil.

LC/MS (m/z, MH+): 514

Intermediate (G). Methyl 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate

To a solution of 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulen-3-yl trifluoromethanesulfonate (F) (10.1 g, 19.67 mmol) in DMF (66 ml) and MeOH (33 ml), were added Pd(dppf)CI2 (909 mg, 1.18 mmol) and diisopropylethylamine (7.21 ml). The black suspension was carbonylated in an autoclave at 70°C under 5 bars of CO for 5 hours. The reaction mixture was filtered, then the filtrate was partially concentrated under reduced pressure. The residue was partitioned between AcOEt and water. The organic phase was washed with water (2x 100 ml), dried over MgS04, and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of DCIW MeOH from 100/0 to 95/05 to give 7.13 g (86%) of methyl 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate (G) as a brown gum.

LC/MS (m/z, MH+): 424

Intermediate (A1 ). 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yltrifluoromethanesulfonate

To a solution of commercially available 2-hydroxy-6,7,8,9-tetrahydro-5H-benzo[7]annulen-5-one (A) (18.5 g, 105 mmol) in DCM (185 ml) and lutidine (13.35 ml, 1 13.505 mmol), cooled at 5°C under argon, was added dropwise trifluoromethanesulfonic anhydride (20.22 ml,

123.29 mmol) while keeping temperature between 10 and 20°C. The reaction mixture was stirred for 1 hour at 5°C then at room temperature for 1 hour.

Then, ice (200 g) was added and the slurry partitioned between water and DCM. The organic phase was washed with aqueous NaHC03 solution, dried over MgS04, filtered off and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of heptane/AcOEt from 100 to 90/10 to give 28.2 g (87%) of 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yl trifluoromethanesulfonate (A1 ) as an orange oil. LC/MS (m/z, MH+): 309

Intermediate (B1 ). Methyl 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulene-2-carboxylate

To a solution of 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulen-2-yl trifluoromethanesulfonate (A1 ) (5.03 g, 16.32 mmol) in DMF (24 ml) and MeOH (12 ml), were added Pd(dppf)CI2 (754 mg, 0.98 mmol) and diisopropylethylamine (6 ml). The black suspension was carbonylated in an autoclave at 70°C under 5 bars of CO for 2.5 hours. The reaction mixture was filtered, then the filtrate was partially concentrated under reduced pressure, and the residue, was partitioned between AcOEt and water. The organic phase was washed with water (2x 75 ml) and aqueous HCI 0.5 N, dried over MgS04 and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of heptane/AcOEt from 100/0 to 90/10 to give 3.4 g (95%) of methyl 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulene-2-carboxylate (B1 ) as a colorless oil.

LC/MS (m/z, MH+): 219

Intermediate (C1 ). Methyl 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate

To a solution of methyl 5-oxo-6,7,8,9-tetrahydro-5H-benzo[7]annulene-2-carboxylate (B1 ) (18,19 g, 83,34 mmol) in DCM (500 ml) and anhydrous pyridine (1 1 ml, 130,56 mmol), cooled at 5°C under argon, was added dropwise trifluoromethanesulfonic anhydride (30 ml, 176,54 mmol). The reaction mixture, a thick suspension, was stirred at room temperature for 24 hours, then ice was added and partitioned between water and DCM. The organic phase was dried over MgS04, filtered off and concentrated under reduced pressure to give 29 g (100%) of methyl 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate (C1 ) as a yellow gum.

LC/MS (m/z, MH+): 351

Intermediate (G). Methyl 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate

To a solution of methyl 9-(trifluoromethanesulfonyloxy)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate (C1 ) (29 g, 82.9 mmol), (3S)-1 -(3-fluoropropyl)-3-[4-(tetramethyl-1 ,3,2-dioxaborolan-2-yl)phenoxy]pyrrolidine (e) (28.9 g, 82.9 mmol), in dioxane (225 ml) were added Pd(dppf)CI2 under argon, complex with DCM (3.73 g, 4.57 mmol) and Cs2C03 1 .5 M aqueous solution (1 1 1.12 ml, 166.68 mmol). The reaction mixture was stirred at 60°C for 1 hour.

After cooling to room temperature, the reaction mixture was poured into a mixture of water (500 ml) and AcOEt (400ml). The organic phase was washed with brine, dried over MgS04, filtered on celite and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of DCM/MeOH from 100/0 to 95/05 to give 23 g (65%) of methyl 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate (G) as a brown gum.

LC/MS (m/z, MH+): 424

Intermediate (H). Methyl 8-bromo-9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro-5H-benzo[7]annulene-3-carboxylate hydrobromide

To a solution of methyl 9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro- 5H-benzo[7]annulene-3-carboxylate (G) (13.93 g, 32.89 mmol), in DCM (150 ml) was added under argon pyridinium tribromide (15.78 g, 44.41 mmol). The reaction mixture was stirred for 1 hour at room temperature. Water (200 ml) was added, organic phase was then dried over MgS04, and concentrated under reduced pressure. The residue was purified by flash chromatography eluting with a gradient of DCM/MeOH from 100/0 to 95/05 to give 16.4 g (85%) of methyl 8-bromo-9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7-dihydro- 5H-benzo[7]annulene-3-carboxylate hydrobromide (H) as a yellow meringue.

LC/MS (m/z, MH+): 502

Intermediate (I). 6-(2,4-dichloro-phenyl)-5-{4-[1 -(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}- -dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester.

To a solution of methyl 8-bromo-9-(4-{[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxy}phenyl)-6,7- dihydro-5H-benzo[7]annulene-3-carboxylate hydrobromide (H) (150 mg, 298.56 μηηοΙ), in dioxane (12 ml) and water (2 ml), was added 2,4-dichlorophenyl-boronic acid (62.67 mg, 328.41 μηιοΙ), Cs2C03 (204.48 mg, 626.97 μπιοΙ), and Pd(dppf)CI2 (14.63 mg, 17.91 mol). The reaction mixture was heated at 90°C for 3 hours, and partitioned between AcOEt and water. The phases were separated and the organic phase washed with brine, dried over MgS04 and concentrated under reduced pressure. The residue was purified by column

chromatography eluting with a mixture of DCM, acetonitrile and MeOH (96/2/2; V/V/V) to give 80 mg (47%) of 6-(2,4-dichloro-phenyl)-5-{4-[1 -(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}-8,9-dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester (I).

LC/MS (m/z, MH+): 568

Compound (1 ). 6-(2,4-dichlorophenyl)-5-[4-[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulen -2-carboxylic acid

To a solution of 6-(2,4-dichloro-phenyl)-5-{4-[1 -(3-fluoro-propyl)-pyrrolidin-3-yloxy]-phenyl}-8,9-dihydro-7H-benzocycloheptene-2-arboxylic acid methyl ester (I) (80 mg, 140.72 μηηοΙ) in MeOH (5 ml) was added a solution of NaOH (562.88 μΙ, 5 M) and the reaction mixture was heated at 60°C for 5 hours and the solvent removed under reduced pressure. The residue was taken up in water (10 ml) and aqueous HCI (5 M) added to pH 7. The slurry was extracted with DCM, dried over MgS04 and concentrated under reduced pressure. The solid was purified by column chromatography eluting with a mixture of DCM, acetonitrile and MeOH (90/5/5; V/V/V) to give 60 mg (77%) of 6-(2,4-dichlorophenyl)-5-[4-[(3S)-1 -(3-fluoropropyl)pyrrolidin-3-yl]oxyphenyl]-8,9-dihydro-7H-benzo[7]annulene-2-carboxylic acid. 1H NMR (400 MHz, DMSO-d6, δ ppm): 1 .68 (m, 1 H); 1 ,79 (dm, J=25.3 Hz, 2 H); 2.07 to 2.23 (m, 5 H); 2.38 (m, 1 H); 2.46 (t, J=7.2 Hz, 2 H); 2.52 (m, 1 H); 2.62 (m, 1 H); 2.55 to 2.89 (m, 3 H); 4.47 (td, J=6.2 and 47.6 Hz, 2 H); 4.72 (m, 1 H); 6.63 (d, J=8.9 Hz, 2 H); 6.71 (m, 3 H); 7.18 (d, J=8.4 Hz, 1 H); 8.26 (dd, J=2.0 and 8.4 Hz, 1 H); 7.58 (d, J=2,0 Hz, 1 H); 7.63 (d, J=8.4 Hz, 1 H); 7.79 (s, 1 H); 12.3 (m, 1 H)

LC/MS (m/z, MH+): 554

//////////////

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/////Amcenestrant, SAR439859, アムセネストラント , Antineoplastic, CANCER

C1CC2=C(C=CC(=C2)C(=O)O)C(=C(C1)C3=C(C=C(C=C3)Cl)Cl)C4=CC=C(C=C4)OC5CCN(C5)CCCF

Tremelimumab


(Light chain)
DIQMTQSPSS LSASVGDRVT ITCRASQSIN SYLDWYQQKP GKAPKLLIYA ASSLQSGVPS
RFSGSGSGTD FTLTISSLQP EDFATYYCQQ YYSTPFTFGP GTKVEIKRTV AAPSVFIFPP
SDEQLKSGTA SVVCLLNNFY PREAKVQWKV DNALQSGNSQ ESVTEQDSKD STYSLSSTLT
LSKADYEKHK VYACEVTHQG LSSPVTKSFN RGEC
(Heavy chain)
QVQLVESGGG VVQPGRSLRL SCAASGFTFS SYGMHWVRQA PGKGLEWVAV IWYDGSNKYY
ADSVKGRFTI SRDNSKNTLY LQMNSLRAED TAVYYCARDP RGATLYYYYY GMDVWGQGTT
VTVSSASTKG PSVFPLAPCS RSTSESTAAL GCLVKDYFPE PVTVSWNSGA LTSGVHTFPA
VLQSSGLYSL SSVVTVPSSN FGTQTYTCNV DHKPSNTKVD KTVERKCCVE CPPCPAPPVA
GPSVFLFPPK PKDTLMISRT PEVTCVVVDV SHEDPEVQFN WYVDGVEVHN AKTKPREEQF
NSTFRVVSVL TVVHQDWLNG KEYKCKVSNK GLPAPIEKTI SKTKGQPREP QVYTLPPSRE
EMTKNQVSLT CLVKGFYPSD IAVEWESNGQ PENNYKTTPP MLDSDGSFFL YSKLTVDKSR
WQQGNVFSCS VMHEALHNHY TQKSLSLSPG K
(Disulfide bridge: L23-L88, L134-L194, L214-H139, H22-H96, H152-H208, H265-H325, H371-H429, H227-H’227, H228-H’228, H231-H’231, H234-H’234)

Tremelimumab 5GGV.png

Fab fragment of tremelimumab (blue) binding CTLA-4 (green). From PDB entry 5GGV.

Tremelimumab

FormulaC6500H9974N1726O2026S52
CAS745013-59-6
Mol weight146380.4722

FDA APPROVED2022/10/21, Imjudo

PEPTIDE, CP 675206

Antineoplastic, Immune checkpoint inhibitor, Anti-CTLA4 antibody
  DiseaseHepatocellular carcinoma

Tremelimumab (formerly ticilimumab, CP-675,206) is a fully human monoclonal antibody against CTLA-4. It is an immune checkpoint blocker. Previously in development by Pfizer,[1] it is now in investigation by MedImmune, a wholly owned subsidiary of AstraZeneca.[2] It has been undergoing human trials for the treatment of various cancers but has not attained approval for any.

Imjudo (tremelimumab) in combination with Imfinzi approved in the US for patients with unresectable liver cancer

PUBLISHED24 October 2022

https://www.astrazeneca.com/media-centre/press-releases/2022/imfinzi-and-imjudo-approved-in-advanced-liver-cancer.html

24 October 2022 07:00 BST
 

Approval based on HIMALAYA Phase III trial results which showed single priming dose of Imjudo added to Imfinzi reduced risk of death by 22% vs. sorafenib
 

AstraZeneca’s Imjudo (tremelimumab) in combination with Imfinzi (durvalumab) has been approved in the US for the treatment of adult patients with unresectable hepatocellular carcinoma (HCC), the most common type of liver cancer. The novel dose and schedule of the combination, which includes a single dose of the anti-CTLA-4 antibody Imjudo 300mg added to the anti-PD-L1 antibody Imfinzi 1500mg followed by Imfinzi every four weeks, is called the STRIDE regimen (Single Tremelimumab Regular Interval Durvalumab).

The approval by the US Food and Drug Administration (FDA) was based on positive results from the HIMALAYA Phase III trial. In this trial, patients treated with the combination of Imjudo and Imfinzi experienced a 22% reduction in the risk of death versus sorafenib (based on a hazard ratio [HR] of 0.78, 95% confidence interval [CI] 0.66-0.92 p=0.0035).1 Results were also published in the New England Journal of Medicine Evidence showing that an estimated 31% of patients treated with the combination were still alive after three years, with 20% of patients treated with sorafenib still alive at the same duration of follow-up.2

Liver cancer is the third-leading cause of cancer death and the sixth most commonly diagnosed cancer worldwide.3,4 It is the fastest rising cause of cancer-related deaths in the US, with approximately 36,000 new diagnoses each year.5,6

Ghassan Abou-Alfa, MD, MBA, Attending Physician at Memorial Sloan Kettering Cancer Center (MSK), and principal investigator in the HIMALAYA Phase III trial, said: “Patients with unresectable liver cancer are in need of well-tolerated treatments that can meaningfully extend overall survival. In addition to this regimen demonstrating a favourable three-year survival rate in the HIMALAYA trial, safety data showed no increase in severe liver toxicity or bleeding risk for the combination, important factors for patients with liver cancer who also have advanced liver disease.”

Dave Fredrickson, Executive Vice President, Oncology Business Unit, AstraZeneca, said: “With this first regulatory approval for Imjudo, patients with unresectable liver cancer in the US now have an approved dual immunotherapy treatment regimen that harnesses the potential of CTLA-4 inhibition in a unique combination with a PD-L1 inhibitor to enhance the immune response against their cancer.”

Andrea Wilson Woods, President & Founder, Blue Faery: The Adrienne Wilson Liver Cancer Foundation, said: “In the past, patients living with liver cancer had few treatment options and faced poor prognoses. With today’s approval, we are grateful and optimistic for new, innovative, therapeutic options. These new treatments can improve long-term survival for those living with unresectable hepatocellular carcinoma, the most common form of liver cancer. We appreciate the patients, their families, and the broader liver cancer community who continue to fight for new treatments and advocate for others.”

The safety profiles of the combination of Imjudo added to Imfinzi and for Imfinzi alone were consistent with the known profiles of each medicine, and no new safety signals were identified.

Regulatory applications for Imjudo in combination with Imfinzi are currently under review in Europe, Japan and several other countries for the treatment of patients with advanced liver cancer based on the HIMALAYA results.

Notes

Liver cancer
About 75% of all primary liver cancers in adults are HCC.3 Between 80-90% of all patients with HCC also have cirrhosis.7 Chronic liver diseases are associated with inflammation that over time can lead to the development of HCC.7

More than half of patients are diagnosed at advanced stages of the disease, often when symptoms first appear.8 A critical unmet need exists for patients with HCC who face limited treatment options.8 The unique immune environment of liver cancer provides clear rationale for investigating medications that harness the power of the immune system to treat HCC.8

HIMALAYA
HIMALAYA was a randomised, open-label, multicentre, global Phase III trial of Imfinzi monotherapy and a regimen comprising a single priming dose of Imjudo 300mg added to Imfinzi 1500mg followed by Imfinzi every four weeks versus sorafenib, a standard-of-care multi-kinase inhibitor.

The trial included a total of 1,324 patients with unresectable, advanced HCC who had not been treated with prior systemic therapy and were not eligible for locoregional therapy (treatment localised to the liver and surrounding tissue).

The trial was conducted in 181 centres across 16 countries, including in the US, Canada, Europe, South America and Asia. The primary endpoint was overall survival (OS) for the combination versus sorafenib and key secondary endpoints included OS for Imfinzi versus sorafenib, objective response rate and progression-free survival (PFS) for the combination and for Imfinzi alone.

Imfinzi
Imfinzi (durvalumab) is a human monoclonal antibody that binds to the PD-L1 protein and blocks the interaction of PD-L1 with the PD-1 and CD80 proteins, countering the tumour’s immune-evading tactics and releasing the inhibition of immune responses.

Imfinzi was recently approved to treat patients with advanced biliary tract cancer in the US based on results from the TOPAZ-1 Phase III trial. It is the only approved immunotherapy in the curative-intent setting of unresectable, Stage III non-small cell lung cancer (NSCLC) in patients whose disease has not progressed after chemoradiotherapy and is the global standard of care in this setting based on the PACIFIC Phase III trial.

Imfinzi is also approved in the US, EU, Japan, China and many other countries around the world for the treatment of extensive-stage small cell lung cancer (ES-SCLC) based on the CASPIAN Phase III trial. In 2021, updated results from the CASPIAN trial showed Imfinzi plus chemotherapy tripled patient survival at three years versus chemotherapy alone.

Imfinzi is also approved for previously treated patients with advanced bladder cancer in several countries.

Since the first approval in May 2017, more than 100,000 patients have been treated with Imfinzi.

As part of a broad development programme, Imfinzi is being tested as a single treatment and in combinations with other anti-cancer treatments for patients with SCLC, NSCLC, bladder cancer, several gastrointestinal (GI) cancers, ovarian cancer, endometrial cancer, and other solid tumours.

Imfinzi combinations have also demonstrated clinical benefit in metastatic NSCLC in the POSEIDON Phase III trial.

Imjudo
Imjudo (tremelimumab) is a human monoclonal antibody that targets the activity of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Imjudo blocks the activity of CTLA-4, contributing to T-cell activation, priming the immune response to cancer and fostering cancer cell death.

Beyond HIMALAYA, Imjudo is being tested in combination with Imfinzi across multiple tumour types including locoregional HCC (EMERALD-3), SCLC (ADRIATIC) and bladder cancer (VOLGA and NILE).

Imjudo is also under review by global regulatory authorities in combination with Imfinzi and chemotherapy in 1st-line metastatic NSCLC based on the results of the POSEIDON Phase III trial, which showed the addition of a short course of Imjudo to Imfinzi plus chemotherapy improved both overall and progression-free survival compared to chemotherapy alone.

AstraZeneca in GI cancers
AstraZeneca has a broad development programme for the treatment of GI cancers across several medicines spanning a variety of tumour types and stages of disease. In 2020, GI cancers collectively represented approximately 5.1 million new diagnoses leading to approximately 3.6 million deaths.9

Within this programme, the Company is committed to improving outcomes in gastric, liver, biliary tract, oesophageal, pancreatic, and colorectal cancers.

Imfinzi (durvalumab) is being assessed in combinations in oesophageal and gastric cancers in an extensive development programme spanning early to late-stage disease across settings.

The Company aims to understand the potential of Enhertu (trastuzumab deruxtecan), a HER2-directed antibody drug conjugate, in the two most common GI cancers, colorectal and gastric cancers. Enhertu is jointly developed and commercialised by AstraZeneca and Daiichi Sankyo.

Lynparza (olaparib) is a first-in-class PARP inhibitor with a broad and advanced clinical trial programme across multiple GI tumour types including pancreatic and colorectal cancers. Lynparza is developed and commercialised in collaboration with MSD (Merck & Co., Inc. inside the US and Canada).

AstraZeneca in immuno-oncology (IO)
Immunotherapy is a therapeutic approach designed to stimulate the body’s immune system to attack tumours. The Company’s immuno-oncology (IO) portfolio is anchored in immunotherapies that have been designed to overcome evasion of the anti-tumour immune response. AstraZeneca is invested in using IO approaches that deliver long-term survival for new groups of patients across tumour types.

The Company is pursuing a comprehensive clinical trial programme that includes Imfinzi as a single treatment and in combination with Imjudo (tremelimumab) and other novel antibodies in multiple tumour types, stages of disease, and lines of treatment, and where relevant using the PD-L1 biomarker as a decision-making tool to define the best potential treatment path for a patient.

In addition, the ability to combine the IO portfolio with radiation, chemotherapy, and targeted small molecules from across AstraZeneca’s oncology pipeline, and from research partners, may provide new treatment options across a broad range of tumours.

AstraZeneca in oncology
AstraZeneca is leading a revolution in oncology with the ambition to provide cures for cancer in every form, following the science to understand cancer and all its complexities to discover, develop and deliver life-changing medicines to patients.

The Company’s focus is on some of the most challenging cancers. It is through persistent innovation that AstraZeneca has built one of the most diverse portfolios and pipelines in the industry, with the potential to catalyse changes in the practice of medicine and transform the patient experience.

AstraZeneca has the vision to redefine cancer care and, one day, eliminate cancer as a cause of death.

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Mechanism of action

Tremelimumab aims to stimulate an immune system attack on tumors. Cytotoxic T lymphocytes (CTLs) can recognize and destroy cancer cells. However, there is also an inhibitory mechanism (immune checkpoint) that interrupts this destruction. Tremelimumab turns off this inhibitory mechanism and allows CTLs to continue to destroy the cancer cells.[3] This is immune checkpoint blockade.

Tremelimumab binds to the protein CTLA-4, which is expressed on the surface of activated T lymphocytes and inhibits the killing of cancer cells. Tremelimumab blocks the binding of the antigen-presenting cell ligands B7.1 and B7.2 to CTLA-4, resulting in inhibition of B7-CTLA-4-mediated downregulation of T-cell activation; subsequently, B7.1 or B7.2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA-4-mediated inhibition.

Unlike Ipilimumab (another fully human anti-CTLA-4 monoclonal antibody), which is an IgG1 isotype, tremelimumab is an IgG2 isotype.[4][5]

Clinical trials

Melanoma

Phase 1 and 2 clinical studies in metastatic melanoma showed some responses.[6] However, based on early interim analysis of phase III data, Pfizer designated tremelimumab as a failure and terminated the trial in April 2008.[1][7]

However, within a year, the survival curves showed separation of the treatment and control groups.[8] The conventional Response Evaluation Criteria in Solid Tumors (RECIST) may underrepresent the merits of immunotherapies. Subsequent immunotherapy trials (e.g. ipilimumab) have used the Immune-Related Response Criteria (irRC) instead.

Mesothelioma

Although it was designated in April 2015 as orphan drug status in mesothelioma,[9] tremelimumab failed to improve lifespan in the phase IIb DETERMINE trial, which assessed the drug as a second or third-line treatment for unresectable malignant mesothelioma.[10][11]

Non-small cell lung cancer

In a phase III trial, AstraZeneca paired tremelimumab with a PD-L1 inhibitor, durvalumab, for the first-line treatment of non-small cell lung cancer.[12] The trial was conducted across 17 countries, and in July 2017, AstraZeneca announced that it had failed to meet its primary endpoint of progression-free survival.[13]

References

  1. ^ Jump up to:a b “Pfizer Announces Discontinuation of Phase III Clinical Trial for Patients with Advanced Melanoma”. Pfizer.com. 1 April 2008. Retrieved 5 December 2015.
  2. ^ Mechanism of Pathway: CTLA-4 Inhibition[permanent dead link]
  3. ^ Antoni Ribas (28 June 2012). “Tumor immunotherapy directed at PD-1”. New England Journal of Medicine. 366 (26): 2517–9. doi:10.1056/nejme1205943. PMID 22658126.
  4. ^ Tomillero A, Moral MA (October 2008). “Gateways to clinical trials”. Methods Find Exp Clin Pharmacol. 30 (8): 643–72. doi:10.1358/mf.2008.30.5.1236622. PMID 19088949.
  5. ^ Poust J (December 2008). “Targeting metastatic melanoma”. Am J Health Syst Pharm. 65 (24 Suppl 9): S9–S15. doi:10.2146/ajhp080461. PMID 19052265.
  6. ^ Reuben, JM; et al. (1 Jun 2006). “Biologic and immunomodulatory events after CTLA-4 blockade with tremelimumab in patients with advanced malignant melanoma”. Cancer. 106 (11): 2437–44. doi:10.1002/cncr.21854. PMID 16615096. S2CID 751366.
  7. ^ A. Ribas, A. Hauschild, R. Kefford, C. J. Punt, J. B. Haanen, M. Marmol, C. Garbe, J. Gomez-Navarro, D. Pavlov and M. Marsha (May 20, 2008). “Phase III, open-label, randomized, comparative study of tremelimumab (CP-675,206) and chemotherapy (temozolomide [TMZ] or dacarbazine [DTIC]) in patients with advanced melanoma”. Journal of Clinical Oncology. 26 (15S): LBA9011. doi:10.1200/jco.2008.26.15_suppl.lba9011.[permanent dead link]
  8. ^ M.A. Marshall, A. Ribas, B. Huang (May 2010). “Evaluation of baseline serum C-reactive protein (CRP) and benefit from tremelimumab compared to chemotherapy in first-line melanoma”. Journal of Clinical Oncology. 28 (15S): 2609. doi:10.1200/jco.2010.28.15_suppl.2609.[permanent dead link]
  9. ^ FDA Grants AstraZeneca’s Tremelimumab Orphan Drug Status for Mesothelioma [1]
  10. ^ “Tremelimumab Fails Mesothelioma Drug Trial”. Archived from the original on 2016-03-06. Retrieved 2016-03-06.
  11. ^ AZ’ tremelimumab fails in mesothelioma trial
  12. ^ “AstraZeneca’s immuno-oncology combo fails crucial Mystic trial in lung cancer | FierceBiotech”.
  13. ^ “AstraZeneca reports initial results from the ongoing MYSTIC trial in Stage IV lung cancer”.

///////////Tremelimumab, Imjudo, APPROVALS 2022, FDA 2022, PEPTIDE, CP 675206, Antineoplastic, Immune checkpoint inhibitor, Anti-CTLA4 antibody

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Futibatinib


Futibatinib (JAN/USAN/INN).png
img

Futibatinib

フチバチニブ

FormulaC22H22N6O3
CAS1448169-71-8
Mol weight418.4485

2022/9/30 FDA APPROVED, Lytgobi

Antineoplastic, Receptor tyrosine kinase inhibitor
  DiseaseCholangiocarcinoma (FGFR2 gene fusion)

1-[(3S)-3-[4-amino-3-[2-(3,5-dimethoxyphenyl)ethynyl]-1H-pyrazolo[3,4-d]pyrimidin-1-yl]-1-pyrrolidinyl]-2-propen-1-one

TAS-120, TAS 120, TAS120; Futibatinib

Futibatinib, also known as TAS-120 is an orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor TAS-120 selectively and irreversibly binds to and inhibits FGFR, which may result in the inhibition of both the FGFR-mediated signal transduction pathway and tumor cell proliferation, and increased cell death in FGFR-overexpressing tumor cells. FGFR is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival and its expression is upregulated in many tumor cell types.

SYN

Patent Document 1: International Publication WO 2007/087395 pamphlet
Patent Document 2: International Publication WO 2008/121742 pamphlet
Patent Document 3: International Publication WO 2010/043865 pamphlet
Patent Document 4: International Publication WO 2011/115937 pamphlet

 

Unlicensed Document 1 : J. Clin. Oncol. 24, 3664-3671 (2006)
Non-licensed Document 2: Mol. Cancer Res. 3, 655-667 (2005)
Non-licensed Document 3: Cancer Res. 70, 2085-2094 (2010)
Non-licensed Document 4: Clin. Cancer Res. 17, 6130-6139 (2011)
Non-licensed Document 5: Nat. Med. 1, 27-31 (1995)

WO2020095452

WO2020096042

WO2020096050

WO2019034075

WO2015008844

WO2015008839

WO2013108809

SYN

US9108973

SYN

Reference Example 1: WXR1

Compound WXR1 was synthesized according to the route reported in patent WO2015008844. 1 H NMR(400MHz, DMSO-d 6 )δ8.40(d,J=3.0Hz,1H),6.93(d,J=2.5Hz,2H),6.74-6.52(m,2H),6.20-6.16( m,1H), 5.74-5.69(m,1H), 5.45-5.61(m,1H), 4.12-3.90(m,2H), 3.90-3.79(m,8H), 2.47-2.30(m,2H). MS m/z: 419.1[M+H] +

PAPER

Bioorg Med Chem, March 2013, Vol.21, No.5, pp.1180-1189

SYN

WO2015008844

PATENT

////////

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Clinical data
Trade namesLytgobi
Other namesTAS-120
License dataUS DailyMed: Futibatinib
Routes of
administration
By mouth
Drug classAntineoplastic
ATC codeL01EN04 (WHO)
Legal status
Legal statusUS: ℞-only [1]
Identifiers
showIUPAC name
CAS Number1448169-71-8
PubChem CID71621331
IUPHAR/BPS9786
DrugBankDB15149
ChemSpider58877816
UNII4B93MGE4AL
KEGGD11725
ChEMBLChEMBL3701238
PDB ligandTZ0 (PDBe, RCSB PDB)
Chemical and physical data
FormulaC22H22N6O3
Molar mass418.457 g·mol−1
3D model (JSmol)Interactive image
showSMILES
showInChI

Futibatinib, sold under the brand name Lytgobi, is a medication used for the treatment of cholangiocarcinoma (bile duct cancer).[1][2] It is a kinase inhibitor.[1][3] It is taken by mouth.[1]

Futibatinib was approved for medical use in the United States in September 2022.[1][2][4]

Medical uses

Futibatinib is indicated for the treatment of adults with previously treated, unresectable, locally advanced or metastatic intrahepatic cholangiocarcinoma harboring fibroblast growth factor receptor 2 (FGFR2) gene fusions or other rearrangements.[1][2]

Names

Futibatinib is the international nonproprietary name (INN).[5]

References

  1. ^ Jump up to:a b c d e f “Lytgobi (futibatinib) tablets, for oral use” (PDF). Archived (PDF) from the original on 4 October 2022. Retrieved 4 October 2022.
  2. ^ Jump up to:a b c https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2022/214801Orig1s000ltr.pdf Archived 4 October 2022 at the Wayback Machine Public Domain This article incorporates text from this source, which is in the public domain.
  3. ^ “Lytgobi (Futibatinib) FDA Approval History”. Archived from the original on 4 October 2022. Retrieved 4 October 2022.
  4. ^ “FDA Approves Taiho’s Lytgobi (futibatinib) Tablets for Previously Treated, Unresectable, Locally Advanced or Metastatic Intrahepatic Cholangiocarcinoma” (Press release). Taiho Oncology. 30 September 2022. Archived from the original on 4 October 2022. Retrieved 4 October 2022 – via PR Newswire.
  5. ^ World Health Organization (2019). “International nonproprietary names for pharmaceutical substances (INN): recommended INN: list 81”. WHO Drug Information. 33 (1). hdl:10665/330896.

External links

//////////Futibatinib, Lytgobi, FDA 2022, APPROVALS 2022, フチバチニブ , ANTINEOPLASTIC, TAS 120

C=CC(N1C[C@@H](N2N=C(C#CC3=CC(OC)=CC(OC)=C3)C4=C(N)N=CN=C42)CC1)=O

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