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Enrupatinib

January 20, 2026 2:32 am / Leave a comment

Enrupatinib

CAS 2222689-47-4

MF C27H26N6O3 MW 482.5 g/mol

6-[3-methoxy-4-[(6-methyl-3-pyridinyl)methoxy]anilino]-3-morpholin-4-ylquinoxaline-5-carbonitrile

colony-stimulating factor 1 receptor (CSF1R) inhibitor, antineoplastic, EI 1071, EI-1071, 9L35RVQ9J6

ENRUPATINIB is a small molecule drug with a maximum clinical trial phase of II and has 1 investigational indication.

EI-1071 is a selective Colony Stimulating Factor-1 Receptor kinase inhibitor.

A Study to Evaluate the Safety, Tolerability and Amount of EI-1071 in Blood in Healthy VolunteersCTID: NCT04238364Phase: Phase 1Status: CompletedDate: 2025-02-25
A Phase 2 Study to Assess the Safety of EI-1071 and the Effects of EI-1071 on Neuroinflammation in Alzheimer’s Disease PatientsCTID: NCT06745583Phase: Phase 2Status: RecruitingDate: 2025-07-28

OriginatorElixiron Immunotherapeutics
Developer4B Technologies; Elixiron Immunotherapeutics
ClassAntidementias; Antineoplastics; Small molecules
Mechanism of ActionMacrophage colony-stimulating factor receptor antagonists
Phase IIAlzheimer’s disease
Phase IAmyotrophic lateral sclerosis; Giant cell tumour of tendon sheath
No development reportedBreast cancer; Colorectal cancer
27 Jul 2025Pharmacodynamics data from preclinical studies in Alzheimer’s disease presented at the Alzheimer’s Association International Conference 2025 (AAIC-2025)
20 Dec 2024Phase-II clinical trials in Alzheimer’s disease (Treatment-experienced) in Taiwan (PO) (NCT06745583)
28 Jul 2024Adverse event data from a phase I trial in Alzheimer’s disease presented at the Alzheimer’s Association International Conference 2024 (AAIC-2024)

SYN

US10689362, Example 54

PAT

https://patentscope.wipo.int/search/en/detail.jsf;jsessionid=FF56F70B79B734C8ED557D6943D76B2E.wapp1nC?docId=WO2025067450&_cid=P12-MKLYYQ-95450-1

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2018071348&_cid=P12-MKLZ1L-03304-1

PAT

Solid dispersion, pharmaceutical composition, and preparation method and use thereforPublication Number: WO-2025067450-A1Priority Date: 2023-09-28
Method of enhanced absorption of quinoxaline type iii receptor tyrosine kinase inhibitorsPublication Number: WO-2025019622-A2Priority Date: 2023-07-18
Quinoxaline compounds as type iii receptor tyrosine kinase inhibitorsPublication Number: US-2019308949-A1Priority Date: 2016-10-10
Quinoxaline Compounds as Type III Receptor Tyrosine Kinase InhibitorsPublication Number: CN-110325515-APriority Date: 2016-10-10
Quinoxaline compounds as type III receptor tyrosine kinase inhibitorsPublication Number: JP-7206188-B2Priority Date: 2016-10-10Grant Date: 2023-01-17
quinoxaline compounds as type III tyrosine kinase receptor inhibitorsPublication Number: BR-112019007271-A2Priority Date: 2016-10-10
Quinoxaline compounds as type III receptor tyrosine kinase inhibitorsPublication Number: AU-2017342928-A1Priority Date: 2016-10-10
QUINOXALINE COMPOUNDS AS TYPE III RECEPTOR TYROSINKINASE INHIBITORSPublication Number: RU-2019113764-APriority Date: 2016-10-10
Quinoxaline compounds as type iii receptor tyrosine receptor inhibitorsPublication Number: IL-265829-APriority Date: 2016-10-10
Quinoxaline compounds as type iii receptor tyrosine kinase inhibitorsPublication Number: CA-3039919-A1Priority Date: 2016-10-10
Quinoxaline compounds as type iii receptor tyrosine kinase inhibitorsPublication Number: WO-2018071348-A1Priority Date: 2016-10-10
Quinoxaline compounds as inhibitors of type III receptor tyrosine kinasePublication Number: CN-110325515-BPriority Date: 2016-10-10Grant Date: 2023-06-20
Quinoxaline compounds as type III receptor tyrosine kinase inhibitorsPublication Number: US-10689362-B2Priority Date: 2016-10-10Grant Date: 2020-06-23

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////////enrupatinib, ANAX, colony-stimulating factor 1 receptor (CSF1R) inhibitor, antineoplastic, EI 1071, EI-1071, 9L35RVQ9J6

Deulorlatinib

January 16, 2026 2:36 am / Leave a comment

Deulorlatinib

CAS 2131126-33-3

MFC21H16²H3FN6O2, MW 409.4 g/mol

(10R)-7-amino-12-fluoro-2-(²H3)methyl-10,16-dimethyl15-oxo-10,15,16,17-tetrahydro-2H-8,4-
(metheno)pyrazolo[4,3-h][2,5,11]benzoxadiazacyclotetradecine-3-carbonitrile
tyrosine kinase inhibitor, antineoplastic, 7PW3UT8C9B, TGRX 326, TGRX-326

Deulorlatinib is an orally bioavailable inhibitor of the receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1), with potential antineoplastic activity. Upon oral administration, deulorlatinib targets, binds to and inhibits the activity of ALK and ROS1, which leads to the disruption of ALK- and ROS1-mediated signaling and the inhibition of cell growth in ALK- and ROS1-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types. ROS1, overexpressed in certain cancer cells, plays a key role in cell growth and survival of cancer cells.

TGRX-326 Chinese Phase III for Advanced Non-small Cell Lung Cancer (NSCLC)CTID: NCT06082635Phase: Phase 3Status: Active, not recruitingDate: 2025-05-18
TGRX-326 Pharmacokinetic Drug InteractionCTID: NCT06294561Phase: Phase 1Status: CompletedDate: 2024-06-27
TGRX-326 Chinese Phase I for Advanced Non-small Cell Lung Cancer (NSCLC)CTID: NCT05441956Phase: Phase 1Status: Active, not recruitingDate: 2025-05-18
TGRX-326 Chinese Phase II for Advanced Non-small Cell Lung Cancer (NSCLC)CTID: NCT05955391Phase: Phase 2Status: Active, not recruitingDate: 2025-05-18

SYN

WO 2017/148325 A1

syn

[US20220024908A1]

https://patentscope.wipo.int/search/en/detail.jsf?docId=US348430040&_cid=P11-MKG9AH-82468-1

Example 6: Synthesis of (10R)-7-amino-12-fluoro-2-(methyl-d₃)-10,16-dimethyl-15-oxo-10,15,16,17-tetrahydro-2H-8,4-(metheno)pyrazolo[4,3-h][2,5,11]benzoxadiazacyclotetradecine-3-carbonitrile (the Compound of Formula (A))

To a 250 mL three-necked flask equipped with magnetic stirring were added the compound of formula (J) (7.0 g, 42.2 mmol) and anhydrous dichloromethane (120 mL), and stirred until the solution became clear. The compound of formula (H) (8.77 g, 46.4 mmol) and then triethylamine (4.69 g, 46.4 mmol) were successively added. The mixture was stirred at room temperature under nitrogen atmosphere for 30 minutes to give a pale yellow clear solution for further use.

To another 500 mL three-necked flask equipped with magnetic stirring was added anhydrous aluminum chloride (6.17 g, 46.4 mmol), and the system was evacuated with suction and purged with nitrogen gas. Anhydrous dichloromethane (60 mL) was added under nitrogen atmosphere, and the mixture was cooled to 0° C. in an ice-water bath. Triethylamine (6.39 g, 63.3 mmol) was slowly added dropwise. After the addition was completed, the mixture was stirred at this temperature for 10 minutes. The above-mentioned solution of raw materials in dichloromethane was slowly added dropwise over 30 minutes. The mixture was reacted with stirring at this temperature for another 2 hours. By TLC (PE:EA=1:1) and HPLC monitoring, the reaction was completed. The reaction was quenched by adding water (200 mL). The organic phase was separated, and the aqueous layer was extracted with dichloromethane (100 mL×2). The organic phases were combined, washed successively with water (100 mL) and then saturated brine (100 mL), dried over anhydrous sodium sulfate, and filtered. The filtrate was concentrated to dryness under reduced pressure to give 12.66 g of a yellow oil in a yield of 94.0% and a purity (HPLC) of >90% (ee>98%). The intermediate is unstable at room temperature, and thus should be directly taken into the next step or stored in a refrigerator at −20° C. LC-MS (APCI): m/z=320.1 (M+1) ⁺. ¹H NMR (300 MHz, CDCl ₃) δ (ppm): 7.92-7.89 (m, 1H), 7.27-7.17 (m, 2H), 7.03-6.97 (m, 1H), 6.84 (s, 1H), 4.92 (q, J=6.3 Hz, 1H), 4.83 (s, 2H), 2.89 (s, 3H), 1.50 (d, J=6.3 Hz, 3H).

Sulfonylation of the Compound of Formula (G) to Form the Compound of Formula (F):

To a 250 mL three-necked flask equipped with magnetic stirring were added the compound of formula (G) (12.6 g, 39.5 mmol) and anhydrous dichloromethane (120 mL), and stirred until the solution became clear. The mixture was cooled in an ice-water bath. Triethylamine (7.98 g, 79.5 mmol) was added, and then methylsulfonyl chloride (5.85 g, 51.4 mmol) was slowly added dropwise. After the addition was completed, the ice bath was removed, and the mixture was reacted with stirring at room temperature under nitrogen atmosphere for 1 hour. TLC (DCM:MeOH=20:1) showed that the reaction was completed. The reaction was quenched by adding ice-water (100 mL). The organic phase was separated, and the aqueous layer was extracted with dichloromethane (50 mL×2). The organic phases were combined, washed successively with water (50 mL) and then saturated brine (50 mL), dried over anhydrous sodium sulfate, and filtered. The filtrate was concentrated to dryness under reduced pressure, and then dissolved in anhydrous acetonitrile (50 mL) for further use.

Alkylation of the Compound of Formula (E-a) with the Compound of Formula (F) to Form the Compound of Formula (D-a):

To another 250 mL three-necked flask equipped with magnetic stirring were added the compound of formula (E-a) (11.2 g, 59.3 mmol) and acetonitrile (200 mL), and cesium carbonate (25.7 g, 79.0 mmol) was added with stirring. The mixture was heated to 50° C. under nitrogen atmosphere, and stirred at this temperature for 30 min. The above-mentioned solution of the compound of formula (F) in acetonitrile was slowly added dropwise at 50° C. over 10 minutes. After the dropwise addition was completed, the mixture was reacted with stirring at this temperature for 2 hours. By TLC (DCM:MeOH=20:1) and HPLC monitoring, the reaction was completed. After cooling to room temperature, the reaction was quenched by adding water (200 mL). The reaction solution was diluted with ethyl acetate (300 mL), stirred for 5 minutes, and then filtered through Celite to remove insoluble solids. The filter cake was washed with ethyl acetate (50 mL). The organic layer was separated from the filtrate, and the aqueous phase was extracted with ethyl acetate (60 mL×2). The organic phases were combined, washed with a saturated aqueous solution of sodium carbonate (100 mL×3) and then saturated brine (60 mL), dried over anhydrous sodium sulfate, and filtered. The filtrate was concentrated to dryness under reduced pressure to give 17.5 g of a brown solid in a yield of 90.1% and a purity (HPLC) of >85% (ee>95%). LC-MS (APCI): m/z=390.1 (M+1) ⁺.

Introduction of Boc Protecting Group into the Compound of Formula (D-a) to Form the Compound of Formula (C):

To a 250 mL single-necked flask equipped with magnetic stirring were added the compound of formula (D-a) (17.5 g, 35.8 mmol) and dichloromethane (200 mL), and stirred until the solution became clear. Triethylamine (14.5 g, 143.2 mmol) and then DMAP (850 mg, 7.2 mmol) were successively added. Boc₂O (23.4 g, 107.4 mmol) was slowly added dropwise, and the mixture was reacted with stirring at room temperature under nitrogen atmosphere overnight. By TLC (DCM:MeOH=20:1) and HPLC monitoring, the reaction was completed. The reaction solution was evaporated under reduced pressure to remove the solvent, and the residue was purified by silica gel column chromatography (EA/PE=0-35%) to give 15.4 g of a white solid in a yield of 62.4% and a purity (HPLC) of >95% (ee>95%). LC-MS (APCI): m/z=590.1 (M+1−100) ⁺. ¹H NMR (300 MHz, CDCl ₃) (δ/ppm): 8.06 (d, J=1.8 Hz, 1H), 7.53-7.48 (m, 1H), 7.24-7.20 (m, 2H), 7.04-6.98 (m, 1H), 6.81 (s, 1H), 5.66-5.59 (m, 1H), 4.89-4.69 (m, 2H), 2.97 (s, 3H), 1.58 (d, J=6.0 Hz, 3H), 1.47 (s, 18H).

Cyclization of the Compound of Formula (C) Using Palladium Catalyst to Form the Compound of Formula (B):

To a 500 mL single-necked flask equipped with magnetic stirring were added the compound of formula (C) (15.4 g, 22.3 mmol) and 2-methyl-2-butanol (300 mL), and stirred until the solution became clear. Potassium acetate (6.56 g, 66.9 mmol) was added. The system was evacuated with suction and purged with nitrogen gas three times. Palladium acetate (0.75 g, 3.35 mmol) and n-butylbis(1-adamantyl)phosphine (1.60 g, 4.46 mmol) were quickly added. The system was evacuated with suction and purged with nitrogen gas three times. The reaction solution was heated to 110° C. under nitrogen atmosphere, and reacted with stirring at this temperature overnight. By TLC (PE:EA=1:1) and HPLC monitoring, the reaction was completed. The reaction solution was cooled to room temperature, diluted with dichloromethane (300 mL), and filtered through Celite to remove insoluble solids. The filter cake was washed with dichloromethane (50 mL). The filtrates were combined, and concentrated to dryness under reduced pressure. To the residue was added acetonitrile (150 mL), and the mixture was heated to reflux for 1 hour. The oil bath was removed, and the mixture was allowed to slowly cool to room temperature. A large amount of a white solid precipitated out, and the precipitated solid was filtered. The filter cake was washed with acetonitrile (10 mL), and dried to give 8.2 g of a white solids in a yield of 60.4% and a purity (HPLC) of >99.5% (ee>99.9%). LC-MS (APCI): m/z=510.1 (M+1−100) ⁺. ¹H NMR (300 MHz, CDCl ₃) (δ/ppm): 8.22 (d, J=1.8 Hz, 1H), 7.29-7.25 (m, 1H), 7.22-7.16 (m, 2H), 7.03-6.96 (m, 1H), 5.76-5.70 (m, 1H), 4.42 (q, J=14.1 Hz, 2H), 3.15 (s, 3H), 1.76 (d, J=6.0 Hz, 3H), 1.44 (s, 18H).

Removal of the Boc from the Compound of Formula (B) Using an Acid to Form the Compound of Formula (A):

To a 250 mL single-necked flask equipped with magnetic stirring were added the compound of formula (B) (8.2 g, 13.5 mmol) and dichloromethane (100 mL), and stirred until the solution became clear. The mixture was cooled in an ice-water bath, and trifluoroacetic acid (20 mL) was slowly added dropwise. After the addition was completed, the ice bath was removed, and the mixture was reacted with stirring at room temperature for 2 hours. By TLC (DCM:MeOH=20:1) and HPLC monitoring, the reaction was completed. The reaction solution was evaporated under reduced pressure to remove the organic solvent. Dichloromethane (100 mL) and a saturated aqueous solution of sodium bicarbonate (60 mL) were added under cooling, and the mixture was stirred for 10 minutes. The organic phase was separated, and the aqueous layer was extracted with dichloromethane (50 mL×2). The organic phases were combined, washed successively with water (30 mL) and then saturated brine (500 mL), dried over anhydrous sodium sulfate, and filtered. The filtrate was concentrated under reduced pressure to give 5.1 g of an amorphous white solid in a yield of 92.6% and a purity (HPLC) of >99.5% (ee>99.9%). LC-MS (APCI): m/z=410.2 (M+1) ⁺. ¹H NMR (300 MHz, CDCl ₃) (δ) ppm 7.79 (d, J=1.8 Hz, 1H), 7.31-7.27 (m, 1H), 7.23-7.19 (m, 1H), 7.06-6.97 (m, 1H), 6.87 (d, J=1.8 Hz, 1H), 5.75-5.70 (m, 1H), 5.09 (br s, 2H), 4.40 (q, J=14.1 Hz, 2H), 3.12 (s, 3H), 1.78 (d, J=6.6 Hz, 3H).

PAT

Preparation method for deuterated macrocyclic compound

Publication Number: US-2022024908-A1

Priority Date: 2018-11-28

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//////deulorlatinib, tyrosine kinase inhibitor, antineoplastic, 7PW3UT8C9B, TGRX 326, TGRX-326

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Casdatifan

January 14, 2026 2:40 am / Leave a comment

Casdatifan

CAS 2709069-30-5

MF C21H17F4NO3S, 439.4 g/mol

(5R,6S,8R)-3,5,6-trifluoro-8-[(1S,2R)-2-fluoro-1-hydroxy-7-(methanesulfonyl)-2,3-dihydro-1H-inden-4-yl]-5,6,7,8-tetrahydronaphthalene-1-carbonitrile

(5R,6S,8R)-3,5,6-trifluoro-8-[(1S,2R)-2-fluoro-1-hydroxy-7-methylsulfonyl-2,3-dihydro-1H-inden-4-yl]-5,6,7,8-tetrahydronaphthalene-1-carbonitrile

(5R,6S,8R)-3,5,6-trifluoro-8-[(1S,2R)-2-fluoro-1-hydroxy-7-methanesulfonyl-2, 3-dihydro-1H-inden-4-yl]-5,6,7,8-tetrahydronaphthalene-1-carbonitrile
hypoxia-inducible factor (HIF) inhibitor, antineoplastic, AB 521, DP73UWL6LE

Casdatifan is an orally bioavailable allosteric inhibitor of hypoxia inducible factor (HIF)-2alpha, with potential antineoplastic activity. Upon oral administration, casdatifan targets and allosterically binds to a hydrophobic pocket on HIF-2alpha leading to a confirmational change that prevents HIF-2alpha heterodimerization with HIF-1beta and binding to the hypoxia response element (HRE) binding site on DNA. This results in decreased transcription and expression of HIF-2alpha downstream target genes, many of which regulate tumor cell growth and survival. Blocking HIF-2alpha reduces the proliferation of HIF-2alpha-expressing tumor cells. HIF-2alpha, a heterodimeric transcription factor overexpressed under hypoxic conditions in many cancer cell types, promotes proliferation, progression and metastasis of tumors.

A Phase 1 Study of AB521 Monotherapy and Combination Therapies in Renal Cell Carcinoma and Other Solid TumorsCTID: NCT05536141Phase: Phase 1Status: RecruitingDate: 2026-01-02
A Relative Bioavailability Study and Food Effect Study of AB521 in Healthy Adult VolunteersCTID: NCT05999513Phase: Phase 1Status: CompletedDate: 2024-10-17
A Study to Investigate the Efficacy and Safety of Volrustomig ± Casdatifan vs Nivolumab + Ipilimumab as 1L Treatment for Advanced ccRCCCTID: NCT07000149Phase: Phase 3Status: Active, not recruitingDate: 2025-11-14
Study of Zanzalintinib (XL092) + AB521 and Zanzalintinib + AB521 + Nivolumab in Participants With Advanced Clear Cell Renal Cell Carcinoma (ccRCC) or Other Advanced Solid Tumors (STELLAR-009)CTID: NCT06191796Phase: Phase 1Status: TerminatedDate: 2025-06-12
Drug-Drug Interaction Study of Casdatifan in Healthy Adult Participants (ARC-29)CTID: NCT06919991Phase: Phase 1Status: CompletedDate: 2025-11-13

SYN

https://pubs.acs.org/doi/10.1021/acs.oprd.4c00497

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2021188769&_cid=P12-MKDEE0-87371-1

Example 215: (5R,6S,8R)-3,5,6-trifluoro-8-[(1S,2R)-2-fluoro-1-hydroxy-7-methanesulfonyl-2, 3-dihydro-1H-inden-4-yl]-5,6,7,8-tetrahydronaphthalene-1-carbonitrile

ANAX LABORATORIES

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PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US442743749&_cid=P12-MKDEE0-87371-1

Example 2: Synthesis of (5R,6S,8R)-3,5,6-trifluoro-8-[(1S,2R)-2-fluoro-1-hydroxy-7-methanesulfonyl-2,3-dihydro-1H-inden-4-yl]-5,6,7,8-tetrahydronaphthalene-1-carbonitrile

Step i: Synthesis of Compound 11

Product 10 of step h (37.85 g, 78.28 mmol, 1.0 equiv.) was dissolved in THF (400 mL) at 23° C. A solution of hydrochloric acid (320 mL, 6M) was added dropwise over 20 min, and the mixture was stirred at 30° C. for 4 h. After this time, the reaction reached completion, as shown by LC/MS (MeCN/H ₂O—20%→100%, 6 min). The reaction mixture was diluted with water (1 L) and EtOAc (0.6 L), back-extracted twice with EtOAc, and washed with water, sat. sol. NaHCO ₃, and brine. The organic layer was dried over Na ₂SO ₄, filtered, and concentrated. The material (32.25 g, 94%) was triturated with CH ₂Cl ₂(45 mL) at 45° C., filtered, and washed with a minimum of cold CH ₂Cl ₂and cold hexanes to afford 11 as a white crystalline solid (26.15 g, 76%, 12:1 dr). ¹H NMR (400 MHZ, DMSO-d ₆) δ 7.96 (ddd, J=8.3, 2.7, 1.3 Hz, 1H), 7.89 (dd, J=8.9, 2.7 Hz, 1H), 7.57 (d, J=8.1 Hz, 1H), 6.66 (d, J=8.1 Hz, 1H), 5.95 (ddd, J=51.2, 13.5, 2.2 Hz, 1H), 5.89 (d, J=5.6 Hz, 1H), 5.47 (ddd, J=10.0, 6.2, 4.9 Hz, 1H), 5.26 (qd, J=52.5, 5.4 Hz, 1H), 5.12 (tddd, J=47.4, 18.7, 10.3, 2.7 Hz, 1H), 4.83 (t, J=5.4 Hz, 1H), 3.30 (s, 3H), 3.28-3.13 (m, 2H), 2.71-2.60 (m, 1H), 2.02-1.85 (m, 1H). ¹⁹F NMR (376 MHZ, DMSO-d ₆) δ −112.3, −179.6, −196.7, −199.4. ESI MS [M+Na] ⁺ for C ₂₁H ₁₇F ₄NO ₃SNa, calcd 462.0, found 461.9.

PAT

Tetralin and tetrahydroquinoline compounds as inhibitors of hif-2alphaPublication Number: US-2023021476-A1Priority Date: 2020-03-19
Tetralin and tetrahydroquinoline compounds as inhibitors of HIF-2Î±Publication Number: US-11407712-B2Priority Date: 2020-03-19Grant Date: 2022-08-09
Tetralin and tetrahydroquinoline compounds as inhibitors of HIF-2alphaPublication Number: US-12103907-B2Priority Date: 2020-03-19Grant Date: 2024-10-01
Tetralin and tetrahydroquinoline compounds as HIF-2Î± inhibitorsPublication Number: CN-115298165-APriority Date: 2020-03-19
Tetralin and tetrahydroquinoline compounds as inhibitors of hif-2alphaPublication Number: US-2021317079-A1Priority Date: 2020-03-19
Tetralin and tetrahydroquinoline compounds as inhibitors of hif-2alphaPublication Number: WO-2021188769-A1Priority Date: 2020-03-19
Tetralin and tetrahydroquinoline compounds as inhibitors of hif-2alphaPublication Number: US-2024254079-A1Priority Date: 2020-03-19
Process for preparing tetralin compoundsPublication Number: US-12145901-B1Priority Date: 2021-09-17Grant Date: 2024-11-19
Tetralin and tetrahydroquinoline compounds as inhibitors of HIF-2alphaPublication Number: US-11787762-B2Priority Date: 2020-03-19Grant Date: 2023-10-17
Tetrahydronaphthalene and tetrahydroquinoline compounds as HIF-2 alpha inhibitorsPublication Number: CN-119118872-APriority Date: 2020-03-19
Tetralin and tetrahydroquinoline compounds as HIF-2Î± inhibitorsPublication Number: CN-115298165-BPriority Date: 2020-03-19Grant Date: 2024-09-17
Tetralin and tetrahydroquinoline compounds as inhibitors of hif-2alphaPublication Number: US-2025214930-A1Priority Date: 2020-03-19

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////////Casdatifan, hypoxia-inducible factor (HIF) inhibitor, antineoplastic, AB 521, DP73UWL6LE

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Cambritaxestat

January 13, 2026 2:32 am / Leave a comment

Cambritaxestat

CAS 1979939-16-6

MFC25H22ClF3N4O2 MW502.9 g/mol

N-[(1S)-1-(4-chlorophenyl)ethyl]-3-[3-[[4-(trifluoromethoxy)phenyl]methyl]imidazo[4,5-b]pyridin-2-yl]propanamide

N-[(1S)-1-(4-chlorophenyl)ethyl]-3-(3-{[4-(trifluoromethoxy)phenyl]methyl}-3H-imidazo[4,5-b]pyridin-2-yl)propanamide
autotaxin inhibitor, antineoplastic, Orphan Drug, IOA 289, IOA-289, IOA289, LYY3P2KA27, CRT 0273750

OriginatorCancer Research Technology; Merck & Co
DeveloperiOnctura
ClassAntifibrotics; Antineoplastics; Small molecules
Mechanism of ActionAngiogenesis inhibitors; Cell proliferation inhibitors; ENPP2 protein inhibitors
Orphan Drug StatusYes – Pancreatic cancer
Phase I/IIPancreatic cancer
Phase ISolid tumours
PreclinicalNon-alcoholic steatohepatitis
14 Oct 2025Efficacy and adverse event data from a phase I/II trial in Pancreatic cancer released by iOnctura
04 Oct 2024Cambritaxestat is still in phase-I development in Solid-tumours (In volunteers) in Italy (PO, Capsule) (NCT05027568)
31 May 2024Efficacy and adverse event data from a phase I/II trial in Pancreatic cancer presented at the 60th Annual Meeting of the American Society of Clinical Oncology (ASCO-2024)

Cambritaxestat is an autotaxin inhibitor.

Cambritaxestat is an orally bioavailable small molecule inhibitor of autotaxin (ATX; ectonucleotide pyrophosphatase/phosphodiesterase family member 2; ENPP2), with potential antifibrotic and antineoplastic activities. Upon oral administration, cambritaxestat targets and binds to both the substrate pocket and the lysophosphatidic acid (LPA) carrier channel of ATX, thereby inhibiting the activity of ATX. This both directly inhibits the proliferation of tumor cells and reduces fibrosis in the tumor microenvironment (TME), allowing lymphocytes to infiltrate into the tumor and enhancing immune responses against tumor cells. ATX, a secreted glycoprotein with lysophospholipase D activity, hydrolyzes lysophosphatidylcholine (LPC) to LPA. LPA-mediated signaling plays an important role in cellular migration, proliferation and survival in fibrotic response. ATX and LPA are overexpressed in many tumors.

A Study to Assess an ATX Inhibitor (IOA-289) in Healthy VolunteersCTID: NCT05027568Phase: Phase 1Status: CompletedDate: 2025-03-20
A Study to Assess an ATX Inhibitor (IOA-289) in Patients with Metastatic Pancreatic CancerCTID: NCT05586516Phase: Phase 1/Phase 2Status: Active, not recruitingDate: 2025-03-20

SYN

WO2016/124939

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2016124939&_cid=P22-MKBYYZ-98558-1

SYN

https://patentscope.wipo.int/search/en/detail.jsf;jsessionid=D2AB83A7D50F3F6B36DBA4001867C8E7.wapp2nC?docId=WO2024246264&_cid=P22-MKBYUT-93851-1

WO2016/124939 describes various ATX inhibitor compounds and their use in the treatment of proliferative disorders in which ATX activity is implicated, including Compound 1.

Compound 1 is example 40 in WO2016/124939, which document is incorporated herein by reference in its entirety. WO2016/124939 describes over 200 examples. Compound 1’s structure is according to Formula I.

PAT

Autotaxin inhibitory compoundsPublication Number: US-10654846-B2Priority Date: 2015-02-06Grant Date: 2020-05-19
Autotaxin inhibitory compoundsPublication Number: EP-3253737-B3Priority Date: 2015-02-06Grant Date: 2024-05-29
Autotaxin inhibitor compoundsPublication Number: ES-2778898-T7Priority Date: 2015-02-06Grant Date: 2024-11-15
Autotaxin inhibitory compoundsPublication Number: EP-3253737-A1Priority Date: 2015-02-06
Home chemokine inhibiting compoundsPublication Number: CN-107428752-BPriority Date: 2015-02-06Grant Date: 2021-06-29
Autotaxin inhibitory compoundsPublication Number: US-11453666-B2Priority Date: 2015-02-06Grant Date: 2022-09-27
Autotaxin Inhibitory CompundsPublication Number: US-2020283435-A1Priority Date: 2015-02-06
Autotaxin inhibitory compoundsPublication Number: WO-2016124939-A1Priority Date: 2015-02-06
A pi3k-delta inhibitor for the treatment of pancreatic cancerPublication Number: WO-2022207648-A1Priority Date: 2021-03-29
A pi3k-delta inhibitor for the treatment of pancreatic cancerPublication Number: EP-4313059-A1Priority Date: 2021-03-29
A pi3k-delta inhibitor for the treatment of pancreatic cancerPublication Number: US-2024216385-A1Priority Date: 2021-03-29
Autotaxin inhibitory compoundsPublication Number: EP-3253737-B1Priority Date: 2015-02-06Grant Date: 2020-01-08
Autotaxin inhibitory compoundsPublication Number: US-2018016274-A1Priority Date: 2015-02-06
Autotaxin (atx) inhibitor for the treatment of pancreatic cancerPublication Number: WO-2022258693-A1Priority Date: 2021-06-09
Autotaxin (atx) inhibitor for the treatment of pancreatic cancerPublication Number: US-2025057820-A1Priority Date: 2021-06-09
Autotaxin (atx) inhibitor for the treatment of pancreatic cancerPublication Number: EP-4351563-A1Priority Date: 2021-06-09
Autotaxin (ATX) inhibitors for the treatment of pancreatic cancerPublication Number: CN-117295496-APriority Date: 2021-06-09
PI3K-Î´ inhibitors for the treatment of pancreatic cancerPublication Number: CN-116997340-APriority Date: 2021-03-29

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Characterization and translational development of IOA-289, a novel autotaxin inhibitor for the treatment of solid tumorsPublication Name: Immuno-Oncology and TechnologyPublication Date: 2023-06PMCID: PMC10205783PMID: 37234285DOI: 10.1016/j.iotech.2023.100384
The IUPHAR Guide to Immunopharmacology: connecting immunology and pharmacologyPublication Name: ImmunologyPublication Date: 2020-03-02PMCID: PMC7160657PMID: 32020584DOI: 10.1111/imm.13175
Discovery of potent inhibitors of the lysophospholipase autotaxinPublication Name: Bioorganic & Medicinal Chemistry LettersPublication Date: 2016-11-15PMID: 27780639DOI: 10.1016/j.bmcl.2016.10.036

///////Cambritaxestat, autotaxin inhibitor, antineoplastic, Orphan Drug, IOA 289, IOA-289, IOA289, LYY3P2KA27, CRT 0273750

Bosmolisib

January 9, 2026 2:52 am / Leave a comment

Bosmolisib

CAS 2055765-77-8

MF 2055765-77-8 MW478.3 g/mol

4-{[(1S)-1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl]amino}pyrido[2,3-d]pyrimidin-5(8H)-one

Pyrido[2,3-d]pyrimidin-5(8H)-one, 4-[[(1S)-1-(4,8-dichloro-1,2-dihydro-1-oxo-2-phenyl-3-isoquinolinyl)ethyl]amino]-

4-[[(1S)-1-(4,8-dichloro-1-oxo-2-phenylisoquinolin-3-yl)ethyl]amino]-8H-pyrido[2,3-d]pyrimidin-5-one
phosphatidylinositol 3-kinase (PI3K) inhibitor, antineoplastic, BR 101801, FJ5CTS1VNJ

A Study of Bosmolisib (BR101801) in Participants With R/R PTCL.CTID: NCT07180771Phase: Phase 2Status: Not yet recruitingDate: 2025-09-18
BR101801 in Adult Patients With Advanced Hematologic Malignancies(Phase I)CTID: NCT04018248Phase: Phase 1Status: CompletedDate: 2025-09-10

Bosmolisib is an orally bioavailable inhibitor of phosphoinositide 3-kinase delta (PI3-kinase subunit delta; PI3K-delta; PI3Kdelta) and DNA-dependent protein kinase (DNA-PK), with potential antineoplastic and immunomodulating activities. Upon oral administration, bosmolisib inhibits the activity of both PI3K-delta and DNA-PK. This prevents PI3K-mediated signaling pathways and may lead to the inhibition of cancer cell growth in PI3K-overexpressing tumor cells. Specifically, since PI3K regulates c-myc expression, inhibition of PI3K signaling may lead to a decrease in proliferation of c-myc-expressing tumor cells. Also, by inhibiting the activity of DNA-PK, bosmolisib interferes with the non-homologous end joining (NHEJ) process and prevents the repair of DNA double strand breaks (DSBs) caused by ionizing radiation or chemotherapeutic treatment. This increases chemo- and radiotherapy cytotoxicity by inhibiting the ability of tumor cells to repair damaged DNA. The PI3K pathway is upregulated in a variety of tumors and plays an important role in regulating cancer cell proliferation, growth, and survival. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks. The enhanced ability of tumor cells to repair DSBs plays a major role in the resistance of tumor cells to chemo- and radiotherapy. In addition, bosmolisib is able to decrease Tregs and increase CD8 lymphocytes.

OriginatorBoryung Pharmaceutical
ClassAntineoplastics; Small molecules
Mechanism of ActionDNA-activated protein kinase inhibitors; Phosphatidylinositol 3 kinase delta inhibitors; Phosphatidylinositol 3 kinase gamma inhibitors
Phase IHaematological malignancies
PreclinicalColorectal cancer
18 Sep 2025Boryung Pharmaceutical plans a phase II trial for Peripheral T Cell Lymphoma and Nodal T-follicular helper cell lymphoma (Second-line therapy or greater) in September 2025 (PO, Capsule) (NCT07180771)
06 Jan 2025Chemical structure information added.
09 Dec 2023Updated efficacy and adverse event data from a phase I trial in Hematological malignancies presented at the 65^th American Society of Hematology Annual Meeting and Exposition (ASH-2023

SYN

WO 2016/204429.

SYN

[WO2019139399A1]

xample 1. Preparation of (S)-4-((1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl)amino)pyrido[2,3-d]pyrimidin-5(8H)-one

[116](S)-4-((1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl)amino)pyrido[2,3-d]pyrimidin-5(8H)-one (4-((1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin -3-yl)ethyl)amino)pyrido[2,3-d]pyrimidin-5(8H)-one) represented by the chemical formula 3 above was prepared by the same method as that described in Example 10 of International Patent Publication No.

WO 2016/204429.

SYN

[WO2016204429]

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2016204429&_cid=P22-MK6A2W-95428-1

<Example 10> Preparation of (S)-4-((l-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl)amino)pyrido [2,3-d]pyrimidin-5(8H)-one

In Example 5, 50 mg (0.113 vol) of (S)-4— ((1-(8-chloro-1—oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl)amino)pyrido [2, 3-d]pyrimidin-5(8H)-one prepared was dissolved in 2 mL of acetic acid, and then 17 mg (0.124 vol) of N—chlorosuccinimide (NCS) was added. The mixture was stirred at 50 ^° C for 15 hours, filtered under reduced pressure, neutralized using an aqueous sodium bicarbonate solution, and then the organic layer extracted by adding dichloromethane and water was dried (Na ₂ SO ₄ ), filtered, concentrated under reduced pressure, and separated by column chromatography (SiO ₂ , eluent: dichloromethane/methanol, 30/1 -> dichloromethane/methanol, 10/1) to afford 25 mg (0.052 mmol, 46% yield) of compound (S)— 4-((1— (4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinolin-3-yl)ethyl)amino)pyrido[2, 3-d]pyramidin-5(8H)-one as a pale yellow solid.

^LH NMR (300 MHz, CDC1₃) δ 10.99 (d, J = 4.8 Hz, 1Ή)， 8.25 (s, 1H) , 7.95(dd, ^JJ = 1.9 Hz, J = 7.5 Hz, 1H)， 7.75 (d, J = 7.8 Hz, 1H) , 7.46-7.62 (m, 6H), 7.20 (d, J = 6.7 Hz, 1H) , 6.3 (d, J = 7.5 Hz, 1H), 5.04 (t , J = 67.2 Hz, 1H) , 1.67 (d, J = 7.2 Hz, 3H) .

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US214732247&_cid=P22-MK69S5-86256-1

Example 10: Preparation of (S)-4-((1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinoline-3-yl)ethyl)amino)pyrido[2,3-d]pyrimidine-5(8H)-one

50 mg (0.113 mmol) of (S)-4-((1-(8-chloro-1-oxo-2-phenyl-1,2-dihydroisoquinoline-3-yl)ethyl)amino)pyrido[2,3-d]pyrimidine-5(8H)-one prepared in Example 5 was dissolved in 2 mL of acetic acid, to which 17 mg (0.124 mmol) of N-chlorosuccinimide (NCS) was added, followed by stirring at 50° C. for 15 hours. The reaction mixture was filtered under reduced pressure. Saturated sodiumbicarbonate aqueous solution was added thereto, followed by neutralization. Dichloromethane and water were added thereto, followed by extraction. The extracted organic layer was dried (Na ₂SO ₄), filtered, and concentrated under reduced pressure. The residue was separated by column chromatography (SiO ₂, eluent: dichloromethane/methanol, 30/1→dichloromethane/methanol, 10/1) to give 25 mg of the target compound (S)-4-((1-(4,8-dichloro-1-oxo-2-phenyl-1,2-dihydroisoquinoline-3-yl)ethyl)amino)pyrido[2,3-d]pyrimidine-5(8H)-one as a pale yellow solid (0.052 mmol, yield: 46%).

¹H NMR (300 MHz, CDCl ₃) δ 10.99 (d, J=4.8 Hz, 1H), 8.25 (s, 1H), 7.95 (dd, J=1.9 Hz, J=7.5 Hz, 1H), 7.75 (d, J=7.8 Hz, 1H), 7.46-7.62 (m, 6H), 7.20 (d, J=6.7 Hz, 1H), 6.3 (d, J=7.5 Hz, 1H), 5.04 (t, J=67.2 Hz, 1H), 1.67 (d, J=7.2 Hz, 3H).

PAT

A pharmaceutical composition for preventing or treating a heteroaryl derivative or a pharmaceutically acceptable salt thereof, a method for producing the same, and a PI3 kinase-related disease containing the heteroaryl derivative as an active ingredient.Publication Number: JP-6808905-B2Priority Date: 2015-06-18Grant Date: 2021-01-06
Heteroaryl derivative or pharmaceutically acceptable salt thereof, method of preparation thereof and pharmaceutical composition to prevent or treat diseases associated with PI3 kinases, which contains the same as active principlePublication Number: ES-2816050-T3Priority Date: 2015-06-18Grant Date: 2021-03-31
Heteroaryl derivative or pharmaceutically acceptable salt thereof, preparation method therefor, and pharmaceutical compostion for preventing or treating diseases associated with pi3 kinases, containing same as active ingredientPublication Number: US-2018105527-A1Priority Date: 2015-06-18
Heteroaryl derivative or pharmaceutically acceptable salt thereof, preparation method therefor, and pharmaceutical composition for preventing or treating diseases associated with pi3 kinases, containing same as active ingredientPublication Number: EP-3312175-B1Priority Date: 2015-06-18Grant Date: 2020-07-22
Heteroaryl derivatives or pharmaceutically acceptable salts thereof, preparation method thereof and pharmaceutical composition for use in preventing or treating pi3 kinase related diseasesPublication Number: TW-I616446-BPriority Date: 2015-06-18Grant Date: 2018-03-01
HETEROARYL DERIVATIVES OR PHARMACEUTICALLY ACCEPTABLE SALTS THEREOF, PROCESS FOR PRODUCING THE SAME, AND PHARMACEUTICAL COMPOSITIONS FOR PREVENTING OR TREATING PI3-KINASE RELATED DISEASES COMPRISING THE SAME AS THE ACTIVE INGREDIENTPublication Number: JP-2018522852-APriority Date: 2015-06-18
Heteroaryl derivative or pharmaceutically acceptable salt thereof, preparation method therefor, and pharmaceutical composition for preventing or treating diseases associated with PI3 kinases, containing same as active ingredientPublication Number: US-10526337-B2Priority Date: 2015-06-18Grant Date: 2020-01-07
Heteroaryl derivative or a pharmaceutically acceptable salt thereof, a method for production thereof and a pharmaceutical composition for preventing or treating diseases associated with pi3 kinases, containing said active substancePublication Number: RU-2719367-C2Priority Date: 2015-06-18Grant Date: 2020-04-17
Heteroaryl derivative or pharmaceutically acceptable salt thereof, preparation method thereof, and pharmaceutical composition comprising same as active ingredient for preventing or treating PI3 kinase-associated diseasesPublication Number: CN-107690433-APriority Date: 2015-06-18

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PI3Kδ/γ inhibitor BR101801 extrinsically potentiates effector CD8+ T cell-dependent antitumor immunity and abscopal effect after local irradiationPublication Name: Journal for ImmunoTherapy of CancerPublication Date: 2022-03PMCID: PMC8921929PMID: 35288465DOI: 10.1136/jitc-2021-003762
Synergistic radiosensitizing effect of BR101801, a specific DNA-dependent protein kinase inhibitor, in various human solid cancer cells and xenograftsPublication Name: American journal of cancer researchPublication Date: 2021PMCID: PMC8640799PMID: 34873471

/////////bosmolisib, phosphatidylinositol 3-kinase (PI3K) inhibitor, antineoplastic, BR 101801, FJ5CTS1VNJ

Beroterkib

January 8, 2026 2:41 am / Leave a comment

Beroterkib

CAS 2095719-92-7

MF C29H31ClFN5O5 MW584.0 g/mol

(2R)-2-(6-{5-chloro-2-[(oxan-4-yl)amino]pyrimidin-4-yl}-1,3-dihydro-2H-1-oxoisoindol-2-yl) -N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide

(2R)-2-[5-[5-chloro-2-(oxan-4-ylamino)pyrimidin-4-yl]-3-oxo-1H-isoindol-2-yl]-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide

(alphaR)-6-[5-chloro-2-[(tetrahydro-2H-pyran-4-yl)amino]-4-pyrimidinyl]-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]-1,3-dihydro-alpha-methyl-1-oxo-2H-isoindole-2-acetamide

(2R)-2-[5-[5-chloro-2-(oxan-4-ylamino)pyrimidin-4-yl]-3-oxo-1H-isoindol-2-yl]-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide
extracellular signal-regulated kinases (ERK) inhibitor, antineoplastic, ASTX029, ASTX 029, 14FDK6ISC9, Beroterkib anhydrous, AT 35029

Beroterkib Anhydrous is the anhydrous form of beroterkib, an orally bioavailable inhibitor of the extracellular signal-regulated kinases (ERK) 1 and 2, with potential antineoplastic activity. Upon administration, beroterkib specifically binds to and inhibits both ERK 1 and 2, thereby preventing the activation of mitogen-activated protein kinase (MAPK)/ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The MAPK/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in the proliferation, differentiation and survival of tumor cells.

Study of ASTX029 in Subjects With Advanced Solid TumorsCTID: NCT03520075Phase: Phase 1/Phase 2Status: CompletedDate: 2025-07-03
Phase I/II Study of a Combination of Decitabine and Cedazuridine (ASTX727) and ASTX029, an ERK Inhibitor, for Patients With RAS Pathway Mutant Myelodysplastic Syndromes and Myelodysplastic/Myeloproliferative NeoplasmsCTID: NCT06284460Phase: Phase 1/Phase 2Status: WithdrawnDate: 2024-10-24
A Phase 1 Study to Evaluate the Effect of Food on Pharmacokinetics of ASTX029CTID: NCT04466514Phase: Phase 1Status: CompletedDate: 2024-08-02

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2017068412&_cid=P21-MK4TZX-17603-1

Example 685: (2R)-2-(6-{5-chloro-2-[(oxan-4-yl)amino]pyrimidin-4-yl}-1-oxo-2,3-dihydro- 1H-isoindol-2-yl)-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide

A stirred solution of (R)-2-(6-(5-chloro-2-((oxan-4-yl)amino)pyrimidin-4-yl)-1-oxoisoindolin-2- yl)propanoic acid (70 mg, 0.168 mmol), (S)-2-amino-2-(3-fluoro-5-methoxyphenyl)ethanol, HCl (41 mg, 0.185 mmol) and triethylamine (0.094 ml, 0.672 mmol) in DMF (1 ml) was treated with TBTU (65 mg, 0.202 mmol) and stirred at room temperature overnight. The mixture was diluted with ethyl acetate (20 ml), was washed successively with 1M KHSO₄ (10 ml), NaHCO₃ (10 ml), brine (2x 10 ml) and then water (4x 10 ml), was dried (MgSO₄) and evaporated. The residue was purified by chromatography (SiO₂, 12 g column, 0- 5% EtOOH in EtOAc) to give a glass, which was triturated with ether (2 ml) to give a solid. The solid was collected by filtration, washed with ether (2x 1 ml) and dried under vacuum at 50°C overnight to give the titlecompound (64.3 mg, 64.3 %) as a cream solid. 1H NMR (DMSO, 400 MHz) δ 8.56 (1H, d), 8.44 (1H, s), 8.07 ‒ 8.00 (1H, m), 7.97 (1H, dd), 7.74 (1H, d), 7.61 (1H, s), 6.76 ‒ 6.64 (3H, m), 4.99 (1H, q), 4.91 (1H, t), 4.86 ‒ 4.70 (2H, m), 4.60 (1H, d), 4.00 ‒ 3.80 (3H, m), 3.76 (3H, s), 3.60 ‒ 3.47 (2H, m), 3.40 ‒ 3.33 (2H, m), 1.84 (2H, d), 1.59 ‒ 1.39 (5H, m). ). LCMS: [M+H]+ = 584.

SYN

US10457669,

https://patentscope.wipo.int/search/en/detail.jsf?docId=US237389744&_cid=P21-MK4U5F-21416-1

Example 685: (2R)-2-(6-{5-chloro-2-[(oxan-4-yl)amino]pyrimidin-4-yl}-1-oxo-2,3-dihydro-1H-isoindol-2-yl)-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide

A stirred solution of (R)-2-(6-(5-chloro-2-((oxan-4-yl)amino)pyrimidin-4-yl)-1-oxoisoindolin-2-yl)propanoic acid (70 mg, 0.168 mmol), (S)-2-amino-2-(3-fluoro-5-methoxyphenyl)ethanol, HCl (41 mg, 0.185 mmol) and triethylamine (0.094 ml, 0.672 mmol) in DMF (1 ml) was treated with TBTU (65 mg, 0.202 mmol) and stirred at room temperature overnight. The mixture was diluted with ethyl acetate (20 ml), was washed successively with 1M KHSO ₄(10 ml), NaHCO ₃(10 ml), brine (2×10 ml) and then water (4×10 ml), was dried (MgSO ₄) and evaporated. The residue was purified by chromatography (SiO ₂, 12 g column, 0-5% EtOOH in EtOAc) to give a glass, which was triturated with ether (2 ml) to give a solid. The solid was collected by filtration, washed with ether (2×1 ml) and dried under vacuum at 50° C. overnight to give the title compound (64.3 mg, 64.3%) as a cream solid. 1H NMR (DMSO, 400 MHz) δ 8.56 (1H, d), 8.44 (1H, s), 8.07-8.00 (1H, m), 7.97 (1H, dd), 7.74 (1H, d), 7.61 (1H, s), 6.76-6.64 (3H, m), 4.99 (1H, q), 4.91 (1H, t), 4.86-4.70 (2H, m), 4.60 (1H, d), 4.00-3.80 (3H, m), 3.76 (3H, s), 3.60-3.47 (2H, m), 3.40-3.33 (2H, m), 1.84 (2H, d), 1.59-1.39 (5H, m).). LCMS: [M+H] ⁺=584.

SYN

US10457669,

PAT

Conjugates comprising hydroxyalkyl starch and a cytotoxic agent and process for their preparationPublication Number: AU-2011276120-B2Priority Date: 2010-07-09Grant Date: 2013-12-19
Conjugates comprising hydroxyalkyl starch and a cytotoxic agent and process for their preparationPublication Number: AU-2011276120-A1Priority Date: 2010-07-09
Combustion modified flexible polyurethane foamPublication Number: GB-2124634-APriority Date: 1982-07-26
Benzolactam compounds as protein kinase inhibitorsPublication Number: ES-2989326-T3Priority Date: 2015-10-21Grant Date: 2024-11-26
Protein kinase inhibitor benzolactam compoundsPublication Number: CN-114948963-APriority Date: 2015-10-21
Benzolactam compounds as protein kinase inhibitorsPublication Number: US-2024368136-A1Priority Date: 2015-10-21
Protein Kinase Inhibitors Benzolactam CompoundsPublication Number: CN-108617166-BPriority Date: 2015-10-21Grant Date: 2022-05-17
Benzolactam compounds as protein kinase inhibitorsPublication Number: CN-114948963-BPriority Date: 2015-10-21Grant Date: 2025-05-27

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REF

Discovery of ASTX029, a clinical candidate which modulates the phosphorylation and catalytic activity of ERK1/2Publication Name: Journal of Medicinal ChemistryPublication Date: 2021-10-06PMID: 34387469DOI: 10.1021/acs.jmedchem.1c00905
ASTX029, a Novel Dual-mechanism ERK Inhibitor, Modulates Both the Phosphorylation and Catalytic Activity of ERKPublication Name: Molecular Cancer TherapeuticsPublication Date: 2021-07-30PMID: 34330842DOI: 10.1158/1535-7163.mct-20-0909

//////////////Beroterkib, extracellular signal-regulated kinases (ERK) inhibitor, antineoplastic, ASTX029, ASTX 029, 14FDK6ISC9, Beroterkib anhydrous, AT 35029

Atirmociclib

January 5, 2026 3:01 am / Leave a comment

Atirmociclib

CAS 2380321-51-5

MF C22H27ClFN5O3,
463.9 g/mol

(3S,4R)-4-[[5-chloro-4-[7-fluoro-2-(2-hydroxypropan-2-yl)-3-propan-2-ylbenzimidazol-5-yl]pyrimidin-2-yl]amino]oxan-3-ol

(3S,4R)-4-({5-chloro-4-[4-fluoro-2-(2-hydroxypropan-2-yl)-1-(propan2-yl)-1H-1,3-benzimidazol-6-yl]pyrimidin-2-yl}amino)oxan-3-ol

1,5-anhydro-3-({5-chloro-4-[4-fluoro-2-(2-hydroxpropan-2-yl)-1-(propan-2-yl)-1H-benzimidazol-6-yl]pyrimidin-2-yl}amino)-2,3-dideoxy-D-threo-pentitol

D-threo-Pentitol, 1,5-anhydro-3-[[5-chloro-4-[4-fluoro-2-(1-hydroxy-1-methylethyl)-1-(1-methylethyl)-1H-benzimidazol-6-yl]-2-pyrimidinyl]amino]-2,3-dideoxy-
cyclin-dependent kinase (CDK) inhibitor, antineoplastic, PF 07220060, S743GOJ5LJ, CDK4/6-IN-6

Atirmociclib is an orally bioavailable inhibitor of cyclin-dependent kinase 4 (CDK4), with potential antineoplastic activity. Upon administration, atirmociclib selectively inhibits CDK4, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and inhibits tumor cell proliferation. CDK4, a serine/threonine kinase, is upregulated in many tumor cell types and plays a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.

Atirmociclib (development code PF-07220060) is an investigational orally bioavailable and CDK4-specific inhibitor being developed by Pfizer for the treatment of various solid tumors, particularly hormone receptor-positive, HER2-negative breast cancer.^[1][2] The safety and efficacy of atirmociclib have not been established, as it remains in clinical development as of September 2025.^[3][4][5]

SYN

https://pubs.acs.org/doi/10.1021/acs.jmedchem.5c02137

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US275481329&_cid=P22-MK0K3I-13424-1

Example A94 (Scheme A-15): Preparation of 1,5-anhydro-3-({5-chloro-4-[4-fluoro-2-(2-hydroxypropan-2-yl)-1-(propan-2-yl)-1H-benzimidazol-6-yl]pyrimidin-2-yl}amino)-2,3-dideoxy-D-threo-pentitol

Step 8: Synthesis of 1,5-anhydro-3-({5-chloro-4-[4-fluoro-2-(2-hydroxypropan-2-yl)-1-(propan-2-yl)-1H-benzimidazol-6-yl]pyrimidin-2-yl}amino)-2,3-dideoxy-D-threo-pentitol (Example A94)

A 2 L three-neck round bottom flask was charged with 2-[6-(2,5-dichloropyrimidin-4-yl)-4-fluoro-1-(propan-2-yl)-1H-benzimidazol-2-yl]propan-2-ol (A-23) (112 g, 292 mmol), 3-amino-1,5-anhydro-2,3-dideoxy-D-threo-pentitol hydrochloride (51.6 g, 336 mmol), and MeCN (1.1 L). DIPEA (132 g, 1.02 mol, 178 mL) was added at room temperature. The reaction mixture was heated to 80° C. (internal temperature) and stirred at the same temperature for 40 h to provide a brown solution. LCMS analysis showed remaining starting material. Additional 3-amino-1,5-anhydro-2,3-dideoxy-D-threo-pentitol hydrochloride (6.73 g, 43.8 mmol) was added at 80° C. (internal temperature) and the reaction was stirred at 80° C. (internal temperature) for an additional 10 h. The reaction mixture was cooled to room temperature and concentrated under vacuum. The residue was taken up in 1:1 EtOAc/H ₂O (1.5 L). Some solids were precipitated. EtOH (100 mL) was added. The organic layer was collected and the aqueous layer was extracted with EtOAc (2×500 mL). The combined organic layers were washed with H ₂O (2×300 mL), dried over Na ₂SO ₄, and filtered. To the filtrate was added sulfhydryl silica gel (Accela, 8 g, 0.7-1.4 mmol/g). The resulting mixture was stirred at room temperature for 1 h and then filtered through a pad of Celite. Treatment with sulfhydryl silica gel was repeated in identical fashion and the filtrate was concentrated to dryness. The crude residue was slurried in MeCN (500 mL) at room temperature for 16 h. The suspension was filtered and the filter cake was washed with MeCN (2×100 mL). The filter cake was slurried again with MeCN (300 mL) at room temperature for 6 h. The mixture was filtered and the filter cake was washed with MeCN (2×100 mL). The filter cake was collected and dried under vacuum and then dried in a drying oven (45° C. for 20 h, 50° C. for 64 h) to provide 1,5-anhydro-3-({5-chloro-4-[4-fluoro-2-(2-hydroxpropan-2-yl)-1-(propan-2-yl)-1H-benzimidazol-6-yl]pyrimidin-2-yl}amino)-2,3-dideoxy-D-threo-pentitol (Example A94) (90 g, 66% yield) as a white solid. ¹H NMR (400 MHz, 80° C., DMSO-d ₆) δ 8.38 (s, 1H), 8.00 (s, 1H), 7.43 (d, J=11.8 Hz, 1H), 7.13 (d, J=7.5 Hz, 1H), 5.80 (hept, J=7.0 Hz, 1H), 5.56 (s, 1H), 4.71 (d, J=5.3 Hz, 1H), 3.91-3.79 (m, 3H), 3.61-3.52 (m, 1H), 3.41-3.31 (m, 1H), 3.12-3.07 (m, 1H), 2.09-2.00 (m, 1H), 1.70 (s, 6H), 1.67-1.52 (m, 7H); ¹⁹F NMR (377 MHz, CDCl ₃) δ −127.2; m/z (ESI+) for (C ₂₂H ₂₇ClFN ₆O ₃), 464.2 (M+H) ⁺; [α] _D ²²=−12.6 (c=0.2, MeOH).

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US275481329&_cid=P22-MK0KHW-23947-1

PAT

2-amino-pyridine or 2-amino-pyrimidine derivatives as cyclin dependent kinase inhibitorsPublication Number: KR-102661053-B1Priority Date: 2018-04-26Grant Date: 2024-04-26
2-amino-pyridine or 2-amino-pyrimidine derivatives as cyclin dependent kinase inhibitorsPublication Number: KR-20230152182-APriority Date: 2018-04-26
Cyclin dependent kinase inhibitorsPublication Number: US-11220494-B2Priority Date: 2018-04-26Grant Date: 2022-01-11
CYCLINE-DEPENDENT KINASE INHIBITORSPublication Number: PE-20201202-A1Priority Date: 2018-04-26
Cyclin dependent kinase inhibitorsPublication Number: US-2022089580-A1Priority Date: 2018-04-26
2-amino-pyridine or 2-amino-pyrimidine derivatives as cyclin dependent kinase inhibitorsPublication Number: HR-P20250254-T1Priority Date: 2018-04-26
Cyclin dependent kinase inhibitorsPublication Number: US-12378232-B2Priority Date: 2018-04-26Grant Date: 2025-08-05
2-amino-pyridine or 2-amino-pyrimidine derivatives as cyclin dependent kinase inhibitorsPublication Number: EP-3784664-B1Priority Date: 2018-04-26Grant Date: 2025-02-19
2-Amino-pyridine or 2-amino-pyrimidine derivatives as cyclin-dependent kinase inhibitorsPublication Number: CN-112313219-BPriority Date: 2018-04-26Grant Date: 2024-04-26

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Mechanism of action

Atirmociclib is designed as a CDK4-specific inhibitor, distinguishing it from dual CDK4/6 inhibitors currently approved for cancer treatment.^[6] The drug targets cyclin-dependent kinase 4, which plays a role in cell cycle regulation.^[1]^[7]^[8]

Atirmociclib functions as a selective inhibitor of the CDK4/cyclin D complex, which plays a crucial role in cell cycle regulation.^[4] The drug works by targeting the CDK4 kinase, rendering the retinoblastoma (Rb)/E2F transcription system inactive, which ultimately leads to cell cycle arrest in the G1 phase.^[4] This mechanism is particularly effective in tumors that have lost Rb cell cycle-suppressive function, a common feature in various solid tumors.^[5]

The selective nature of atirmociclib represents a significant advancement over existing dual CDK4/6 inhibitors.^[6] By specifically targeting CDK4 while limiting CDK6 inhibition, atirmociclib is designed to maintain antitumor efficacy while potentially reducing dose-limiting hematologic toxicities, particularly neutropenia, which is believed to be primarily driven by CDK6 inhibition.^[9]

Clinical development

Atirmociclib is currently being evaluated in clinical trials for the treatment of advanced solid tumors.^[1] Clinical studies are ongoing with estimated completion dates extending to 2027–2028, reflecting the early stage of development for this investigational compound.^[1]

Preclinical research published in Cancer Cell in March 2025 reported atirmociclib as a next-generation CDK4-selective inhibitor with enhanced anti-tumor activity and reduced predicted toxicity compared to FDA-approved dual CDK4/6 inhibitors, though these findings require validation in clinical studies.^[6]

Preclinical studies

Preclinical research has demonstrated that atirmociclib exhibits enhanced anti-tumor activity compared to FDA-approved dual CDK4/6 inhibitors while showing reduced predicted toxicity.^[6] Studies have shown that CDK4-selective inhibition can provide improved preclinical anti-tumor efficacy and safety profiles compared to dual CDK4/6 inhibition strategies.^[10]

The preclinical development program has explored combination approaches with various therapeutic modalities, including endocrine therapy, CDK2 inhibition, HER2 antibodies, and immune checkpoint inhibitors.^[6] These combination strategies are designed to counter resistance mechanisms to CDK4 inhibition and expand the potential therapeutic applications of cell cycle targeting therapy.^[6]

Clinical trials

Atirmociclib has entered clinical development as part of Pfizer’s extensive oncology pipeline.^[11] The clinical program is evaluating atirmociclib both as a single agent and in combination with other therapeutic approaches, particularly focusing on patients with hormone receptor-positive, HER2-negative breast cancer.^[9]^[12]^[13]^[14]^[15]^[16]^[17]

Early clinical studies have included heavily pretreated patient populations, including those who have previously received CDK4/6 inhibitor therapy.^[9] This approach allows for the evaluation of atirmociclib’s potential to overcome resistance to existing CDK4/6 inhibitors and provide therapeutic benefit in patients with limited treatment options.^[9]

Safety profile and toxicity

One of the key differentiating features of atirmociclib is its potential for improved safety profile compared to existing dual CDK4/6 inhibitors.^[6] The selective targeting of CDK4 while limiting CDK6 inhibition is specifically designed to reduce neutropenia, the most common dose-limiting toxicity associated with current CDK4/6 inhibitors.^[18]

The rationale for this approach is based on preclinical evidence suggesting that neutropenia is primarily driven by CDK6 inhibition rather than CDK4 inhibition.^[18] By selectively targeting CDK4, atirmociclib aims to maintain therapeutic efficacy while potentially allowing for higher or more sustained dosing without the dose-limiting hematologic toxicities that can compromise treatment outcomes with existing agents.^[18]

Regulatory status

As of September 2025, atirmociclib remains an investigational drug that has not received approval from the FDA or other regulatory agencies.^[5] The compound is part of Pfizer’s oncology development pipeline.^[5]

References

Pfizer (2 February 2025). A Phase 1/2A Study Evaluating the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Anti-Tumor Activity of Pf-07220060 as a Single Agent and as Part of Combination Therapy in Participants With Advanced Solid Tumors (Report). clinicaltrials.gov.
Shapiro GI (March 2017). “The evolving role of cyclin-dependent kinase inhibitors in cancer management”. Clinical Advances in Hematology & Oncology. 15 (3): 174–177. PMID 28398270.
“CDK4 inhibitor PF-07220060”. http://www.cancer.gov. 2 February 2011. Retrieved 3 September 2025.
“Pfizer Pipeline”. Pfizer.
“Atirmociclib PF-07220060”. Pfizer Oncology Development. Retrieved 3 September 2025.
Chang J, Lu J, Liu Q, Xiang T, Zhang S, Yi Y, et al. (March 2025). “Single-cell multi-stage spatial evolutional map of esophageal carcinogenesis”. Cancer Cell. 43 (3): 380–397.e7. doi:10.1016/j.ccell.2025.02.009. PMID 40068596.
Topacio BR, Zatulovskiy E, Cristea S, Xie S, Tambo CS, Rubin SM, et al. (May 2019). “Cyclin D-Cdk4,6 Drives Cell-Cycle Progression via the Retinoblastoma Protein’s C-Terminal Helix”. Molecular Cell. 74 (4): 758–770.e4. doi:10.1016/j.molcel.2019.03.020. PMC 6800134. PMID 30982746.
Helsten T, Kato S, Schwaederle M, Tomson BN, Buys TP, Elkin SK, et al. (July 2016). “Cell-Cycle Gene Alterations in 4,864 Tumors Analyzed by Next-Generation Sequencing: Implications for Targeted Therapeutics”. Molecular Cancer Therapeutics. 15 (7): 1682–1690. doi:10.1158/1535-7163.MCT-16-0071. PMID 27196769.
“ESMO 2024 – combos could be the way forward for CDK2”. ApexOnco. 15 September 2024.
Palmer CL, Boras B, Pascual B, Li N, Li D, Garza S, et al. (March 2025). “CDK4 selective inhibition improves preclinical anti-tumor efficacy and safety”. Cancer Cell. 43 (3): 464–481.e14. doi:10.1016/j.ccell.2025.02.006. PMID 40068598.
“Pfizer Highlights Diverse Oncology Portfolio and Combination Approaches at ESMO 2024”. Pfizer. 2024.
Pfizer (12 August 2025). A Phase 1/2a Dose Escalation and Expansion Study to Evaluate Safety, Tolerability, Pharmacokinetic, Pharmacodynamic, and Anti-Tumor Activity of Pf-07248144 in Participants With Advanced or Metastatic Solid Tumors (Report). clinicaltrials.gov.
Pfizer (2 July 2025). An Interventional Safety and Efficacy Phase 1/2, Open-Label Study to Investigate Tolerability, Pk, and Antitumor Activity of Vepdegestrant (Arv-47/Pf-07850327), an Oral Proteolysis Targeting Chimera, in Combination With Pf-07220060 in Participants Aged 18 Years and Older With Er+/her2- Advanced or Metastatic Breast Cancer (Report). clinicaltrials.gov.
Pfizer (14 November 2024). A Phase 1/2, Open-Label, Multicenter, Dose Escalation and Dose Expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Antitumor Activity of PF-07220060 in Combination With Pf-07104091 Plus Endocrine Therapy in Participants With Advanced Solid Tumors (Report). clinicaltrials.gov.
Pfizer (17 June 2025). (FOURLIGHT-3) (Report). clinicaltrials.gov.
Pfizer (13 March 2025). An Interventional, Open-Label, Randomized, Multicenter Phase 3 Study of PF-07220060 Plus Letrozole Compared to cdk4/6 Inhibitor Plus Letrozole in Participants Over 18 Years of Age With Hormone Receptor (Hr)-Positive, her2-Negative Advanced/Metastatic Breast Cancer Who Have Not Received Any Prior Systemic Anticancer Treatment for Advanced/Metastatic Disease (FOURLIGHT-1) (Report). clinicaltrials.gov.
Pfizer (15 November 2024). An Interventional, Open-Label, Randomized, Multicenter, Phase 2 Study of Pf-07220060 Plus Letrozole Compared to Letrozole Alone in Postmenopausal Women 18 Years or Older With Hormone Receptor-Positive, her2-Negative Breast Cancer in the Neoadjuvant Setting (Report). clinicaltrials.gov.
“Pfizer dials down its atirmociclib ambitions”. ApexOnco. 1 May 2025.

Identifiers

IUPAC name
CAS Number	2380321-51-5
PubChem CID	146219790
ChemSpider	115009592
UNII	S743GOJ5LJ
KEGG	D12834
ChEMBL	ChEMBL5187755
Chemical and physical data
Formula	C₂₂H₂₇ClFN₅O₃
Molar mass	463.94 g·mol⁻¹
3D model (JSmol)	Interactive image
SMILES
InChI

///////////Atirmociclib, cyclin-dependent kinase (CDK) inhibitor, antineoplastic, PF 07220060, S743GOJ5LJ, CDK4/6-IN-6

Asaretoclax

January 4, 2026 2:34 am / Leave a comment

Asaretoclax

CAS 2363074-01-3

MF C47H57F2N7O7S, MW 902.1 g/mol

4-[4-[[2-[3-(difluoromethyl)-1-bicyclo[1.1.1]pentanyl]-4,4-dimethylcyclohexen-1-yl]methyl]piperazin-1-yl]-N-[4-[(4-hydroxy-4-methylcyclohexyl)methylamino]-3-nitrophenyl]sulfonyl-2-(1H-pyrrolo[2,3-b]pyridin-5-yloxy)benzamide

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)benzamide

B-cell lymphoma 2 (Bcl-2) inhibitor, antineoplastic, GY6FD5FXA3, HY 159817, ABT 263

Asaretoclax is an orally bioavailable inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon oral administration, asaretoclax targets, binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.

SYN

US11318134,

https://patentscope.wipo.int/search/en/detail.jsf?docId=US309776623&_cid=P21-MJZ42N-73938-1

Example 34

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1l-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)benzamide

Intermediate 18

4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrobenzenesulfonamide

Intermediate 18 was prepared following a procedure described in WO2014/165044A1. LC/MS (ESI) m/z 344.1 [M+H] ⁺.

Intermediate 30

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)benzoic Acid

Step 1: Methyl 2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)benzoate (Intermediate 30-1) was prepared following the procedure described in Step 1, Route C for Intermediate 28 using Intermediate 24 in place of Intermediate 22. LCMS (ESI) m/z 591.2 [M+H] ⁺.

Step 2: Intermediate 30 was prepared following the procedure described in Step 5, Route B for Intermediate 26 using Intermediate 30-1 in place of methyl 2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((4,4-dimethyl-2-(3-methylbicyclo[1.1.1]pentan-1-yl)cyclohex-1-en-1-yl)methyl)piperazin-1-yl)benzoate. LCMS (ESI) m/z 577.5[M+H] ⁺.

Example 34 was prepared following General Procedure A using Intermediate 30 and Intermediate 18. ¹H NMR (400 MHz, DMSO-d ₆) δ 11.70 (s, 1H), 11.40 (br s, 1H), 8.59-8.49 (m, 2H), 8.04 (d, J=2.0 Hz, 1H), 7.78 (d, J=8.8 Hz, 1H), 7.53-7.48 (m, 3H), 7.06 (d, J=9.2 Hz, 1H), 6.72 (d, J=7.2 Hz, 1H), 6.38 (s, 1H), 6.25 (s, 1H), 5.99 (t, J=56.8 Hz, 1H), 4.25 (s, 1H), 3.33-3.25 (m, 2H), 3.18-3.05 (m, 4H), 2.97 (s, 2H), 2.40-2.28 (m, 4H), 2.05-1.95 (m, 2H), 1.94 (s, 6H), 1.71-1.59 (m, 5H), 1.58-1.49 (m, 2H), 1.39-1.28 (m, 2H), 1.27-1.20 (m, 2H), 1.18-1.09 (m, 2H), 1.10 (s, 3H), 0.83 (s, 6H); LC/MS (ESI) m/z 902.6 [M+H] ⁺.

SYN

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US384526484&_cid=P21-MJZ3XL-69589-1

PAT

Benzamide compounds

Publication Number: US-2021009543-A1

Priority Date: 2018-01-10

Benzamide compoundsPublication Number: CN-118084904-APriority Date: 2018-01-10
Benzamide compoundsPublication Number: EP-4556469-A1Priority Date: 2018-01-10
Benzamide compounds as bci inhibitors for the treatment of hivPublication Number: EP-3740487-B1Priority Date: 2018-01-10Grant Date: 2025-01-08
Benzamide compoundsPublication Number: US-11344546-B2Priority Date: 2018-01-10Grant Date: 2022-05-31
Benzamide compoundsPublication Number: US-11318134-B2Priority Date: 2018-01-10Grant Date: 2022-05-03

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/////////Asaretoclax, B-cell lymphoma 2 (Bcl-2) inhibitor, antineoplastic, GY6FD5FXA3, HY 159817, ABT 263

Zomiradomide

December 22, 2025 2:37 am / Leave a comment

Zomiradomide

CAS 2655656-99-6

MF C45H48F3N7O6S MW871.97

N-[2-[4-[[6-[2-[[2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindol-4-yl]amino]ethyl]-2-azaspiro[3.3]heptan-2-yl]methyl]cyclohexyl]-5-(2-hydroxypropan-2-yl)-1,3-benzothiazol-6-yl]-6-(trifluoromethyl)pyridine-2-carboxamide
N-[2-[trans-4-[[6-[2-[[2-(2,6-Dioxo-3-piperidinyl)-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl]amino]ethyl]-2-azaspiro[3.3]hept-2-yl]methyl]cyclohexyl]-5-(1-hydroxy-1-methylethyl)-6-benzothiazolyl]-6-(trifluoromethyl)-2-pyridinecarboxamide

antineoplastic, IRAK degrader-1, AQ5UXV5646

Zomiradomide is an orally active PROTAC degrader for IRAK4 (DC₅₀=6 nM), thereby inhibiting the NF-κB signaling pathway. Zomiradomide acts also as a molecular glue, recruiting Ikaros and Aiolos, and mediating their degradation (DC₅₀ for Ikaros is 1 nM), thereby activating the type I IFN signaling pathway.

Zomiradomide is a small molecule protein degrader of interleukin-1 receptor-associated kinase 4 (IRAK4) and the immunomodulatory imide drug (IMiD) substrates Ikaros (IKZF1) and Aiolos (IKZF3), with potential immunomodulating and antineoplastic activities. Upon administration, zomiradomide modulates the E3 (ubiquitin) ligase and targets IRAK4, Ikaros and Aiolos for ubiquitination. This induces proteasome-mediated degradation of IRAK4, Ikaros and Aiolos. The degradation of IRAK4 inhibits IRAK4-mediated signaling and prevents the activation of IRAK4-mediated nuclear factor-kappa B (NF-kB) signaling and decreases the expression of inflammatory cytokines and certain pro-survival factors. This inhibits the proliferation of IRAK4-overactivated tumor cells, which are found in cells harboring MYD88 activating mutations or those with overactivated toll-like receptor (TLR) pathways. The degradation of the transcription factors Ikaros and Aiolos leads to a downregulation of other proteins, including interferon regulatory factor 4 (IRF4), which upregulates type I interferon signaling and further inhibits NF-kB activation. This leads to apoptosis and the inhibition of tumor cell proliferation. IRAK4, a serine/threonine-protein kinase that plays a key role in both the TLR and IL-1R signaling pathways, is activated though the adaptor protein MYD88 and links the TLR and IL-1R signaling pathway to the NF-kB pathway.

SYN

WO2022027058

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2022027058&_cid=P20-MJGJKA-81687-1

Example 1. Synthesis of N-[2-[4-[[6-[2-[[2-(2,6-dioxo-3-piperidyl)-1,3-dioxo-isoindolin-4-yl]amino]ethyl]-2- azaspiro[3.3]heptan-2-yl]methyl]cyclohexyl]-5-(1-hydroxy-1-methyl-ethyl)-1,3-benzothiazol-6-yl]-6-(trifluoromethyl)pyridine-2-carboxamide (Compound A)

[00349] To a solution of 4-[2-(2-azaspiro[3.3]heptan-6-yl)ethylamino]-2-(2,6-dioxo-3-piperidyl)isoindoline -1,3-dione (75.8 mg, 148 umol, TFA salt, Intermediate ATH) in THF (2 mL) was added TEA (15.0 mg, 148 umol), then the mixture stirred at 25 °C for 10 min. Next, HOAc (8.92 mg, 148 umol) and N-[2-(4-formylcyclohexyl)-5-(1-hydroxy-1-methyl-ethyl)-1,3-benzothiazol-6-yl]-6-(trifluoromethyl)pyridine-2-carboxamide (73.0 mg, 148 umol, Intermediate BAX) were added to the mixture and the mixture was stirred at 25 °C for 20 minutes, then NaBH(OAc)₃ (62.9 mg, 297 umol) was added to the mixture at 0 °C. The reaction mixture was stirred at 0-25 °C for 2 hours. On completion, the reaction mixture was quenched with H2O (1 mL) and concentrated in vacuo. The residue was purified by prep-HPLC (column: Phenomenex Synergi C18150*25*10 um; mobile phase: [water(0.225%FA)-ACN]; B%: 31%-58%, 9 min) to give the title compound (59.1 mg, 41% yield) as a yellow solid.¹H NMR (400 MHz, DMSO-d6) δ 12.54 (s, 1H), 11.09 (s, 1H), 9.06 (s, 1H), 8.49 – 8.44 (m, 1H), 8.38 (t, J = 8.0 Hz, 1H), 8.19 (d, J = 8.0 Hz, 1H), 7.88 (s, 1H), 7.58 (t, J = 8.0 Hz, 1H), 7.10 – 6.99 (m, 2H), 6.47 (t, J = 5.6 Hz, 1H), 6.07 (s, 1H), 5.05 (dd, J = 5.6, 12.8 Hz, 1H), 3.54 – 3.47 (m, 2H), 3.25 – 3.18 (m, 4H), 3.06 – 2.99 (m, 1H), 2.93 – 2.83 (m, 1H), 2.63 – 2.56 (m, 1H), 2.54 (s, 3H), 2.30 – 2.21 (m, 2H), 2.30 – 2.21 (m, 3H), 2.06 – 1.99 (m, 1H), 1.88 – 1.77 (m, 4H), 1.68 – 1.61 (m, 8H), 1.58 – 1.49 (m, 2H), 1.45 – 1.36 (m, 1H), 1.15 – 1.02 (m, 2H); LC-MS (ESI+) m/z 872.2 (M+H)⁺.

PAT

Irak degraders and uses thereofPublication Number: US-2024131016-A1Priority Date: 2019-12-17
Irak degraders and uses thereofPublication Number: EP-4076520-A1Priority Date: 2019-12-17
IRAK degraders and uses thereofPublication Number: US-11779578-B2Priority Date: 2019-12-17Grant Date: 2023-10-10
IRAK degraders and uses thereofPublication Number: US-11707457-B2Priority Date: 2019-12-17Grant Date: 2023-07-25
Methods of treating mutant lymphomasPublication Number: US-2024316004-A1Priority Date: 2020-07-30
Methods of treating mutant lymphomasPublication Number: US-2022054453-A1Priority Date: 2020-07-30
Irak degraders and uses thereofPublication Number: US-2023144292-A1Priority Date: 2019-12-17
Irak degraders and uses thereofPublication Number: WO-2021127190-A1Priority Date: 2019-12-17
Irak degraders and uses thereofPublication Number: US-2021228562-A1Priority Date: 2019-12-17
Irak4 degraders and uses thereofPublication Number: EP-4463166-A1Priority Date: 2022-01-14
Methods of treating mutant lymphomasPublication Number: WO-2022027058-A1Priority Date: 2020-07-30
Methods of treating mutated lymphomaPublication Number: CN-116133692-APriority Date: 2020-07-30
Methods of treating mutant lymphomasPublication Number: US-11857535-B2Priority Date: 2020-07-30Grant Date: 2024-01-02
Methods of treating mutant lymphomasPublication Number: EP-4188374-A1Priority Date: 2020-07-30
Irak4 degraders and uses thereofPublication Number: WO-2024191788-A1Priority Date: 2023-03-10
Formulations for treating cancerPublication Number: WO-2024163751-A1Priority Date: 2023-02-01
Irak4 degraders and uses thereofPublication Number: WO-2024148049-A1Priority Date: 2023-01-04
Irak4 degraders and uses thereofPublication Number: US-2023277519-A1Priority Date: 2022-01-14
Irak4 degraders and uses thereofPublication Number: WO-2023137439-A1Priority Date: 2022-01-14

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[1]. Weiss Matthew M. Preparation of benzothiazole derivatives as IRAK degraders and uses thereof. World Intellectual Property Organization, WO2021127190 A1. 2021-06-24.[2]. Zeng S, et al. Current advances and development strategies of orally bioavailable PROTACs. Eur J Med Chem. 2023 Dec 5;261:115793. [Content Brief][3]. Weiss MM, et al., Discovery of KT-413, a Targeted Protein Degrader of IRAK4 and IMiD Substrates Targeting MYD88 Mutant Diffuse Large B-Cell Lymphoma. J Med Chem. 2024 Jul 11;67(13):10548-10566. [Content Brief]

/////////zomiradomide, antineoplastic, IRAK degrader-1, AQ5UXV5646

Zemirciclib

December 19, 2025 2:10 am / Leave a comment

Zemirciclib

CAS 2057509-72-3

MF C22H28ClN5O2, 429.9 g/mol

(1S,3R)-3-acetamido-N-[5-chloro-4-(5,5-dimethyl-5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl)pyridin-2-
yl]cyclohexane-1-carboxamide

(1S,3R)-3-acetamido-N-[5-chloro-4-(5,5-dimethyl-4,6-dihydropyrrolo[1,2-b]pyrazol-3-yl)pyridin-2-yl]cyclohexane-1-carboxamide

(1S,3R)-3-acetamido-N-(5-chloro-4-(5,5-dimethyl-5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl)pyridin-2-yl)cyclohexanecarboxamide

cyclin-dependent kinase inhibitor, antineoplastic, AZD 4573, UNII-E5XSP3X68B

Zemirciclib is a selective, short-acting inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon intravenous administration, zemirciclib binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins. This induces cell cycle arrest and apoptosis, and leads to a reduction in tumor cell proliferation. CDK9 regulates elongation of transcription through phosphorylation of RNA polymerase II at serine 2 (p-Ser2-RNAPII). It is upregulated in various tumor cell types and plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.

AZD-4573 is a small molecule drug with a maximum clinical trial phase of II and has 1 investigational indication.

AZD4573 in Novel Combinations With Anti-cancer Agents in Patients With Advanced Blood CancerCTID: NCT04630756Phase: Phase 1/Phase 2Status: CompletedDate: 2025-04-09
AZD4573 as Monotherapy or in Combinations With Anti-cancer Agents in Patients With r/r PTCL or r/r cHLCTID: NCT05140382Phase: Phase 2Status: CompletedDate: 2024-08-28
Study to Assess Safety, Tolerability, Pharmacokinetics and Antitumor Activity of AZD4573 in Relapsed/Refractory Haematological MalignanciesCTID: NCT03263637Phase: Phase 1Status: CompletedDate: 2021-10-22

SYN

Large-Scale Synthesis of AZD4573Publication Name: SynfactsPublication Date: 2022-05-17DOI: 10.1055/s-0041-1738312
From Structure Modification to Drug Launch: A Systematic Review of the Ongoing Development of Cyclin-Dependent Kinase Inhibitors for Multiple Cancer TherapyPublication Name: Journal of Medicinal ChemistryPublication Date: 2022-04-29PMID: 35485642DOI: 10.1021/acs.jmedchem.1c02064
Lessons Learned from Past Cyclin-Dependent Kinase Drug Discovery EffortsPublication Name: Journal of Medicinal ChemistryPublication Date: 2022-03-02PMID: 35235745DOI: 10.1021/acs.jmedchem.1c02190
Discovery of AZD4573, a Potent and Selective Inhibitor of CDK9 That Enables Short Duration of Target Engagement for the Treatment of Hematological MalignanciesPublication Name: Journal of Medicinal ChemistryPublication Date: 2020-12-11PMID: 33306391DOI: 10.1021/acs.jmedchem.0c01754
A comprehensive insight on the recent development of Cyclic Dependent Kinase inhibitors as anticancer agentsPublication Name: European Journal of Medicinal ChemistryPublication Date: 2020-10-01PMID: 32707525DOI: 10.1016/j.ejmech.2020.112571
Recent Developments in the Biology and Medicinal Chemistry of CDK9 Inhibitors: An UpdatePublication Name: Journal of Medicinal ChemistryPublication Date: 2020-08-31PMID: 32866383DOI: 10.1021/acs.jmedchem.0c00744
AZD4573 Is a Highly Selective CDK9 Inhibitor That Suppresses MCL-1 and Induces Apoptosis in Hematologic Cancer CellsPublication Name: Clinical cancer research : an official journal of the American Association for Cancer ResearchPublication Date: 2020-02-14PMID: 31699827DOI: 10.1158/1078-0432.ccr-19-1853
A New CDK9 Inhibitor on the Block to Treat Hematologic MalignanciesPublication Name: Clinical cancer research : an official journal of the American Association for Cancer ResearchPublication Date: 2020-02-14PMID: 31843752DOI: 10.1158/1078-0432.ccr-19-3670
Cyclin dependent kinase (CDK) inhibitors as anticancer drugs: Recent advances (2015–2019)Publication Name: Bioorganic & Medicinal Chemistry LettersPublication Date: 2019-10-15PMID: 31477350DOI: 10.1016/j.bmcl.2019.126637

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2017001354&_cid=P22-MJC84G-87476-1

Example 14: (1S,3R)-3-acetamido-N-(5-chloro-4-(5,5-dimethyl-5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl)pyridin-2-yl)cyclohexanecarboxamide

PAT

COMPOUNDS DERIVED FROM POLYCYCLIC AMIDE AS CDK9 INHIBITORS, COMPOSITION AND THEIR USESPublication Number: BR-122019013677-B1Priority Date: 2015-06-29
Polycyclic amide derivatives as CDK9 inhibitorsPublication Number: KR-102663113-B1Priority Date: 2015-06-29Grant Date: 2024-05-02
Methods of treating a ras protein-related disease or disorderPublication Number: US-2025049810-A1
Chemical compoundsPublication Number: TW-I723028-BPriority Date: 2015-06-29Grant Date: 2021-04-01
Chemical compoundsPublication Number: US-2021171541-A1Priority Date: 2015-06-29
POLYCYCLIC AMIDA DERIVATIVES AS CDK9 INHIBITORSPublication Number: HR-P20211970-T1Priority Date: 2015-06-29
Pyridine and pyrimidine derivativesPublication Number: US-11352369-B2Priority Date: 2015-06-29Grant Date: 2022-06-07
Chemical compoundsPublication Number: US-2022340592-A1Priority Date: 2015-06-29

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/////////Zemirciclib, cyclin-dependent kinase inhibitor, antineoplastic, AZD 4573, UNII-E5XSP3X68B

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Discovery Solutions, Supporting the chemistry needs of clients in the Medical, Analytical and Bio Sciences

Discovery Solutions, Supporting the chemistry needs of clients in the Medical, Analytical and Bio Sciences

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Example 685: (2R)-2-(6-{5-chloro-2-[(oxan-4-yl)amino]pyrimidin-4-yl}-1-oxo-2,3-dihydro-1H-isoindol-2-yl)-N-[(1S)-1-(3-fluoro-5-methoxyphenyl)-2-hydroxyethyl]propanamide

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Step 8: Synthesis of 1,5-anhydro-3-({5-chloro-4-[4-fluoro-2-(2-hydroxypropan-2-yl)-1-(propan-2-yl)-1H-benzimidazol-6-yl]pyrimidin-2-yl}amino)-2,3-dideoxy-D-threo-pentitol (Example A94)

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Example 34

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1l-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)benzamide

Intermediate 18

4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrobenzenesulfonamide

Intermediate 30

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(4-((2-(3-(difluoromethyl)bicyclo[1.1.1]pentan-1-yl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)benzoic Acid

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