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ORGANIC SPECTROSCOPY

Read all about Organic Spectroscopy on ORGANIC SPECTROSCOPY INTERNATIONAL 

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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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Iberdomide


Iberdomide

CAS 1323403-33-3

as HCl: 1560678-63-8

MW 449.5 g/mol, C25H27N3O5

(S)-3-(4-((4-(Morpholinomethyl)benzyl)oxy)-1-oxoisoindolin-2-yl)piperidine-2,6-dione

(3S)-3-[7-[[4-(morpholin-4-ylmethyl)phenyl]methoxy]-3-oxo-1H-isoindol-2-yl]piperidine-2,6-dione

8/13/2026, APPROVAL 2026, FDA 2026, Zenbexus, cc-220, cc 220, 8V66F27X44, 79L3645KFI

To be used in combination with daratumumab and hyaluronidase-fihj and dexamethasone for adults with multiple myeloma who have received at least one prior line of therapy, including a proteasome inhibitor and an immunomodulatory agent

Iberdomide is a modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with immunomodulating and pro-apoptotic activities. Upon administration, iberdomide specifically binds to the cereblon (CRBN) part of the ligase complex, thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3) which are transcriptional repressors in T-cells. This leads to a reduction of their protein levels, and the modulation of the immune system, including activation of T-lymphocytes. In addition, this leads to a downregulation of other proteins, including interferon regulatory factor 4 (IRF4), which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.

Iberdomide, sold under the brand name Zenbexus, is an anti-cancer medication used for the treatment of multiple myeloma.[1] It is a cereblon-modulating protein degrader[1] and a thalidomide analog.[2]. It is taken By mouth.[1]

Iberdomide was approved for medical use in the United States in August 2026.[3]

Medical uses

Iberdomide is indicated in combination with daratumumab, hyaluronidase, and dexamethasone for the treatment of adults with multiple myeloma who have received at least one prior line of therapy including a proteasome inhibitor and an immunomodulatory agent.[3]

Society and culture

Legal status

Iberdomide was approved for medical use in the United States in August 2026.[12] The U.S. Food and Drug Administration (FDA) granted the application for iberdomide priority review, breakthrough therapy, and orphan drug designations.[3]

Names

Iberdomide is the international nonproprietary name.[13]

Iberdomide is sold under the brand name Zenbexus.[14]

SYN

compound 6 [PMID: 28425720]

SYN

https://pubs.acs.org/oprdfk/article-abstract/28/1/46/975719/Process-Development-and-Kilogram-Scale-Manufacture?redirectedFrom=fulltext

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2011100380&_cid=P12-MSZHNS-67589-1

5.2 3-[4-(4-MORPHOLIN-4-YLMETHYL-BENZYLOXY)-1-OXO- 1,3-DIHYDRO-ISOINDOL-2-YL]-PIPERIDINE-2,6-DIONE

Step 3 : To the THF solution of methyl 5-amino-4-(4-(4- (morpholinomethyl)benzyloxy)-1-oxoisoindolin-2-yl)-5-oxopentanoate (40 g, 83 mmol), was added potassium 2-methylpropan-2-olate (9.80 g, 87 mmol) portion wise at 0°C. The mixture was stirred at this temperature for 30 minutes. To the reaction mixture, was added 45 mL of 1N HCl solution, followed by 200 mL of saturated NaHCO3 solution. The mixture was diluted with 500 mL of EtOAc at 0°C, stirred for 5 minutes and separated. The organic layer was washed with water (50 mL × 3) and brine (100 mL), and concentrated on rota-vap to give a white solid, which was stirred in diethyl ether (300 mL) to give a suspension. The suspension was filtered to give 3-[4-(4-morpholin-4-ylmethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-piperidine-2,6-dione as white solid (28.5g, 72% yield): HPLC: Waters Symmetry C18, 5μm, 3.9 × 150 mm, 1 mL/min, 240 nm, gradient to 95/5 acetonitrile/0.1% H3PO4 in 5 min,: tR = 4.78 min (98.5%); mp: 209-21 1 °C; 1H NMR (DMSO-d6) δ 1.86 – 2.09 (m, 1H, CHH), 2.29 – 2.38 (m, 4H, CH2,CH2), 2.44 (dd, J = 4.3, 13.0 Hz, 1H, CHH), 2.53 – 2.64 (m, 1H, CHH), 2.82 – 2.99 (m, 1H, CHH), 3.46 (s, 2H, CH2), 3.52 – 3.61 (m, 4H, CH2,CH2), 4.18 – 4.51 (m, 2H, CH2), 5.11 (dd, J = 5.0, 13.3 Hz, 1H, NCH), 5.22 (s, 2H, CH2), 7.27 – 7.38 (m, 5H, Ar), 7.40 – 7.53 (m, 3H, Ar), 10.98 (s, 1H, NH); 13C NMR (DMSO-d6) δ 22.36, 31.21, 45.09, 51.58, 53.14, 62.10, 66.17, 69.41,

114.97, 115.23, 127.64, 128.99, 129.81, 129.95, 133.31, 135.29, 137.68, 153.50, 168.01,

170.98, 172.83; LCMS: 465; Anal Calcd for C25H27N3O5 + 0.86 H2O: C, 64.63; H, 6.22; N,

9.04; Found: C, 64.39; H, 6.11; N, 8.89; H2O, 3.24.

5.61 (S)-3-[4-(4-MORPHOLIN-4-YLMETHYL-BENZYLOXY)-1-OXO-1,3- DIHYDRO-ISOINDOL-2-YL]-PIPERIDINE-2,6-DIONE

[386] Step 1 : Preparation of (S)-4-[4-(4-Bromomethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-4-carbamoyl-butyric acid methyl ester

To a 2-L round bottom flask was charged methyl 5-amino-4-(4-hydroxy-1-oxoisoindolin-2-yl)-5-oxopentanoate (30 g, 103 mmol), 1,4-bis(bromomethyl)benzene (81 g, 308 mmol) and potassium carbonate (14.19 g, 103 mmol) and acetonitrile (1.2 L). The mixture was stirred at room temperature for 10 min and heated to 50°C for 12 hours. The reaction mixture was allowed to cool to room temperature. The mixture was filtered and the filtrate was concentrated on rota-vap. The resulted solid was dissolved in CH2Cl2 and loaded on 2 silica gel columns (330 g each) eluted using CH2Cl2/MeOH to give 4-[4-(4-bromomethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-4-carbamoyl-butyric acid methyl ester as white solid (40g, 82%). 1H NMR (DMSO-d6) δ 1.98 – 2.13 (m, 1H, CHH), 2.14 – 2.23 (m, 1H, CHH), 2.23 – 2.32 (m, 2H, CHH, CHH), 3.50 (s, 3H, CH3), 4.34 – 4.63 (m, 2H, CH2), 4.67 – 4.80 (m, 3H, CH2, NCH), 5.25 (s, 4H, CH2), 7.19 (s, 1H, NHH), 7.24 – 7.34 (m, 2H, Ar), 7.41 – 7.54 (m, 5H, Ar), 7.58 (br. s., 1H, NHH)

[387] Step 2: Preparation of (S)-4-Carbamoyl-4-[4-(4-morpholin-4-ylmethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-butyric acid methyl ester

To the CH2Cl2 solution of methyl 5-amino-4-(4-(4-(bromomethyl)benzyloxy)-1-oxoisoindolin-2-yl)-5-oxopentanoate (36.5 g, 77 mmol) was added morpholine (14.72 ml, 169 mmol) at 0 °C. The mixture was stirred at 0 °C for 1 hr. The mixture was added 200 mL of CH2Cl2, washed with water (100mL × 2) and brine (100 ml), dried in Na2SO4 and concentrated to give (S)-4-Carbamoyl-4-[4-(4-morpholin-4-ylmethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-butyric acid methyl ester as white foam (39 g, 100%). M.p. 66-68 °C; Waters Symmetry C-18, 3.9 X 150 mm, 5 micro, 1 mL/min, 240 nm, isocratic 15/85 CH3CN/ 0.1% H3PO4 in H2O: 7.92 min (99%). 1H NMR (DMSO-d6) δ 2.00 – 2.12 (m, 1HH CHH), 2.14 – 2.22 (m, 1H, CHH), 2.22 – 2.29 (m, 2H, CHH,CHH), 2.30 – 2.39 (m, 4H, CH2,CH2), 3.46 (s, 2H, CH2), 3.50 (s, 3H, CH3), 3.53 – 3.63 (m, 4H, CH2,CH2), 4.28 – 4.59 (m, 2H, CH2), 4.73 (dd, J= 4.7, 10.2 Hz, 1H, NCH), 5.22 (s, 2H, CH2), 7.14 – 7.23 (m, 1H, NHH), 7.26 – 7.39 (m, 4H, Ar), 7.41 – 7.51 (m, 3H, Ar), 7.58 (s, 1H, NHH). 13C NMR (DMSO-d6) δ 24.82, 30.33, 44.78, 51.24, 53.12, 53.38, 62.09, 66.14, 69.35, 114.66, 115.12, 127.60, 129.00, 129.55, 130.18, 133.43, 135.31, 137.66, 153.42, 167.84, 171.73, 172.46; Anal Calcd for C26H31N3O6+ 0.3 H2O: C% 64.13; H% 6.54; N% 8.63; Found: C% 63.89; H% 6.39; N% 8.56.

[388] Step 3: Preparation of (S)-3-[4-(4-morpholin-4-ylmethyl-benzyloxy)-1-oxo- 1 , 3-dihydro-isoindol-2-yl]-piperidine-2,6-dione

To the THF solution of (S)-methyl 5-amino-4-(4-(4-(morpholinomethyl)benzyloxy)-1-oxoisoindolin-2-yl)-5-oxopentanoate (45 g, 93 mmol) was added potassium 2-methylpropan-2-olate (10.49 g, 93 mmol) portion wise (2g X5) at -78 °C. The mixture was stirred at this temperature for 30 min then was added 250 mL of 1N HCl solution followed by 200 mL of saturated NaHCO3 solution. The mixture was extracted with CH2Cl2 (150 mLx2). The organic layer was washed with water (50 mL × 3) and brine (100 mL), concentrated on rota-vap to give a white solid, which was then recrystallized from CH3CN

(100 mL) to give (S)-3-[4-(4-morpholin-4-ylmethyl-benzyloxy)-1-oxo-1,3-dihydro-isoindol-2-yl]-piperidine-2,6-dione as white solid (32g, 76%). mp: 140-142 °C. LC-MS m/e= 450. HPLC: Waters Symmetry C18, 5μm, 3.9 x 150 mm, 1 mL/min, 240 nm, isocratic

15/85 CH3CN/0.1% H3PO4 in 5 min,: tR = 5.61 min (99.5%); Chiral AGP C 18 4.0 × 150 mm, 5 μm 10/90 i-propanol/ 10 mM NH4Ac in 20 min,: tR = 10.07 min (99.5%); 1H NMR

(DMSO-d6) δ 2.28 – 2.38 (m, 4H, CH2,CH2), 2.44 (dd, J= 4.2, 13.1 Hz, 1H, CHH), 2.53- 2.63 (m, 1H, CHH), 2.79 – 3 02 (m, 1H, CHH), 3.49 – 3.69 (m, 4H, CH2,CH2), 4.11 – 4.52

(m, 2H, CH2), 5.11 (dd, J= 5.1, 13.2 Hz, 1H, NCH), 5.22 (s, 2H, CH2), 7.33 (d, J= 7.7 Hz,

4H, Ar), 7.40 – 7.52 (m, 3H, Ar), 10.97 (s, ΙΗ, ΝΗ). 13C NMR (DMSO-d6) δ 22.33, 31.18,

45.06, 51.55, 53.11, 62.07, 66.14, 69.38, 114.96, 115.20, 127.61, 128.97, 129.78, 129.93,

133.28, 135.27, 137.67, 153.48, 167.97, 170.95, 172.80. LC-MS: 465; Anal Calcd for

C25H27N3O5 C: 66.80%; H: 6.05%; N: 9.35%. Found: C:66.59%; H:5.79%; N:9.26%.

PAT

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References

References

  1.  “U.S. Prescribing Information” (PDF). Packageinserts.bms.com. Retrieved 18 August 2026.
  2.  Gao, Shaobing; Wang, Shichao; Song, Yongping (December 2020). “Novel immunomodulatory drugs and neo-substrates”. Biomarker Research. 8 (1): 2. doi:10.1186/s40364-020-0182-y. PMC 6953231. PMID 31938543.
  3.  “FDA grants accelerated approval to iberdomide with daratumumab and hyaluronidase-fihj and dexamethasone for multiple myeloma”. U.S. Food and Drug Administration (FDA). 13 August 2026. Retrieved 16 August 2026. Public Domain This article incorporates text from this source, which is in the public domain.
  4.  Ye, Ying; Gaudy, Allison; Schafer, Peter; Thomas, Michael; Weiss, Daniel; Chen, Nianhang; et al. (May 2021). “First-in-Human, Single- and Multiple-Ascending-Dose Studies in Healthy Subjects to Assess Pharmacokinetics, Pharmacodynamics, and Safety/Tolerability of Iberdomide, a Novel Cereblon E3 Ligase Modulator”. Clinical Pharmacology in Drug Development. 10 (5): 471–485. doi:10.1002/cpdd.869. PMC 8246954. PMID 32969202.
  5.  Bjorklund, Chad C.; Kang, Jian; Amatangelo, Michael; Polonskaia, Ann; Katz, Mark; Chiu, Hsiling; et al. (April 2020). “Iberdomide (CC-220) is a potent cereblon E3 ligase modulator with antitumor and immunostimulatory activities in lenalidomide- and pomalidomide-resistant multiple myeloma cells with dysregulated CRBN”. Leukemia. 34 (4): 1197–1201. doi:10.1038/s41375-019-0620-8. ISSN 1476-5551. PMC 7214241. PMID 31719682.
  6.  van de Donk, Niels W.C.J.; Popat, Rakesh; Larsen, Jeremy; Minnema, Monique C.; Jagannath, Sundar; Oriol, Albert; et al. (5 November 2020). “First Results of Iberdomide (IBER; CC-220) in Combination with Dexamethasone (DEX) and Daratumumab (DARA) or Bortezomib (BORT) in Patients with Relapsed/Refractory Multiple Myeloma (RRMM)”. Blood. 136 (Supplement 1): 16–17. doi:10.1182/blood-2020-137743. S2CID 228828103.
  7.  Thieblemont, Catherine; Munoz, Javier; Tucci, Alessandra; Visco, Carlo; Cartron, Guillaume; Corradini, Paolo; et al. (15 November 2022). “Iberdomide (CC-220) Monotherapy or in Combination with an Anti-CD20 Monoclonal Antibody As Effective Therapy in Patients with Relapsed/Refractory Lymphoma: Early Results from a Phase 1/2 Study”. Blood. 140 (Supplement 1): 569–572. doi:10.1182/blood-2022-162559. S2CID 256795199.
  8.  Lonial, Sagar; Amatangelo, Michael; Popat, Rakesh; Minnema, Monique C.; Zonder, Jeffrey A.; Larsen, Jeremy; et al. (13 November 2019). “Translational and Clinical Evidence of a Differentiated Profile for the Novel CELMoD, Iberdomide (CC-220)”. Blood. 134 (Supplement_1): 3119. doi:10.1182/blood-2019-124298. S2CID 209233746.
  9.  Amatangelo, Michael; Bjorklund, Chad C.; Kang, Jian; Polonskaia, Ann; Viswanatha, Sridevi; Thakurta, Anjan (29 November 2018). “Iberdomide (CC-220) Has Synergistic Anti-Tumor and Immunostimulatory Activity Against Multiple Myeloma in Combination with Both Bortezomib and Dexamethasone, or in Combination with Daratumumab in Vitro”. Blood. 132 (Supplement 1): 1935. doi:10.1182/blood-2018-99-113383. S2CID 91382999.
  10.  Lonial, Sagar; Popat, Rakesh; Hulin, Cyrille; Jagannath, Sundar; Oriol, Albert; Richardson, Paul G; et al. (November 2022). “Iberdomide plus dexamethasone in heavily pretreated late-line relapsed or refractory multiple myeloma (CC-220-MM-001): a multicentre, multicohort, open-label, phase 1/2 trial”. The Lancet Haematology. 9 (11): e822–e832. doi:10.1016/S2352-3026(22)00290-3. PMID 36209764. S2CID 252779185.
  11.  Merrill, Joan T.; Werth, Victoria P.; Furie, Richard; van Vollenhoven, Ronald; Dörner, Thomas; Petronijevic, Milan; et al. (17 March 2022). “Phase 2 Trial of Iberdomide in Systemic Lupus Erythematosus”. New England Journal of Medicine. 386 (11): 1034–1045. doi:10.1056/NEJMoa2106535. PMID 35294813. S2CID 247499089.
  12.  Feuerstein, Adam (14 August 2026). “FDA clears Bristol multiple myeloma therapy, marking debut of new drug class”. STAT. Retrieved 14 August 2026.
  13.  World Health Organization (2018). “International nonproprietary names for pharmaceutical substances (INN): recommended INN: list 79”. WHO Drug Information. 32 (1). hdl:10665/330941.
  14.  “U.S. FDA Grants Accelerated Approval to Bristol Myers Squibb’s First CELMoD Therapy Zenbexus, in Combination with Daratumumab and Hyaluronidase-fihj and Dexamethasone (ZDd) for Patients with Multiple Myeloma, as Early as First Relapse”. Bristol Myers Squibb (Press release). 13 August 2026. Retrieved 16 August 2026.

External links

Clinical data
Trade namesZenbexus
Other namesCC-220
AHFS/Drugs.comzenbexus
License dataUS DailyMed: Iberdomide
Routes of
administration
By mouth
Drug classCereblon-modulating protein degrader
ATC codeNone
Legal status
Legal statusUS: ℞-only[1]
Identifiers
IUPAC name
CAS Number1323403-33-3as HCl: 1560678-63-8
PubChem CID67335295as HCl: 72793904
IUPHAR/BPS9618
DrugBankDB12101
ChemSpider52085251
UNII8V66F27X44as HCl: 79L3645KFI
KEGGD11134as HCl: D11135
ChEMBLChEMBL3989927
Chemical and physical data
FormulaC25H27N3O5
Molar mass449.507 g·mol−1
3D model (JSmol)Interactive imageas HCl: Interactive image
SMILES
InChI

////////iberdomide, ANAX LABS, APPROVAL 2026, FDA 2026, Zenbexus, APPROVAL 2026, FDA 2026, Zenbexus, cc-220, cc 220, 8V66F27X44, 79L3645KFI

#iberdomide, #ANAX LABS, #APPROVAL 2026, #FDA 2026, #Zenbexus, #APPROVAL 2026, #FDA 2026, #Zenbexus, #cc-220, #cc 220, #8V66F27X44, #79L3645KFI

Zidesamtinib


Zidesamtinib

CAS 2739829-00-4

MF C22H22FN7O MW419.5 g/mol

(19R)-3-ethyl-16-fluoro-10,19-dimethyl-20-oxa-3,4,9,10,11,23-hexazapentacyclo[19.3.1.02,6.08,12.013,18]pentacosa-1(25),2(6),4,8,11,13(18),14,16,21,23-decaen-22-amine

To treat adults with locally advanced or metastatic ROS1-positive non-small cell lung cancer after receiving a ROS1 kinase inhibitor

FDA 2026, APPROVALS 2026, Jideytro, NVL-520, NUV-520, NU-520, NVL 520, NUV 520, NU 520, MX5KQV5XHC

Zidesamtinib (sold under the brand name Jideytro) is an oral, highly selective, next-generation kinase inhibitor approved by the U.S. Food and Drug Administration (FDA) on July 22, 2026, to treat adults with locally advanced or metastatic ROS1-positive non-small cell lung cancer (NSCLC) who have previously been treated with at least one ROS1 kinase inhibitor. Developed originally by Nuvalent and subsequently acquired by GSK, it represents a major milestone as GSK’s first approved therapeutic targeting lung cancer.

Mechanism of Action

Zidesamtinib functions by targeting and inhibiting the receptor tyrosine kinase c-ros oncogene 1 (ROS1). It is custom-engineered to solve the primary clinical challenges that limit previous therapies:

  • Overcoming Resistance Mutations: It binds tightly to wild-type ROS1 and remains robustly active against a broad array of treatment-emergent point mutants. This includes G2032R (the most common solvent-front resistance mutation), as well as S1986Y/F, L2026M, and D2033N mutations.
  • Blood-Brain Barrier Penetration: It features high central nervous system (CNS) penetrance to effectively treat and control brain metastases, which are frequent in aggressive ROS1-positive cancers.
  • TRK-Sparing Design: Unlike older dual-acting inhibitors, it deliberately avoids inhibiting the structurally similar tropomyosin receptor kinase (TRK) family. This minimizes off-target TRK-related neurological toxicities like severe dizziness and ataxia.

Clinical Trial Outcomes

The FDA approval was heavily supported by data from the ongoing global, single-arm, Phase 1/2 ARROS-1 clinical trial (N=117 heavily pretreated patients):

  • Overall Response: Delivered an Objective Response Rate (ORR) of 44% in patients who had exhausted alternative TKI options.
  • Subgroup Efficacy: Achieved a 51% ORR in patients who had received only one prior ROS1 inhibitor, a 54% ORR in those harboring the G2032R mutation, and an intracranial ORR of 48% for patients with active brain metastases.
  • Durability: Showed prolonged disease control, with a 12-month duration of response (DOR) rate standing at 69%.

Administration and Side Effects

Jideytro is formulated as an oral tablet taken once daily, with or without food. It demonstrates a highly tolerable safety profile, with only a 10% dose reduction rate and a 2% treatment discontinuation rate due to adverse events.

  • Common Adverse Reactions (≥ 15%): Edema (swelling), peripheral neuropathy, constipation, fatigue, and dyspnea (shortness of breath).
  • Warnings & Precautions: Includes risks of mild CNS reactions (dizziness, cognitive alterations), QTc interval prolongation, skeletal fractures, pancreatic toxicity, and interstitial lung disease (ILD)/pneumonitis.

Zidesamtinib, sold under the brand name Jideytro, is an anti-cancer medication used for the treatment of previously treated locally advanced or metastatic ROS1+ non-small cell lung cancer.[1][2][3] It is taken by mouth once daily.[1][2][3]

Medical uses

Indication

Zidesamtinib is a prescription medicine used to treat adults with non-small cell lung cancer that has spread within the chest or other parts of the body and is caused by an abnormal ROS1 gene, and who have received a ROS1 kinase inhibitor.[1][2][3]

Mechanism of action

Zidesamtinib is a kinase inhibitor that works by blocking ROS1, an abnormal protein that drives some lung cancers to grow, including forms that have become resistant to earlier ROS1 treatments.[4] Jideytro also works on the related proteins ALK and TRK. In laboratory and animal studies, Zidesamtinib stopped cancer cells with ROS1 changes from growing and slowed tumor growth, including tumors in the brain.[2]

PAT

Example 5 [US383715659]

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2023056405&_cid=P10-MRYBTX-59205-1

Scheme 3. Synthesis of Compound 1.

[00548] Synthesis of Compound 5. To a reactor was charged THF (10 vol ), water (1 vol ), followed by Compound 6 (850.0 g, 2.68 mol, 1 equiv.) and Compound 7 (534.0 g, 3.22 mol, 1.2 equiv ) at 20~30°C. The solids were completely dissolved at 20~30°C while stirring for 15 min and K2CO3 (1.11 kg, 3 equiv.) was added in portions over 10-15 min at 20~30°C. The reaction mixture was fully refdled with nitrogen, and was added Pd(dppf)C12 (78.5 g, 0.04 equiv.) in one portion under nitrogen. The reaction mixture was fully refdled with nitrogen again, then heated to 60-65 °C and stirred at 60~65°C for 16 h under nitrogen. The reaction mixture was cooled to 20~30°C, fdtered through a 10 cm celite pad (2X, 2.4 kg celite). The combined fdtrates were washed with EtOAc (10 vol., 21 L) and separated. The organic phase was washed with water (5 vol., 10.5 L) and separated. The organic phase was stirred for 1 h at 40-45°C in 5 w% aqueous L-cysteine (2.0 eq., 1.61 kg in 30.6 kg water) and separated. The organic phase was washed with water (5 vol., 10.5 L) and separated. The resulting organic phase was concentrated at 45-50°C in vacuum to afford crude product as a light brown oil (2.28 kg). To the crude product was charged MTBE (228 mL, 0.1 vol. relative to crude product), heated to 50°C over 15 min, followed by isopropyl ether (2.28 L, 1 vol.) dropwise over 1 h at 45~50°C, then cooled to 10°C over 2 h. A large amount of solids came out and the resulting slurry was stirred for 2 h at 10-15°C. The solids were collected by fdtration, dried in oven at 45°C for 16 h to get crude Compound 5 as a pale-yellow solid (1.67 kg, 96.3% /220 nm, >99.9%/220 nm chiral purity). 1.67 kg of crude Compound 5 was purified by silica gel chromatography (EtOAc/ n-heptane=l: 1, 2.5X silica gel, 100-200 meshes) to get Compound 5 as an off-white solid (1.58 kg, 99.6%/220 nm, >99.9%/220 nm chiral purity, 97.9 w%, 72% yield). H NMR (400 MHz, DMSO) 5 7.44 (dd, J = 10.5, 2.5

Hz, 1H), 7.36 (s, 1H), 7.22 (dd, J = 8.3, 6.0 Hz, 1H), 7.16 – 7.08 (m, 2H), 5.25 (d, J = 4.2 Hz, 1H), 4.86 – 4.68 (m, 1H), 4.14 (s, 3H), 4.00 (q, J = 7.2 Hz, 2H), 3.72 (s, 2H), 1.27 (t, J = 7.3 Hz, 3H), 1.11 (d, J = 6.3 Hz, 3H). MS (ESI, m/z): 330.20 (M + H)+.

[00549] In another example, a similar procedure was run in a 0.5:2 biphasic mixture of toluene and water (2.5 vol.) with a catalystic amount (e.g. 0.002 mol equiv.) Pd(Amphos)C12 (instead of 0.04 mol equiv. of PdidppfhCE) used as the catalyst. Potassium phosphate (K3PO4 3 H2O) substituted potassium carbonate (K2CO3) 3.0 mol equiv. as the base, and the amount of Compound 7 employed was 1.02 mol equiv. The improved process was conducted at 50 °C. At the end of the reaction, the organic layer was fdtered and treated with activated carbon and concentrated, and the final material was crystallized from toluene/heptane/water to give Compound 5 in 92% yield and 99.9% purity.

[00550] Synthesis of Compound 3. To a 50 L reactor was charged dichloromethane (11.25 L), Compound 5 (750 g, >99.9%/220 nm chiral purity) and triethylamine (920.0 g) at r t. (20~30°C). The resulting mixture was refilled with nitrogen and cooled to 0°C. To it was added a solution of MS2O (793.0 g) in dichloromethane (3.75 L) drop-wise over 45 min while keeping the temperature at 0~5°C. The reaction mixture was stirred at 0~5°C for 1 h under nitrogen. The reaction mixture was quenched with cooled water (7.5 L) at 5~15°C and separated. The organic phase was washed with cooled water (3.75 L) and separated. The organic phase was dried over anhydrous Na2SC>4, filtered and concentrated at 25~30°C in vacuum to around 2 vol., then switched to n-heptane (2.25 L) and concentrated at 25~30°C in vacuum to around 2 vol. of Compound 3 in n-heptane. n-heptane /EtOAc (3.0 L, lOv/lv) was added to the above mixture and the mixture was slurried for 1 h at 0~10°C under nitrogen and filtered. The filter cake was washed with n-heptane (1.5 L), dried in vacuum at 25~30°C for 5 h to afford Compound 3 as an off-white solid (845 g, 98.9 w%, 99.98%/220 nm chiral purity, 91% yield). H NMR (400 MHz, CDC13) 5 7.35 (dd, J = 9.6, 2.5 Hz, 1H), 7.24 – 7.18 (m, 2H), 7.12 (s, 1H), 7.08 (td, J = 8.3, 2.6 Hz, 1H), 5.78 (d, J = 6.4 Hz, 1H), 4.21 (s, 3H), 4.05 (q, J = 7.3 Hz, 2H), 3.90 – 3.76 (m, 2H), 2.78 (s, 3H), 1.58 (d, J = 6.5 Hz, 3H), 1.40 (t, J = 7.3 Hz, 3H). MS (ESI, m/z): 408.20 (M + H)+.

[00551] In another example, triethylamine base (1.3 mol equiv.), MS2O (1.2 mol equiv.), and dichloromethane solvent (10 vol) were used. The reaction mixture was quenched with aqueous sodium bicarbonate to remove excess MS2O, and crystallization from dichloromenthane/hexane results in 98% yield with 100% purity of Compound 3.

[00552] Synthesis of Compound 2. A 20 L reactor was refilled with nitrogen, then charged with DMA (12.6 L) at r.t. (20~25°C) To the reactor was charged Compound 4 (390.0 g) and Compound 3 (840.0 g, 99.98%/220 nm chiral purity) in one portion at 20~25°C through a dry nitrogen flow. The reaction mixture was heated to 35°C over 15 min and stirred for 5-10 min at 35~40°C to get a clear solution. To the reaction mixture was charged powder K3PO4 (875.0 g) in one portion at 35~45°C. After complete addition, the resulting mixture was heated to 60°C over 20 min and stirred at 58~63°C for 1.5 h through a dry nitrogen flow. The reaction mixture was cooled to 25~30°C, filtered through a celite pad (5 cm, 1.5 kg) and rinsed the filter cake with EtOAc (2 L, 2-3 vol.). The filtrate was poured into water (16.8 L, 20 vol.) at 0-10°C, extracted with EtOAc (10 L, 12 vol.) and separated. The aqueous phase was extracted with EtOAc (5 L, 6 vol.). The combined organic phases were washed with water (5 L*3, 6 vol. *3), concentrated at 50°C in vacuum to afford crude product as a gray solid (956 g). The crude product was dissolved in EtOAc (950 mL, 1 vol. relative to crude product) at 35~40°C, then was added dropwise n-heptane (950 mL, 1 vol. relative to crude product) at 30~40°C over 20 min. The resulting mixture was cooled to 20~25°C over 30 min and stirred for 1 h at 30-40°C. Some solids came out slowly and n-heptane (1.9 L, 2 vol. relative to crude product) was added dropwise to the slurry mixture at 20~25°C over 30 min. The precipitates were stirred at 15~20°C for 3 h and filtered. The filter cake was washed with n-heptane (1.5 L) and dried in oven at 45-50°C for 16 h to afford Compound 2 as a pale-yellow solid (743 g, 98.6%/220 nm, 96.9 w%, 99.98%/220 nm chiral purity, 0.48%KF, 72% yield). H NMR (400 MHz, DMSO) 5 7.54 (dd, J = 10.2, 2.7 Hz, 1H), 7.51 (d, J = 1.9 Hz, 1H), 7.42 (s, 1H), 7.31 (dd, J = 8.5, 5.8 Hz, 1H), 7.22 (td, J = 8.4, 2.7 Hz, 1H), 7.17 (s, 1H), 6.92 (d, J = 1.8 Hz, 1H), 6.14 (s, 2H), 5.47 (q, J = 6.0 Hz, 1H), 4.22 (s, 3H), 4.02 (q, J = 7.3 Hz, 2H), 3.78 (q, J = 16.1 Hz, 2H), 1.40 (d, J = 6.3 Hz, 3H), 1.29 (t, J = 7.3 Hz, 3H). MS (ESI, m/z): 500.30 (M + H)+.

[00553] In another example, a process was developed where Compound 4 (1.1 mol equiv. to Compound 3) was used. Potassium phosphate base (K2PO4, 4. 1 mol equiv.) and DMA (16 vol.) were substituted with cesium carbonate (CS2CO3, 2.2 mol equiv.) and NMP (5.6 vol.). The reaction was carried out at 20~30°C. Following completion of the reaction, the crude product was precipitated with water. The material was then dissolved in ethyl acetate, washed with water, and treated with activated carbon. The product is subsequently crystallized from toluene/ethyl acetate/heptane to give Compound 2 in 80% yield and 99.9% purity.

[00554] Synthesis of Compound 1. To a reactor was charged t-AmOH (20 vol.), Compound 2 (700.0 g, 99.99% chiral purity) and potassium pivalate (588.0 g). The reaction mixture was fully refilled with nitrogen. To the reaction mixture was added cataCXium A (120.4 g) and Pd(OAc)2 (37.8 g) at r.t. under nitrogen. The resulting mixture was heated to 100°C and stirred for 18 h under nitrogen. The reaction mixture was cooled to 30°C , filtered through a celite pad and washed the filter cake with EtOAc (3 vol.). The filtrate was washed with water (5 vol. *2) and separated. The upper organic phase was concentrated in vacuum to afford a brown oil. The oil was dissolved in EtOAc (27 L) then added 5w% aqueous L-cysteine (0.98 kg in 18.6 kg water), stirred for 1 h at 40~45°C and separated. The organic phase was washed with water (6.75 L) and separated. 5w% aqueous L-cysteine (0.98 kg in 18.6 kg water) was charged to the above organic phase, stirred for 1 h at 40~45°C and separated. The organic phase was washed with water (6.75 L.) and separated. The organic phase was concentrated in vacuum at 45~50°C to afford a brown solid (1.12 kg). The crude solid (1.12 kg) was further purified by silica gel chromatography eluted with EtOAc/DCM (dry loading, 3X, 100-200 meshes, EtOAc:DCM=l : 1) to afford a pale-yellow solid ( 1.02 kg). The solid was dissolved in EtOAc (600 mL, 2 vol.) at 50~60°C, then was added n-heptane (1.8 L, 6 vol.) dropwise over 50 min at 50~60°C. A large of solids came out during addition. The resulting slurry was cooled to 15~20°C over 50 min and stirred for 30 min at 15~20°C. The slurry was concentrated in vacuum at 45~50°C to 2-3 vol. mixture, n-heptane (1.2 L, 4 vol.) was added to the

above mixture (2-3 vol.), concentrated in vacuum at 45~50°C to 2-3 vol. mixture. The mixture was cooled to 10~15°C over 2 h, stirred at 10~15°C for 1 h and filtered. The filtered cake was rinsed with n-heptane (600 mb) and dried in vacuum at 50°C for 20 h to afford Form 1 of Compound 1 as an off-white solid (280 g, 99.0%). H NMR (400 MHz, DMSO) 57.79 (dd, J = 10.3, 2.2 Hz, 1H), 7.58 (s, 1H), 7.43 (d, J = 1.8 Hz, 1H), 7.24 – 7.16 (m, 2H), 6.13 (s, 2H), 6.08 (d, J = 1.7 Hz, 1H), 5.31 – 5.23 (m, 1H), 4.16 (s, 3H), 4.05 – 3.94 (m, 2H), 3.78 (d, J = 15.6 Hz, 1H), 2.98 (d, J = 15.5 Hz, 1H), 1.71 (d, J = 6.2 Hz, 3H), 1.26 (t, J = 7.2 Hz, 3H). MS (ESI, m/z): 420.30 (M + H)+. XRPD (FIG. 1), TG/DTA (FIG. 2), DSC (FIG. 3), DVS (FIG. 4), and FT-IR (FIG. 5) results for a sample of Form 1 were obtained.

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References

References

  1.  “JIDEYTRO™ (zidesamtinib) for Patients”. Jideytro. 2026-02-05. Retrieved 2026-07-23.
  2.  “Jideytro: Uses, Dosage, Side Effects & Warnings”. Drugs.com. Retrieved 2026-07-23.
  3.  “Nuvalent Announces FDA Acceptance of New Drug Application for Zidesamtinib for the Treatment of TKI Pre-treated Patients with Advanced ROS1-positive NSCLC”. Nuvalent Investors. Retrieved 2026-07-23.
  4.  Wespiser M, Gille R, Pérol M (2026). “ROS1-positive non-small cell lung cancer: from genomics to treatment decisions”. Frontiers in Oncology. 16 1739598. doi:10.3389/fonc.2026.1739598. PMC 12907153. PMID 41704605.
  5.  “New FDA Drug Approvals for 2026”. Drugs.com. Retrieved 2026-07-23.
  6.  Center for Drug Evaluation and Research (2026-07-22). “Novel Drug Approvals for 2026”. FDA.

PAT

Clinical data
Pronunciationjih-DAY-troh[1][2]
Trade namesJideytro
Other namesNUV-520; NVL 520
AHFS/Drugs.comjideytro
Routes of
administration
By mouth
Drug classTyrosine kinase inhibitor
Legal status
Legal statusUS: ℞-only
Identifiers
IUPAC name
CAS Number2739829-00-4
PubChem CID166560233
IUPHAR/BPS12392
DrugBankDB21623
ChemSpider128922073
UNIIMX5KQV5XHC
KEGGD12899
ChEBICHEBI:747901
ChEMBLChEMBL5314497
Chemical and physical data
FormulaC22H22FN7O
Molar mass419.464 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

////////zidesamtinib, anax labs, CANCER, FDA 2026, APPROVALS 2026, Jideytro, NVL-520, NUV-520, NU-520, NVL 520, NUV 520, NU 520, MX5KQV5XHC

#zidesamtinib, #anax labs, #CANCER, FDA 2026, #APPROVALS 2026, #Jideytro, #NVL-520, #NUV-520, #NU-520, #NVL 520, #NUV 520, #NU 520, #MX5KQV5XHC

Gedatolisib


Gedatolisib

Approvals 3026, FDA 2026, 7/14/2026, Revtorpyk

PF-05212384; PF-5212384; PKI-587
CAS 1197160-78-3
Chemical Formula: C32H41N9O4
Molecular Weight: 615.72
1-(4-{[4-(Dimethylamino)-1-piperidinyl]carbonyl}phenyl)-3-{4-[4,6-di(4-morpholinyl)-1,3,5-triazin-2-yl]phenyl}urea
3-{4-[bis(morpholin-4-yl)-1,3,5-triazin-2-yl]phenyl}-1-{4-[4-(dimethylamino)piperidine-1-carbonyl]phenyl}urea
N-[4-[[4-(Dimethylamino)-1-piperidinyl]carbonyl]phenyl]-N’-[4-[4,6-di(4-morpholinyl)-1,3,5-triazin-2-yl]phenyl]urea
гедатолисиб [Russian] [INN]
غيداتوليسيب [Arabic] [INN]
吉达利塞 [Chinese] [INN]

1-(4-(4-(Dimethylamino)piperidine-1-carbonyl)phenyl)-3-(4-(4,6-dimorpholino-1,3,5-triazin-2-yl)phenyl)urea

Urea, N-[4-[[4-(dimethylamino)-1-piperidinyl]carbonyl]phenyl]-N’-[4-(4,6-di-4-morpholinyl-1,3,5-triazin-2-yl)phenyl]-

96265TNH2R

In combination with fulvestran, to treat hormone receptor-positive, human epidermal growth factor receptor 2-negative, locally advanced or metastatic breast cancer without a PIK3CA mutation detected following progression on or after treatment with at least one line of endocrine therapy in the metastatic setting

Gedatolisib, sold under the brand name Revtorpyk, is an anti-cancer drug used for the treatment of breast cancer.[1] It is under development by Celcuity, Inc. Gedatolisib is a kinase inhibitor.[1] The mechanism of action is accomplished by binding the different p110 catalytic subunit isoforms of PI3K and the kinase site of mTOR.[2] Gedatolisib is administered by intravenous infusion.[1]

Gedatolisib was approved for medical use in the United States in July 2026.[1][3]

Medical uses

Gedatolisib is indicated in combination with fulvestrant, with or without palbociclib, for the treatment of adults with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative locally advanced or metastatic breast cancer without a PIK3CA mutation detected following progression on or after treatment with at least one line of endocrine therapy in the metastatic setting.[1]

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=US42900900&_cid=P22-MRVGV9-51327-1

Example 76

Preparation of 1-(4-(4-(dimethylamino)piperidine-1-carbonyl)phenyl)-3-(4-(4,6-dimorpholino-1,3,5-triazin-2-yl)phenyl)urea

      To the solution of 4-(3-(4-(4,6-dimorpholino-1,3,5-triazin-2-yl)phenyl)ureido)benzoic acid (50 mg; 0.099 mmol), Hunig’s base (103 μL, 0.594 mmol), HBTU (188 mg, 0.495 mmol) in 2 mL of NMP was reacted according to example 68 with N,N-dimethylpiperidin-4-amine (51 mg, 0.396 mmol). Evaporated the solvent and purified by HPLC to give the product (30.6 mg, 52% yield); MS (ESI) m/z=616.7.

PATENT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2010096619&_cid=P22-MRVGV9-51327-1

Scheme 1

Preparation of 1-(4-(4-(dimethylamino) piperidine-1-carbonyl)phenyl-3-(4-(4,6- dimorpholino-1 ,3,5-triazine-2-yl)phenyl) urea (9)

To a slurry of 4-(3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2- yl)phenyl)ureido)benzoic acid (7, 45.5 g, 0.09 mol) in dry THF (1.6 L) heated to 50 0C was added N,N’-carbonyl diimidazole (28 g, 0.17 mol). The reaction mixture was heated for 2 hours and followed by dimethylaminopiperidine (8, 23.5 g, 0.18 mol) and stirred at 53 0C for 16 hours. The reaction mixture was cooled to the room temperature and filtered. The cake was washed with 2-propanol and air-dried to give 97 % pure white powder in 88% yield (49.2 g, 0.08 mol). To the solids stirred in dimethyl acetamide (DMAC, 165 ml) at 70° C for 1 hour was added 2-propanol (640 ml) and the mixture was stirred at 65 0C for additional 1 hour. The solids were filtered, washed with 2-propanol and dried in a vacuum oven at 700C for 16 hour to give crystalline white powder (45 g) with >99% purity. The above-mentioned work up process and crystallization procedure gave a Pd residue of 20 ppm. Alternate procedures for the formation of 1-(4-(4-(dimethylamino) piperidine-1 – carbonyl)phenyl-3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2-yl)phenyl) urea (9)

To the solution of 4-(4,6-dimorpholin-4-yl-1 ,3,5-triazin-2-yl) aniline (4, 18 g, 0.052 mol) in dichloromethane (300 ml) was added methyl 4-isocyanato benzoate (5, 10.5 g, 0.061 mol) and the reaction mixture was stirred for 5 hours. The separated solids were filtered, washed with ether and air dried to give beige solids (21 g, 0.04 mol). Yield 77%. 90 % pure by HPLC; Mass: 520.1 (M+H). Preparation of 4-(3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2-yl)phenyl)ureido) benzoic acid (7)

The mixture of methyl 4-(3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2-yl)ureido)benzoate (6, 21 g, 0.04mol) and lithium hydroxide monohydrate (3.8 g, 0.09 mol) in THF (120 ml), MeOH (60 ml), and water (60 ml) was heated at 80 0C for 3 hours. The dark brown solution was cooled to room temperature and made acidic with concentrated HCI. The solids were filtered, washed with water, washed with acetone , washed with ether, and dried in a vacuum oven at 60 0C for 48 hours to give off white solids of 4-(3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2-yl)phenyl)ureido) benzoic acid (19.2 g, 0.038 mol). Mass: 506.3 (M+H)+; Yield.94%. 1 -(4-(4-(dimethylamino) piperidine-1 -carbonyl)phenyl-3-(4-(4,6-dimorpholino- 1 ,3,5-triazine-2-yl)phenyl) urea (9)

The suspension of 4-(3-(4-(4,6-dimorpholino-1 ,3,5-triazine-2-yl)phenyl)ureido) benzoic acid (7, 17 g, 33.66 mmol) and N-(3-dimethylaminopropyl)ethyl carbodiimide hydrochloride (9.5 g, 49.5 mmol) in THF (200 ml) and acetonitrile (50 ml) was stirred for 10 min and followed by addition of 1-hydroxybenzotriazole hydrate (6.4 g, 47.88 mmol). The reaction mixture was stirred for 30 min and 4-dimethylaminopiperidine (8, 8.86 g, 69.2 mmol) was added by drops. After being stirred for additional 16 hours, the reaction mixture was concentrated to min. The solids were filtered and washed thoroughly with water (very fine suspension). The cake was slurred in hot ethanol, filtered and dried in a vacuum oven at 68 0C for 16 hours to give off white solids (10.3 g, 16.77 mmol). M. p. 238-240 0C. 99 % pure. Mass: 616.3 (M+H)+; Yield 50 %.

PATENT

WO 2009143317

WO 2010096619

WO 2012148540

WO 2014151147

PATENT

US 20170119778

PAPER

Journal of Medicinal Chemistry (2010), 53(6), 2636-2645

http://pubs.acs.org/doi/abs/10.1021/jm901830p

J. Med. Chem., 2010, 53 (6), pp 2636–2645

DOI: 10.1021/jm901830p

Abstract

The PI3K/Akt signaling pathway is a key pathway in cell proliferation, growth, survival, protein synthesis, and glucose metabolism. It has been recognized recently that inhibiting this pathway might provide a viable therapy for cancer. A series of bis(morpholino-1,3,5-triazine) derivatives were prepared and optimized to provide the highly efficacious PI3K/mTOR inhibitor 1-(4-{[4-(dimethylamino)piperidin-1-yl]carbonyl}phenyl)-3-[4-(4,6-dimorpholin-4-yl-1,3,5-triazin-2-yl)phenyl]urea 26 (PKI-587). Compound 26 has shown excellent activity in vitro and in vivo, with antitumor efficacy in both subcutaneous and orthotopic xenograft tumor models when administered intravenously. The structure−activity relationships and the in vitro and in vivo activity of analogues in this series are described.

Preparation of 1-(4-{[4-(Dimethylamino)piperidin-1-yl]carbonyl}phenyl)-3-[4-(4,6-dimorpholin-4- yl-1,3,5-triazin-2-yl)phenyl]urea (26)

MS (ESI) m/z = 616.7. HRMS: calcd for C32H41N9O4 + H+, 616.335 43; found (ESI-FTMS, [M + H]+), 616.334 24. Purity by analytical HPLC 99.3%. (Prodigy ODS3, 0.46 cm × 15 cm, 20 min gradient acetonitrile in water, trifluoroacetic acid, detector wavelengths, 215 and 254 nm.) 1H NMR (DMSO-d6) δ 1.29−1.36 (m, 6H), 2.6 (m, 4H), 2.9 (m,1H), 3.3 (m, 4H), 3.6 (m, 8H), 3.7 (m, 8H), 7.3 (d, J = 8.3 Hz, 2H), 7.51−7.57 (m, 4H), 8.3 (d, J = 8.3 Hz 2H), 8.9 (s, 1H), 9.0 (s, 1H) ppm. Anal. Calcd for C32H41N9O4: C 62.42%, H 6.71%, N 20.47%. Found: C 62.34%, H 6.67%, N 20.39%.

PAPER

Bioorganic & Medicinal Chemistry Letters (2011), 21(16), 4773-4778.

http://www.sciencedirect.com/science/article/pii/S0960894X11008468

PAPER

New and Practical Synthesis of Gedatolisib

http://pubs.acs.org/doi/10.1021/acs.oprd.7b00298

Org. Process Res. Dev., Article ASAP

DOI: 10.1021/acs.oprd.7b00298

Abstract

A new, practical, and convergent synthetic route of gedatolisib, an antitumor agent, is developed on a hectogram scale which avoids the Pd coupling method. The key step is adopting 6-(4-nitrophenyl)-1,3,5-triazine-2,4-diamine and 2,2′-dichlorodiethyl ether to prepare the key 4,4′-(6-(4-nitrophenyl)-1,3,5-triazine-2,4-diyl)dimorpholine in 77% yield and 98.8% purity. Gedatolisib is obtained in 48.6% yield over five simple steps and 99.3% purity (HPLC). Purification methods of the intermediates and the final product involved in the route are given.

off-white solid. 1H NMR (400 MHz, DMSO-d6): δ 1.46 (brs, 2H), 1.89 (brs, 2H), 2.29 (s, 6H), 2.94 (brs, 2H), 3.76 (m, 8H), 3.89 (m, 8H), 7.09 (d, J = 8.4 Hz, 2H), 7.20 (d, J = 8.4 Hz, 2H), 7.50 (d, J = 8.7 Hz, 2H), 8.28 (s, 1H), 8.31 (d, J = 8.6 Hz, 2H), 8.48 (s, 1H). ESI-MS (m/z) 615.9 (M + H). HPLC conditions: Column: Agilent Eclipse XDB-C18 (250 mm × 4.6 mm × 5 μm); Detection: 254 nm; Flow rate: 0.8 mL/min; Temperature: 30 °C; Injection load: 1 μL; Solvent: MeOH; Concentration: 0.5 mg/mL; Run time: 20 min; Mobile phase A: water; Mobile phase B: MeOH/TEA = 100:0.1; Gradient program: time (min): 20; % of mobile phase A: 10; % of mobile phase B: 90; tR = 2.598 min, purity: 99.34%

  • Zhao, X.; Tan, Q.; Zhang, Z.; Zhao, Y. Med. Chem. Res. 2014, 23, 5188– 5196 DOI: 10.1007/s00044-014-1084-z
  • Khafizova, G.; Potoski, J. R. PCT Int. Appl. WO 2010096619, 2010.
  • Venkatesan, A. M.; Chen, Z.; Dehnhardt, C. M.; Dos Santos, O.; Delos Santos, E. G.; Zask, A.; Verheijen, J. C.; Kaplan, J. A.; Richard, D. J.; Ayral-Kaloustian, S.; Mansour, T. S.; Gopalsamy, A.; Curran, K. J.; Shi, M. PCT Int. Appl. WO 2009143317, 2009.

REFERENCES

1: Gedaly R, Galuppo R, Musgrave Y, Angulo P, Hundley J, Shah M, Daily MF, Chen C, Cohen DA, Spear BT, Evers BM. PKI-587 and sorafenib alone and in combination on inhibition of liver cancer stem cell proliferation. J Surg Res. 2013 Nov;185(1):225-30. doi: 10.1016/j.jss.2013.05.016. Epub 2013 May 25. PubMed PMID: 23769634.

2: Gedaly R, Angulo P, Hundley J, Daily MF, Chen C, Evers BM. PKI-587 and sorafenib targeting PI3K/AKT/mTOR and Ras/Raf/MAPK pathways synergistically inhibit HCC cell proliferation. J Surg Res. 2012 Aug;176(2):542-8. doi: 10.1016/j.jss.2011.10.045. Epub 2011 Nov 21. PubMed PMID: 22261591.

3: Dehnhardt CM, Venkatesan AM, Chen Z, Delos-Santos E, Ayral-Kaloustian S, Brooijmans N, Yu K, Hollander I, Feldberg L, Lucas J, Mallon R. Identification of 2-oxatriazines as highly potent pan-PI3K/mTOR dual inhibitors. Bioorg Med Chem Lett. 2011 Aug 15;21(16):4773-8. doi: 10.1016/j.bmcl.2011.06.063. Epub 2011 Jun 21. PubMed PMID: 21763134.

4: Mallon R, Feldberg LR, Lucas J, Chaudhary I, Dehnhardt C, Santos ED, Chen Z, dos Santos O, Ayral-Kaloustian S, Venkatesan A, Hollander I. Antitumor efficacy of PKI-587, a highly potent dual PI3K/mTOR kinase inhibitor. Clin Cancer Res. 2011 May 15;17(10):3193-203. doi: 10.1158/1078-0432.CCR-10-1694. Epub 2011 Feb 15. PubMed PMID: 21325073.

5: Venkatesan AM, Chen Z, dos Santos O, Dehnhardt C, Santos ED, Ayral-Kaloustian S, Mallon R, Hollander I, Feldberg L, Lucas J, Yu K, Chaudhary I, Mansour TS. PKI-179: an orally efficacious dual phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) inhibitor. Bioorg Med Chem Lett. 2010 Oct 1;20(19):5869-73. doi: 10.1016/j.bmcl.2010.07.104. Epub 2010 Jul 30. PubMed PMID: 20797855.

6: Venkatesan AM, Dehnhardt CM, Delos Santos E, Chen Z, Dos Santos O, Ayral-Kaloustian S, Khafizova G, Brooijmans N, Mallon R, Hollander I, Feldberg L, Lucas J, Yu K, Gibbons J, Abraham RT, Chaudhary I, Mansour TS. Bis(morpholino-1,3,5-triazine) derivatives: potent adenosine 5′-triphosphate competitive phosphatidylinositol-3-kinase/mammalian target of rapamycin inhibitors: discovery of compound 26 (PKI-587), a highly efficacious dual inhibitor. J Med Chem. 2010 Mar 25;53(6):2636-45. doi: 10.1021/jm901830p. PubMed PMID: 20166697.

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References

References

  1.  https://celcuity.com/revtorpyk/REVTORPYK_PI_2026.pdf
  2.  Dehnhardt CM, Venkatesan AM, Chen Z, Delos-Santos E, Ayral-Kaloustian S, Brooijmans N, et al. (August 2011). “Identification of 2-oxatriazines as highly potent pan-PI3K/mTOR dual inhibitors”. Bioorganic & Medicinal Chemistry Letters. 21 (16): 4773–8. doi:10.1016/j.bmcl.2011.06.063. PMID 21763134.
  3.  “FDA approves gedatolisib with fulvestrant, with or without palbociclib, for HR-positive, HER2-negative locally advanced or metastatic breast cancer”. U.S. Food and Drug Administration (FDA). 14 July 2026. Retrieved 20 July 2026. Public Domain This article incorporates text from this source, which is in the public domain.
  4.  Sabatini DM (November 2017). “Twenty-five years of mTOR: Uncovering the link from nutrients to growth”. Proceedings of the National Academy of Sciences of the United States of America. 114 (45): 11818–11825. Bibcode:2017PNAS..11411818S. doi:10.1073/pnas.1716173114. PMC 5692607. PMID 29078414.
  5.  Tian T, Li X, Zhang J (February 2019). “mTOR Signaling in Cancer and mTOR Inhibitors in Solid Tumor Targeting Therapy”. International Journal of Molecular Sciences. 20 (3): 755. doi:10.3390/ijms20030755. PMC 6387042. PMID 30754640.
  6.  Hua H, Kong Q, Zhang H, Wang J, Luo T, Jiang Y (July 2019). “Targeting mTOR for cancer therapy”. Journal of Hematology & Oncology. 12 (1) 71. doi:10.1186/s13045-019-0754-1. PMC 6612215. PMID 31277692.
  7.  Vanhaesebroeck B, Perry MW, Brown JR, André F, Okkenhaug K (October 2021). “PI3K inhibitors are finally coming of age”. Nature Reviews. Drug Discovery. 20 (10): 741–769. doi:10.1038/s41573-021-00209-1. PMC 9297732. PMID 34127844. S2CID 235437841.
  8.  Millis SZ, Ikeda S, Reddy S, Gatalica Z, Kurzrock R (December 2016). “Landscape of Phosphatidylinositol-3-Kinase Pathway Alterations Across 19 784 Diverse Solid Tumors”. JAMA Oncology. 2 (12): 1565–1573. doi:10.1001/jamaoncol.2016.0891. PMID 27388585.
  9.  Anderson EJ, Mollon LE, Dean JL, Warholak TL, Aizer A, Platt EA, et al. (2020). “A Systematic Review of the Prevalence and Diagnostic Workup of PIK3CA Mutations in HR+/HER2- Metastatic Breast Cancer”. International Journal of Breast Cancer. 2020 3759179. doi:10.1155/2020/3759179. PMC 7322582. PMID 32637176.
  10.  Clinical trial number NCT01420081 for “A Study Of Two Dual PI3K/mTOR Inhibitors, PF-04691502 And PF-05212384 In Patients With Recurrent Endometrial Cancer” at ClinicalTrials.gov
  11.  Clinical trial number NCT01925274 for “A Study Of PF-05212384 Plus Irinotecan Vs Cetuximab Plus Irinotecan In Patients With KRAS And NRAS Wild Type Metastatic Colorectal Cancer” at ClinicalTrials.gov
  12.  Clinical trial number NCT02438761 for “PF-05212384 (PKI-587) for t-AML/MDS or de Novo Relapsed or Refractory Acute Myeloid Leukemia (AML)” at ClinicalTrials.gov
  13.  Clinical trial number NCT03698383 for “Phase II Study of Herzuma® Plus Gedatolisib in Patients With HER-2 Positive Metastatic Breast Cancer” at ClinicalTrials.gov
  14.  Clinical trial number NCT03911973 for “Gedatolisib Plus Talazoparib in Advanced Triple Negative or BRCA1/2 Positive, HER2 Negative Breast Cancers” at ClinicalTrials.gov
  15.  Clinical trial number NCT03065062 for “Study of the CDK4/6 Inhibitor Palbociclib (PD-0332991) in Combination With the PI3K/mTOR Inhibitor Gedatolisib (PF-05212384) for Patients With Advanced Squamous Cell Lung, Pancreatic, Head & Neck and Other Solid Tumors” at ClinicalTrials.gov
  16.  Clinical trial number NCT02626507 for “Phase I Study of Combination of Gedatolisib With Palbociclib and Faslodex in Patients With ER+/HER2- Breast Cancer” at ClinicalTrials.gov
  17.  “Celcuity Announces FDA Approval of Revtorpyk (gedatolisib) for the Treatment of HR+/HER2-, PIK3CA Wild-Type Locally Advanced or Metastatic Breast Cancer” (Press release). Celcuity. 14 July 2026. Retrieved 20 July 2026 – via GlobeNewswire.
  18.  World Health Organization (2015). “International nonproprietary names for pharmaceutical substances (INN): recommended INN: list 73”. WHO Drug Information. 29 (1). hdl:10665/331088.

External links

  • Clinical trial number NCT05501886 for “Gedatolisib Plus Fulvestrant With or Without Palbociclib vs Standard-of-Care for the Treatment of Patients With Advanced or Metastatic HR+/HER2- Breast Cancer (VIKTORIA-1) (VIKTORIA-1)” at ClinicalTrials.gov
Clinical data
Trade namesRevtorpyk
Other namesPF-05212384; PKI-587
AHFS/Drugs.comrevtorpyk
License dataUS DailyMed: Gedatolisib
Routes of
administration
Intravenous infusion
Drug classAntineoplastic
ATC codeNone
Legal status
Legal statusUS: ℞-only[1]
Identifiers
IUPAC name
CAS Number1197160-78-3
PubChem CID44516953
IUPHAR/BPS7940
DrugBankDB11896
ChemSpider24644946
UNII96265TNH2R
KEGGD10635
ChEMBLChEMBL592445
CompTox Dashboard (EPA)DTXSID40152557 Edit this at Wikidata
Chemical and physical data
FormulaC32H41N9O4
Molar mass615.739 g·mol−1
3D model (JSmol)Interactive image
SMILES

/////////Gedatolisib, anax labs, approvals 3026, FDA 2026, PF 05212384, PF 5212384, PKI-587, PF-05212384, PF-5212384, PKI 587, gedatolisib, antitumor agent, PHASE 3, PFIZER, гедатолисиб , غيداتوليسيب , 吉达利塞 , 96265TNH2R

O=C(NC1=CC=C(C2=NC(N3CCOCC3)=NC(N4CCOCC4)=N2)C=C1)NC5=CC=C(C(N6CCC(N(C)C)CC6)=O)C=C5

 Journal of Medicinal Chemistry (2017), 60(17), 7524-7538 PQR 309

#Gedatolisib, #anax labs, #approvals 3026, #FDA 2026, #PF 05212384, #PF 5212384, #PKI-587, #PF-052123842, #PF-5212384; #PKI 587, #gedatolisib, #antitumor agent, #PHASE 3, #PFIZER, #гедатолисиб , #غيداتوليسيب , #吉达利塞 , #96265TNH2R

Gadoquatrane


Gadoquatrane

CAS2048221-65-2MW2579.0 g/mol

FDA 2026, APPROVALS 2026, Ambelvist, OZG7J613HK, BAY-1747846, BAY 1747846

2-[4,10-bis(carboxylatomethyl)-7-[1-oxo-1-[[2-oxo-2-[[3-[[2-[2-[4,7,10-tris(carboxylatomethyl)-1,4,7,10-tetrazacyclododec-1-yl]propanoylamino]acetyl]amino]-2,2-bis[[[2-[2-[4,7,10-tris(carboxylatomethyl)-1,4,7,10-tetrazacyclododec-1-yl]propanoylamino]acetyl]amino]methyl]propyl]amino]ethyl]amino]propan-2-yl]-1,4,7,10-tetrazacyclododec-1-yl]acetate;tetrakis(gadolinium(3+))

TETRAGADOLINIUM (4,10-BIS(CARBOXYLATOMETHYL)-7-(3,6,12,15-TETRAOXO-16-(4,7,10-TRIS-(CARBOXYLATOMETHYL)-1,4,7,10-TETRAAZACYCLODODECAN-1-YL)-9,9-BIS(((((2-(4,7,10-TRIS-(CARBOXYLATOMETHYL)-1,4,7,10-TETRAAZACYCLODODECAN-1-YL)PROPANOYL)AMINO)ACETYL)-AMINO)METHYL)-4,7,11,14-TETRAAZAHEPTADECAN-2-YL)-1,4,7,10-TETRAAZACYCLODODECAN-1-YL)ACETATE

To detect and visualize lesions with abnormal vascularity, in conjunction with MRI

Gadoquatrane (marketed as AMBELVIST®) is a low-dose, macrocyclic gadolinium-based contrast agent (GBCA) developed by Bayer for use in magnetic resonance imaging (MRI). It is designed to enhance the visualization of lesions in the central nervous system (CNS) and other body regions in adult and pediatric patients.

Core Highlights:

  • Lower Gadolinium Exposure: It requires a dose of 0.04 mmol/kg, which results in 60% less gadolinium exposure compared to standard macrocyclic GBCAs.
  • Regulatory Approval: The FDA approved it in June 2026 for use in adults and pediatric patients, including term neonates. It was also approved in Japan in March 2026.
  • Efficacy & Safety: Phase III clinical trials (the QUANTI studies) showed it effectively detects lesions with abnormal vascularity while maintaining an efficacy and safety profile comparable to other standard macrocyclic agents.
  • Structure: Gadoquatrane features a tetrameric, macrocyclic structure that gives it high relaxivity and stability in the body

SYN

https://patents.google.com/patent/US20250114485A1

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PAT

/////////gadoquatrane, anax labs, FDA 2026, APPROVALS 2026, Ambelvist, OZG7J613HK, BAY-1747846, BAY 1747846

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Zidebactam


Zidebactam

FDA 2026, APPROVALS 2026

To treat complicated urinary tract infections, including pyelonephritis, caused by designated susceptible microorganisms

CAS 1436861-97-0, UNII: YPM97423DB, Wockhardt Biopharm, WCK-5107, WCK5107

Molecular Formula, C13-H21-N5-O7-S
Molecular Weight, 391.4029

Disclosed in PCT International Patent Application No. PCT/IB2012/054290D

  • 01 Aug 2015 Phase-I clinical trials in Bacterial infections (In volunteers, Combination therapy) in USA (IV) (NCT02532140)

trans- sulphuric acid mono-[2-(N’-[(R)-piperidin-3-carbonyl]-hydrazinocarbonyl)-7-oxo-l,6-diaza-bicyclo[3.2.1]oct-6-yl] ester

(2S, 5R)-sulphuric acid mono-[2-(N’-[(R)-piperidin-3-carbonyl]-hydrazinocarbonyl)-7-oxo-l,6-diaza-bicyclo[3.2.1]oct-6-yl] ester

(1R,2S,5R)-l,6-Diazabicyclo [3.2.1] octane-2-carboxylic acid, 7-oxo-6-(sulfooxy)-, 2-[2-[(3R)-3-piperidinylcarbonyl]hydrazide]

trans- sulphuric acid mono-[2-(N’-[(R)-piperidin-3-carbonyl]-hydrazinocarbonyl)-7-oxo-l,6-diaza-bicyclo[3.2.1]oct-6-yl] ester

(2S, 5R)-sulphuric acid mono-[2-(N’-[(R)-piperidin-3-carbonyl]-hydrazinocarbonyl)-7-oxo-l,6-diaza-bicyclo[3.2.1]oct-6-yl] ester

(lR,2S,5R)-l,6-Diazabicyclo [3.2.1] octane-2-carboxylic acid, 7-oxo-6-(sulfooxy)-, 2-[2-[(3R)-3 -piperidinylcarbonyl] hydrazide]

1,6-Diazabicyclo(3.2.1)octane-2-carboxylic acid, 7-oxo-6-(sulfooxy)-, 2-(2-((3R)-3-piperidinylcarbonyl)hydrazide), (1R,2S,5R)-


Zidebactam potassium
  cas is  1706777-49-2

Zidebactam (WCK-5107) is an antibiotic adjuvant drug which acts as a beta-lactamase inhibitor, preventing the breakdown of other antibiotic drugs.[1]

PATENT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2019016393&_cid=P20-MPYVFE-00532-1

PATENT

http://www.google.com/patents/WO2013030733A1?cl=en

Figure imgf000022_0001

Scheme-1

Figure imgf000023_0001

Example-2

trans-sulfuric acid mono-r2-(N,-r(R)-piperidin-3-carbonyll-hvdrazinocarbonyl)-7-oxo-l,6- diaza-bicyclo Γ3.2.11 oct-6-νΠ ester

Step-1: Preparation of trans-3-[N’-(6-benzyloxy-7-oxo-l,6-diaza-bicyclo[3.2.1]octane-2-carbonyl)-hydrazinocarbonyl]-(R)-piperidin-l-carboxylic acid tert-butyl ester:

By using the procedure described in Step-1 of Example- 1 above, and by using trans-6-benzyloxy-7-oxo-l,6-diaza-bicyclo[3.2.1]octane-2-carboxylic acid (25 gm, 0.084 mol), N,N-dimethyl formamide (625 ml), EDC hydrochloride (24 gm, 0.126 mol), HOBt (16.96 gm, 0.126 mol), (R)-N-tert-butoxycarbonyl-piperidin-3-carboxylic acid hydrazide (21.40 gm , 0.088 mol) to provide the title compound in 17.0 gm quantity, 41% yield as a white solid.

Analysis: MS (ES+) CzsHasNsOe = 502.1 (M+l);

I^NMR (CDCI3) = 8.40 (br s, IH), 7.34-7.44 (m, 5H), 5.05 (d, IH), 4.90 (d, IH), 4.00 (br d, IH), 3.82 (br s, IH), 3.30 (br s, IH), 3.16-3.21 (m, IH), 3.06 (br d, IH), 2.42 (br s, IH), 2.29-2.34 (m, IH), 1.18-2.02 (m, 4H), 1.60-1.75 (m, 4H), 1.45-1.55 (m, 2H),1.44 (s, 9H).

Step-2: Preparation of trans-3-[N’-(6-hydroxy-7-oxo-l,6-diaza-bicyclo[3.2.1]octane-2-carbonyl)-hydrazinocarbonyl]-(R)-piperidin-l-carboxylic acid tert-butyl ester:

By using the procedure described in Step-2 of Example- 1 above, and by using trans-3-[N ‘ -(6-benzyloxy-7-oxo- 1 ,6-diaza-bicyclo [3.2.1 ]octane-2-carbonyl)-hydrazinocarbonyl] -(R)-piperidin-l-carboxylic acid tert-butyl ester (16.5 gm , 0.033 mol), methanol (170 ml) and 10% palladium on carbon (3.5 gm) to provide the title compound in 13.5 gm quantity as a pale pink solid and it was used for the next reaction immediately.

Analysis: MS (ES+) CiglfeNsOe = 411.1 (M+l);

Step-3: Preparation of tetrabutylammonium salt of trans-3-[N’-(6-sulfooxy-7-oxo-l,6-diaza-bicyclo [3.2.1] octane-2-carbonyl)-hydrazinocarbonyl] -(R)-piperidin- 1 -carboxylic acid tert-butyl ester:

By using the procedure described in Step-3 of Example- 1 above, and by using trans-3-[N’-(6-hydroxy-7-oxo-l,6-diaza-bicyclo[3.2.1]octane-2-carbonyl)-hydrazinocarbonyl]-(R)-piperidin-1 -carboxylic acid tert-butyl ester (13.5 gm , 0.033 mol), pyridine (70 ml) and pyridine sulfur trioxide complex (26.11 gm, 0.164 mol), 0.5 N aqueous potassium dihydrogen

phosphate solution (400 ml) and tetrabutylammonium sulphate (9.74 gm, 0.033 mol) to provide the title compound in 25 gm quantity as a yellowish solid, in quantitative yield.

Analysis: MS (ES-) 
as a salt = 490.0 (M-l) as a free sulfonic acid;

Step-4: trans-sulfuric acid mono-[2-(N’-[(R)-piperidin-3-carbonyl]-hydrazinocarbonyl)-7-oxo-l,6-diaza-bicyclo[3.2.1]oct-6-yl]ester:

By using the procedure described in Step-4 of Example- 1 above, and by using tetrabutylammonium salt of trans-3-[N’-(6-sulfooxy-7-oxo-l,6-diaza-bicyclo[3.2.1]octane-2-carbonyl)-hydrazinocarbonyl]-(R)-piperidin-l-carboxylic acid tert-butyl ester (24 gm , 0.032 mmol), dichloromethane (60 ml) and trifluoroacetic acid (60 ml) to provide the title compound in 10 gm quantity as a white solid, in 79% yield.

Analysis: MS (ES-)= C13H21N5O7S = 390.2 (M-l) as a free sulfonic acid;

HXNMR (DMSO-d6) = 9.97 (d, 2H), 8.32 (br s, 2H), 4.00 (br s, IH), 3.81 (d, IH), 3.10-3.22 (m, 3H), 2.97-3.02 (m, 2H), 2.86-2.91 (m, IH), 2.65-2.66 (m, IH), 1.97-2.03 (m, IH), 1.57-1.88 (m, 7H).

-32.6°, (c 0.5, water).

PATENT

WO 2015110885

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2015110885

PATENT

WO 2014135931

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014135931

Clinical data
License dataUS DailyMed: Zidebactam
Legal status
Legal statusInvestigational
Identifiers
IUPAC name
CAS Number1436861-97-0
PubChem CID77846445
DrugBankDB13090
ChemSpider44209501
UNIIYPM97423DB
ChEMBLChEMBL4533605
Chemical and physical data
FormulaC13H21N5O7S
Molar mass391.40 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

References

  1.  Karvouniaris M, Almyroudi MP, Abdul-Aziz MH, Blot S, Paramythiotou E, Tsigou E, et al. (April 2023). “Novel Antimicrobial Agents for Gram-Negative Pathogens”. Antibiotics. 12 (4). Basel, Switzerland: 761. doi:10.3390/antibiotics12040761. PMC 10135111. PMID 37107124.

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References

///////ZIDEBACTAM, ANAX LABS, FDA 2026, APPROVALS 2026, Cypsedo, WCK-5107, WCK 5107, YPM97423DB

#ZIDEBACTAM, #ANAX LABS, #FDA 2026, #APPROVALS 2026, #Cypsedo, #WCK-5107, #WCK 5107, #YPM97423DB

see………http://apisynthesisint.blogspot.in/2015/11/wck-5107-in-phase-1-from-wockhardt.html

SEE BACTAM SERIES…………..http://apisynthesisint.blogspot.in/p/bactam-series.html

C1C[C@H](CNC1)C(=O)NNC(=O)[C@@H]2CC[C@@H]3C[N@]2C(=O)N3OS(=O)(=O)O

or

O=C(NNC(=O)[C@@H]2CC[C@@H]1CN2C(=O)N1OS(=O)(=O)O)[C@@H]3CCCNC3

C1CC(CNC1)C(=O)NNC(=O)C2CCC3CN2C(=O)N3OS(=O)(=O)[O-].[Na+]

Cipepofol


Cipepofol

CAS1637741-58-2

MW 204.31 g/mol MF C14H20O

2-[(1R)-1-cyclopropylethyl]-6-propan-2-ylphenol

FDA 2026, APPROVALS 2026, Cypsedo, HSK 3486, CS-0064163, GTPL 10812, HSK-3486, HY-116152, M3WGS532VY

  • OriginatorSichuan Haisco Pharmaceutical
  • ClassCyclopropanes; General anaesthetics; Phenols; Small molecules
  • Mechanism of ActionGABA A receptor agonists
  • RegisteredAnaesthesia; Sedation
  • 10 Apr 2026Sichuan Haisco Pharmaceutical plans a phase III trial for Anesthesia (In Children, In adolescents) (IV) in May 2026 (NCT07510945)
  • 28 Aug 2024No recent reports of development identified for preclinical development in Sedation in USA (IV, Infusion)
  • 01 Aug 2024Zhongda Hospital plans a clinical trial for Sedation (IV) in August 2024 (NCT06538883)

To induce general anesthesia in adults undergoing surgery

Cipepofol (also known as ciprofol or HSK3486) is a novel, short-acting intravenous anesthetic and sedative. As a structural analog of propofol, it targets \(GABA_{A}\) receptors but is 4 to 6 times more potent. It offers faster recovery, improved cardiovascular stability, and significantly less injection pain than propofol.

Key Clinical Advantages

  • Superior Efficacy: Requires a lower dose to achieve the same sedative depth as propofol.
  • Better Safety Profile: Associated with a lower incidence of injection pain, reduced respiratory depression, and better hemodynamic (blood pressure) stability.
  • Fast Acting: Characterized by rapid onset and quick recovery times, making it ideal for procedures like gastrointestinal endoscopy, bronchoscopy, and general anesthesia induction.

Recent Developments

  • FDA Approval: Cipepofol (sold under the brand name CYPSEDO) officially received U.S. FDA marketing approval, becoming the first China-originated innovative intravenous anesthetic to enter the global market.
  • Ongoing Trials: Clinical trials and post-marketing studies are actively evaluating its safety in specific populations, such as elderly patients and children.

Cipepofol (INNTooltip International Nonproprietary Name, USANTooltip United States Adopted Name), also known as ciprofol or by its developmental code name HSK3486, is a general anesthetic related to propofol which is used for anesthesia and sedation.[1][2][3][4] The drug is used by intravenous infusion.[1] A short-acting and highly selective γ-aminobutyric acid positive allosteric modulator,[5] ciprofol is 4 to 6 times more potent than other phenol derivatives such as propofol or fospropofol.[6]

In May 2026, cipepofol was approved by the US FDA.[7] Manufactured by Haisco Pharmaceutical Group of Chengdu, Sichuan, China, ciprofol underwentphase I and II trials in Australia and China.[8][9][10] In these early studies, ciprofol was comparable in efficacy to propofol and was associated with fewer adverse events.[4][6][11][12][13][14][15][16][17][18]

Physical properties

Ciprofol is an optically active 2,6-disubstituted alkylphenol with a cyclopropylethyl group incorporated at the second carbon atom. This cyclopropyl group increases the steric effects and introduces stereoselective effects over its anesthetic properties. These properties appear to increase the anesthetic potency of ciprofol, when compared with propofol.[9]

Medical use

Ciprofol is used for the intravenous induction of general anesthesia.[3][4] Studies published in 2022 and 2023 found it was efficacious as a general anesthetic in patients undergoing gynecological surgery[6][11] and kidney transplantation,[19] as well as for endoscopic procedures such as bronchoscopy,[15][20] esophagogastroduodenoscopy and colonoscopy.[21][22]

Ciprofol has also been used for sedation of critically ill patients undergoing mechanical ventilation in the intensive care unit,[23] as well as for the treatment of agitation and delirium in that patient population.[24] When combined with mild therapeutic hypothermia, ciprofol may also be useful as a cerebral protective agent in the setting of cerebral ischemia-reperfusion injury.[25]

Experimental use

In experimental models of isoproterenol-induced myocardial infarction (using mice as subjects), ciprofol appears to protect the heart against oxidative damage, inflammation and apoptosis of cardiac muscle cells.[26]

SYN

US20240132445,

https://patentscope.wipo.int/search/en/detail.jsf?docId=US428011434&_cid=P12-MPW0XO-91017-1

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014180305&_cid=P12-MPW0R4-87054-1

Example 16

[-cyclopropylethyl] -6 -isopropylphenol (compound 16)

2- [(lR)-l-cyclopropylethyl]-6-isopropyl -phenol

Preparation methods of Examples 16-17:

2-(1-Cyclopropylethyl-6-isopropylphenol (compound 3) 600 mg was used for resolution. Preparation conditions: (Instrument: Agilent 1260/CH-Y-J0404; Column: CHIRALPAK OJ-H (4.6 mm < 250 mm, 5 μm) No.: OJ-H-27; Mobile phase: A: isopropanol, B: n-hexane; Flow rate: 1.0 mL/min; Back pressure: 100 bar; Column temperature: 35°C; Wavelength: 210 nm; Period: 10 min)

Two optical isomers were obtained after separation: peak 1 (retention time: 10.72 min, 280 mg, pale yellow liquid, ee%=99%) and peak 2 (retention time: 13.58 min, 280 mg, pale yellow liquid, ee%=99%).

峰 1 : MS m/z(ESI): 203.1(Ml).

toMR (400 MHz,CDCl3 ) : δ 7.14(dd, 1H), δ 7.08(dd, 1H), 6.91 (t, 1H), 4.93 (s, 1H), 3.22-3.14(m, 1H), 2.55-2.48 (m, 1H), 1.33 (d, 6H), 1.28 (d, 3H), 1.10-1.05 (m, 1H), 0.60-0.58 (m, 1H), 0.49-0.46 (m, 1H), 0.25-0.18 (m, 2H).

峰 2: MS m/z(ESI): 203.1(Ml).

iHNMR (400 MHz,CDCl3) : 57.14(dd, 1H), δ 7.08(dd, 1H), 6.93 (t, 1H), 4.93 (s 1H), 3.22-3.15(m, 1H), 2.55-2.48 (m, 1H), 1.32 (d, 6H), 1.28 (d, 3H), 1.10-1.04 (m, 1H), 0.60-0.58 (m, 1H), 0.49-0.46 (m, 1H), 0.25-0.18 (m, 2H).

PAT

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References

References

  1.  “Sichuan Haisco Pharmaceutical”. AdisInsight. 28 August 2024. Retrieved 1 October 2025.
  2.  “Ciprofol (Cipepofol): A γ-Aminobutyric Acid Receptor Agonist for Induction of Anesthesia”. Chemistry and Pharmacology of Drug Discovery. Wiley. 2024. pp. 251–274. doi:10.1002/9781394225156.ch12. ISBN 978-1-394-22512-5. Retrieved 1 October 2025.
  3.  Wang X, Wang X, Liu J, Zuo YX, Zhu QM, Wei XC, et al. (March 2022). “Effects of ciprofol for the induction of general anesthesia in patients scheduled for elective surgery compared to propofol: a phase 3, multicenter, randomized, double-blind, comparative study”. European Review for Medical and Pharmacological Sciences. 26 (5): 1607–1617. PMID 35302207.
  4.  Zeng Y, Wang DX, Lin ZM, Liu J, Wei XC, Deng J, et al. (February 2022). “Efficacy and safety of HSK3486 for the induction and maintenance of general anesthesia in elective surgical patients: a multicenter, randomized, open-label, propofol-controlled phase 2 clinical trial”. European Review for Medical and Pharmacological Sciences. 26 (4): 1114–1124. PMID 35253166.
  5.  Liao J, Li M, Huang C, Yu Y, Chen Y, Gan J, et al. (2022). “Pharmacodynamics and Pharmacokinetics of HSK3486, a Novel 2,6-Disubstituted Phenol Derivative as a General Anesthetic”. Frontiers in Pharmacology. 13 830791. doi:10.3389/fphar.2022.830791. PMC 8851058. PMID 35185584.
  6.  Chen BZ, Yin XY, Jiang LH, Liu JH, Shi YY, Yuan BY (August 2022). “The efficacy and safety of ciprofol use for the induction of general anesthesia in patients undergoing gynecological surgery: a prospective randomized controlled study”. BMC Anesthesiology. 22 (1) 245. doi:10.1186/s12871-022-01782-7. PMC 9347095. PMID 35922771.
  7.  “Novel Drug Approvals for 2026”. U.S. Food and Drug Administration. 29 May 2026. Retrieved 31 May 2026.
  8.  Lu M, Liu J, Wu X, Zhang Z (2023). “Ciprofol: A Novel Alternative to Propofol in Clinical Intravenous Anesthesia?”. BioMed Research International. 2023 7443226. doi:10.1155/2023/7443226. PMC 9879693. PMID 36714027.
  9.  Qin L, Ren L, Wan S, Liu G, Luo X, Liu Z, et al. (May 2017). “Design, Synthesis, and Evaluation of Novel 2,6-Disubstituted Phenol Derivatives as General Anesthetics”. Journal of Medicinal Chemistry. 60 (9): 3606–3617. doi:10.1021/acs.jmedchem.7b00254. PMID 28430430.
  10.  Nair A, Seelam S (2022). “Ciprofol- a game changing intravenous anesthetic or another experimental drug!”. Saudi Journal of Anaesthesia. 16 (2): 258–259. doi:10.4103/sja.sja_898_21. PMC 9009555. PMID 35431734.
  11.  Man Y, Xiao H, Zhu T, Ji F (March 2023). “Study on the effectiveness and safety of ciprofol in anesthesia in gynecological day surgery: a randomized double-blind controlled study”. BMC Anesthesiology. 23 (1) 92. doi:10.1186/s12871-023-02051-x. PMC 10039513. PMID 36964501.
  12.  Chen X, Guo P, Yang L, Liu Z, Yu D (2022). “Comparison and Clinical Value of Ciprofol and Propofol in Intraoperative Adverse Reactions, Operation, Resuscitation, and Satisfaction of Patients under Painless Gastroenteroscopy Anesthesia”. Contrast Media & Molecular Imaging. 2022 9541060. doi:10.1155/2022/9541060. PMC 9314164. PMID 35935320.
  13.  Zhong J, Zhang J, Fan Y, Zhu M, Zhao X, Zuo Z, et al. (May 2023). “Efficacy and safety of Ciprofol for procedural sedation and anesthesia in non-operating room settings”. Journal of Clinical Anesthesia. 85 111047. doi:10.1016/j.jclinane.2022.111047. PMID 36599219. S2CID 255468218.
  14.  Liang P, Dai M, Wang X, Wang D, Yang M, Lin X, et al. (June 2023). “Efficacy and safety of ciprofol vs. propofol for the induction and maintenance of general anaesthesia: A multicentre, single-blind, randomised, parallel-group, phase 3 clinical trial”. European Journal of Anaesthesiology. 40 (6): 399–406. doi:10.1097/EJA.0000000000001799. PMC 10155686. PMID 36647565.
  15.  Luo Z, Tu H, Zhang X, Wang X, Ouyang W, Wei X, et al. (March 2022). “Efficacy and Safety of HSK3486 for Anesthesia/Sedation in Patients Undergoing Fiberoptic Bronchoscopy: A Multicenter, Double-Blind, Propofol-Controlled, Randomized, Phase 3 Study”. CNS Drugs. 36 (3): 301–313. doi:10.1007/s40263-021-00890-1. PMC 8927014. PMID 35157236.
  16.  Hu C, Ou X, Teng Y, Shu S, Wang Y, Zhu X, et al. (November 2021). “Sedation Effects Produced by a Ciprofol Initial Infusion or Bolus Dose Followed by Continuous Maintenance Infusion in Healthy Subjects: A Phase 1 Trial”. Advances in Therapy. 38 (11): 5484–5500. doi:10.1007/s12325-021-01914-4. PMC 8523013. PMID 34559359.
  17.  Teng Y, Ou M, Wang X, Zhang W, Liu X, Liang Y, et al. (September 2021). “Efficacy and safety of ciprofol for the sedation/anesthesia in patients undergoing colonoscopy: Phase IIa and IIb multi-center clinical trials”. European Journal of Pharmaceutical Sciences. 164 105904. doi:10.1016/j.ejps.2021.105904. PMID 34116176.
  18.  Zhu Q, Luo Z, Wang X, Wang D, Li J, Wei X, et al. (April 2023). “Efficacy and safety of ciprofol versus propofol for the induction of anesthesia in adult patients: a multicenter phase 2a clinical trial”. International Journal of Clinical Pharmacy. 45 (2): 473–482. doi:10.1007/s11096-022-01529-x. PMC 10147789. PMID 36680620.
  19.  Qin K, Qin WY, Ming SP, Ma XF, Du XK (July 2022). “Effect of ciprofol on induction and maintenance of general anesthesia in patients undergoing kidney transplantation”. European Review for Medical and Pharmacological Sciences. 26 (14): 5063–5071. PMID 35916802.
  20.  Wu B, Zhu W, Wang Q, Ren C, Wang L, Xie G (2022). “Efficacy and safety of ciprofol-remifentanil versus propofol-remifentanil during fiberoptic bronchoscopy: A prospective, randomized, double-blind, non-inferiority trial”. Frontiers in Pharmacology. 13 1091579. doi:10.3389/fphar.2022.1091579. PMC 9812563. PMID 36618929.
  21.  Li J, Wang X, Liu J, Wang X, Li X, Wang Y, et al. (August 2022). “Comparison of ciprofol (HSK3486) versus propofol for the induction of deep sedation during gastroscopy and colonoscopy procedures: A multi-centre, non-inferiority, randomized, controlled phase 3 clinical trial”. Basic & Clinical Pharmacology & Toxicology. 131 (2): 138–148. doi:10.1111/bcpt.13761. PMC 9543620. PMID 35653554.
  22.  Long YQ, Feng CD, Ding YY, Feng XM, Liu H, Ji FH, et al. (2022). “Esketamine as an Adjuvant to Ciprofol or Propofol Sedation for Same-Day Bidirectional Endoscopy: Protocol for a Randomized, Double-Blind, Controlled Trial With Factorial Design”. Frontiers in Pharmacology. 13 821691. doi:10.3389/fphar.2022.821691. PMC 8975265. PMID 35370640.
  23.  Liu Y, Yu X, Zhu D, Zeng J, Lin Q, Zang B, et al. (May 2022). “Safety and efficacy of ciprofol vs. propofol for sedation in intensive care unit patients with mechanical ventilation: a multi-center, open label, randomized, phase 2 trial”. Chinese Medical Journal. 135 (9): 1043–1051. doi:10.1097/CM9.0000000000001912. PMC 9276409. PMID 34924506.
  24.  Liu GL, Wu GZ, Ge D, Zhou HJ, Cui S, Gao K, et al. (2023). “Efficacy and safety of ciprofol for agitation and delirium in the ICU: A multicenter, single-blind, 3-arm parallel randomized controlled trial study protocol”. Frontiers in Medicine. 9 1024762. doi:10.3389/fmed.2022.1024762. PMC 9868613. PMID 36698817.
  25.  Wang YC, Wu MJ, Zhou SL, Li ZH (January 2023). “Protective effects of combined treatment with ciprofol and mild therapeutic hypothermia during cerebral ischemia-reperfusion injury”. World Journal of Clinical Cases. 11 (3): 487–492. doi:10.12998/wjcc.v11.i3.487. PMC 9923870. PMID 36793629.
  26.  Yang Y, Xia Z, Xu C, Zhai C, Yu X, Li S (2022). “Ciprofol attenuates the isoproterenol-induced oxidative damage, inflammatory response and cardiomyocyte apoptosis”. Frontiers in Pharmacology. 13 1037151. doi:10.3389/fphar.2022.1037151. PMC 9723392. PMID 36483733.
  27.  Vittori A, Di Fabio C, Cascella M, Marinangeli F, Francia E, Mascilini I, et al. (January 2026). “Advantages of Ciprofol with Special Consideration of Pediatric Anesthesia”. Children (Basel, Switzerland). 13 (2). doi:10.3390/children13020188. PMC 12939459. PMID 41749542.
  28.  Liu SB, Yao X, Tao J, Yang JJ, Zhao YY, Liu DW, et al. (March 2023). “Population total and unbound pharmacokinetics and pharmacodynamics of ciprofol and M4 in subjects with various renal functions”. British Journal of Clinical Pharmacology. 89 (3): 1139–1151. doi:10.1111/bcp.15561. PMID 36217805. S2CID 252818288.
  29.  Hu Y, Li X, Liu J, Chen H, Zheng W, Zhang H, et al. (December 2022). “Safety, pharmacokinetics and pharmacodynamics of a novel γ-aminobutyric acid (GABA) receptor potentiator, HSK3486, in Chinese patients with hepatic impairment”. Annals of Medicine. 54 (1): 2769–2780. doi:10.1080/07853890.2022.2129433. PMC 9559057. PMID 36217101.
  30.  Li X, Yang D, Li Q, Wang H, Wang M, Yan P, et al. (2021). “Safety, Pharmacokinetics, and Pharmacodynamics of a Single Bolus of the γ-aminobutyric Acid (GABA) Receptor Potentiator HSK3486 in Healthy Chinese Elderly and Non-elderly”. Frontiers in Pharmacology. 12 735700. doi:10.3389/fphar.2021.735700. PMC 8430033. PMID 34512361.
  31.  Ding YY, Long YQ, Yang HT, Zhuang K, Ji FH, Peng K (December 2022). “Efficacy and safety of ciprofol for general anaesthesia induction in elderly patients undergoing major noncardiac surgery: A randomised controlled pilot trial”. European Journal of Anaesthesiology. 39 (12): 960–963. doi:10.1097/EJA.0000000000001759. PMID 36214498. S2CID 252779399.
  32.  Duan G, Lan H, Shan W, Wu Y, Xu Q, Dong X, et al. (April 2023). “Clinical effect of different doses of ciprofol for induction of general anesthesia in elderly patients: A randomized, controlled trial”. Pharmacology Research & Perspectives. 11 (2) e01066. doi:10.1002/prp2.1066. PMC 9944862. PMID 36811327. S2CID 257098376.
  33.  Yang Y, Xia Z, Xu C, Zhai C, Yu X, Li S (2022). “Ciprofol attenuates the isoproterenol-induced oxidative damage, inflammatory response and cardiomyocyte apoptosis”. Frontiers in Pharmacology. 13 1037151: 1037151. doi:10.3389/fphar.2022.1037151. PMC 9723392. PMID 36483733.
  34.  Bian Y, Zhang H, Ma S, Jiao Y, Yan P, Liu X, et al. (January 2021). “Mass balance, pharmacokinetics and pharmacodynamics of intravenous HSK3486, a novel anaesthetic, administered to healthy subjects”. British Journal of Clinical Pharmacology. 87 (1): 93–105. doi:10.1111/bcp.14363. PMID 32415708. S2CID 218658207.

Further reading

Clinical data
Other namesCiprofol; CS-0064163; CS0064163; GTPL10812; GTPL-10812; HSK-3486; HSK3486; HY-116152; HY116152; (R)-2-(1-Cyclopropylethyl)-6-isopropylphenol
Routes of
administration
Intravenous infusion[1]
Drug classGABAA receptor positive allosteric modulator
Pharmacokinetic data
MetabolismLiver glucuronidation
ExcretionKidney
Identifiers
IUPAC name
CAS Number1637741-58-2 
PubChem CID86301664
DrugBankDB16295 
ChemSpider76794458 
UNIIM3WGS532VY
KEGGD12449 
ChEMBLChEMBL4094894 
Chemical and physical data
FormulaC14H20O
Molar mass204.313 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

////////cipepofol, FDA 2026, APPROVALS 2026, Cypsedo, HSK 3486, CS-0064163, GTPL 10812, HSK-3486, HY-116152, M3WGS532VY, ANAESTHETIC

#cipepofol, #FDA 2026, #APPROVALS 2026, #Cypsedo, #HSK 3486, #CS-0064163, #GTPL 10812, #HSK-3486, #HY-116152, #M3WGS532VY, #ANAESTHETIC

Baxdrostat


CLICK LINK https://newdrugapprovals.org/2025/08/31/baxdrostat/

Sonrotoclax


Sonrotoclax

CAS 2383086-06-2

MW 890.1 g/mol, MFC49H59N7O7S

FDA APPROVED 5/13/2026, Beqalzi, APPROVALS 2026, BGB-11417, BGB 11417, 30R67U9KYS

N-[4-[(4-hydroxy-4-methylcyclohexyl)methylamino]-3-nitrophenyl]sulfonyl-4-[2-[(2S)-2-(2-propan-2-ylphenyl)pyrrolidin-1-yl]-7-azaspiro[3.5]nonan-7-yl]-2-(1H-pyrrolo[2,3-b]pyridin-5-yloxy)benzamide

To treat adults with relapsed or refractory mantle cell lymphoma after at least two lines of systemic therapy, including a Bruton’s tyrosine kinase inhibitor

Sonrotoclax is a potent, orally active Bcl2 inhibitor. Sonrotoclax has effective cell killing effect against a variety of lymphoma and leukemia cell lines.

Regulatory Status & Primary Indication

On May 13, 2026, the U.S. Food and Drug Administration (FDA) granted accelerated approval to sonrotoclax for treating adult patients with relapsed or refractory mantle cell lymphoma (MCL). [1]

  • Eligibility Requirement: Patients must have undergone at least two prior lines of systemic therapy, which must include a Bruton’s tyrosine kinase (BTK) inhibitor.
  • Clinical Performance: In the supporting Phase 1/2 BGB-11417-201 trial, sonrotoclax demonstrated an overall response rate (ORR) of 52% and a median time to response of 1.9 months

Sonrotoclax 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, sonrotoclax specifically binds to and inhibits the activity of the pro-survival protein Bcl-2. This restores apoptotic processes and inhibits cell proliferation in Bcl-2-overexpressing tumor cells. Bcl-2, a protein that belongs to the Bcl-2 family, is overexpressed in various tumor cell types and plays an important role in the negative regulation of apoptosis. Its tumor expression is associated with increased drug resistance and cancer cell survival.

Sonrotoclax is an investigational new drug that is being evaluated for the treatment of hematologic malignancies, particularly chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).[1] It is a potent and selective BCL2 inhibitor that can overcome resistance associated with BCL2 mutations, such as the G101V variant, which limits the effectiveness of first-generation inhibitors like venetoclax.[2]

SYN

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)-4-(2-((S)-2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzamide (hereinafter sonrotoclax).

SYN

2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)-4-(2-((S)-2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzamide

Step 9: 2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)-4-(2-((S)-2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzamide

      A mixture of (S)-2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(2-(2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzoic acid (44 g, 78 mmol), 4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrobenzenesulfonamide (26.8 g, 78 mmol), TFA (15.7 g, 156 mmol), EDCl (19.4 g, 101 mmol) and DMAP (19 g, 156 mmol) in anhydrous DCM (880 mL) was stirred overnight at room temperature. The reaction was monitored by HPLC. After starting material of (S)-2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-4-(2-(2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzoic acid was consumed completely, the reaction mixture was heated to ˜35° C. and N 1,N 1-dimethylethane-1,2-diamine (17.2 g, 195 mmol) was added in one portion. The reaction was stirred for another 12 hours. The mixture was washed twice with 10 wt % aq. AcOH solution (300 mL×2) and then washed with saturated aq. NaHCO 3 (300 mL×2). The organic layer was collected and concentrated to about 90 mL. 22 g of silica gel was added and stirred for 2 hours. After filtration, 180 mL EA was added into the filtrate at reflux and further stirred for 5 hours. After the mixture was cooled to room temperature, the precipitate was filtered and then the wet cake was washed twice with EA (180 mL). After drying in vacuum at 80-90° C., the desired compound was obtained (48 g, yield: 69.5%). 1H NMR (DMSO-d 6) δ ppm: 11.65 (s, 1H), 11.11 (br, 1H), 8.58-8.39 (m, 2H), 8.00 (d, J=2.8 Hz, 1H), 7.74 (d, J=8.8 Hz, 1H), 7.57-7.37 (m, 4H), 7.30-7.10 (m, 3H), 7.00 (d, J=9.2 Hz, 1H), 6.65 (d, J=1.2 Hz, 1H), 6.35 (s, 1H), 6.17 (s, 1H), 4.24 (s, 1H), 3.39-3.20 (m, 5H), 3.04-2.88 (m, 4H), 2.23 (s, 1H), 1.94-1.47 (m, 11H), 1.44-1.26 (m, 7H), 1.19 (d, J=8.0 Hz, 3H), 1.14 (d, J=8.0 Hz, 3H), 1.10 (s, 4H). MS (ESI, m/e) [M+1] + 889.9.

SYN

Example F43: 2-((1H-pyrrolo[2,3-b]pyridin-5-yl)oxy)-N-((4-((((1r,4r)-4-hydroxy-4-methylcyclohexyl)methyl)amino)-3-nitrophenyl)sulfonyl)-4-(2-((S)-2-(2-isopropylphenyl)pyrrolidin-1-yl)-7-azaspiro[3.5]nonan-7-yl)benzamide

PAT

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References

References

  1.  “Sonrotoclax – BeiGene”. AdisInsight. Springer Nature Switzerland AG.
  2.  Tomkins O, D’Sa S (2024). “Review of BCL2 inhibitors for the treatment of Waldenström’s macroglobulinaemia and non-IgM lymphoplasmacytic lymphoma”. Frontiers in Oncology. 14 1490202. doi:10.3389/fonc.2024.1490202. PMC 11570586. PMID 39558954.
Clinical data
Pronunciation/sɒnˈroʊtəklæks/
son-ROH-tə-klaks
Identifiers
IUPAC name
CAS Number2383086-06-2
PubChem CID149553242
ChemSpider129309008
UNII30R67U9KYS
KEGGD12883
ChEMBLChEMBL5314951
Chemical and physical data
FormulaC49H59N7O7S
Molar mass890.11 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

/////////sonrotoclax, anax labs, FDA 2026, APPROVALS 2026, Beqalzi, BGB-11417, BGB 11417, 30R67U9KYS, accelerated approval

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Vepdegestrant


Vepdegestrant

CAS 2229711-08-2

MW 723.9 g/mol, C45H49N5O4

(3S)-3-[6-[4-[[1-[4-[(1R,2S)-6-hydroxy-2-phenyl-1,2,3,4-tetrahydronaphthalen-1-yl]phenyl]piperidin-4-yl]methyl]piperazin-1-yl]-3-oxo-1H-isoindol-2-yl]piperidine-2,6-dione

5/1/2026, FDA 2026, APROVALS 2026, Veppanu, ARV 471, WC1U3R1YMI, PF 07850327

To treat estrogen receptor-positive, human epidermal growth factor receptor 2-negative, ESR1-mutated advanced or metastatic breast cancer with disease progression following at least one line of endocrine therapy

On May 1, 2026, the FDA approved vepdegestrant (Veppanu), a first-in-class oral PROTAC estrogen receptor (ER) degrader developed by Arvinas and Pfizer, for adults with ER-positive, HER2-negative, ESR1-mutated advanced or metastatic breast cancer who have progressed on endocrine therapy. It demonstrated significant progression-free survival (PFS) improvements compared to fulvestrant.

Key Details About Vepdegestrant (Veppanu):

  • Mechanism of Action: As an oral PROTAC (Proteolysis-Targeting Chimera), vepdegestrant targets the estrogen receptor for degradation, designed to be more effective than traditional endocrine therapies, particularly in ESR1-mutated tumors.
  • Approved Indication: For treating adults with ER+/HER2-, ESR1-mutated advanced/metastatic breast cancer (detected by Guardant360 CDx) after at least one line of endocrine therapy.
  • Dosage: The recommended dose is 200 mg taken orally once daily with food.
  • Clinical Efficacy (VERITAC-2): In trials, vepdegestrant showed a significantly longer PFS compared to intramuscular fulvestrant.
  • Side Effects & Risks: Common side effects include decreased white blood cell counts, increased liver function tests, muscle/bone pain, fatigue, and nausea. Warnings include embryo-fetal toxicity and QTc interval prolongation (heart rhythm issues).
  • Companion Diagnostic: Guardant360 CDx was approved alongside the drug to identify patients with ESR1 mutations

Vepdegestrant (developmental code name ARV-471) is an investigational oral proteolysis-targeting chimera (PROTAC) compound that targets the estrogen receptor for protein degradation. It is being developed for the treatment of estrogen receptor-positive, HER2-negative (ER+/HER2-) breast cancer by Arvinas and Pfizer.[1][2][3]

Mechanism of action

Vepdegestrant is designed as a PROTAC that recruits the ubiquitin-proteasome system to target the estrogen receptor for degradation.[4] The compound contains both an E3 ubiquitin ligase-binding moiety and an estrogen receptor-binding domain, intended to bring these proteins into proximity to trigger ubiquitination and subsequent proteasomal degradation of the ER protein.[5] In laboratory studies, vepdegestrant demonstrated ER degradation in ER-positive breast cancer cell lines with reported DC50 values of approximately 1-2 nM.[6]

Vepdegestrant is an orally available hetero-bifunctional molecule and selective estrogen receptor (ER) alpha-targeted protein degrader, using the proteolysis targeting chimera (PROTAC) technology, with potential antineoplastic activity. Vepdegestrant is composed of an ER alpha ligand attached to an E3 ligase recognition moiety. Upon oral administration,vepdegestrant targets and binds to the ER ligand binding domain on ER alpha. E3 ligase is recruited to the ER by the E3 ligase recognition moiety and ER alpha is tagged by ubiquitin. This causes ubiquitination and degradation of ER alpha by the proteasome. This decreases ER alpha protein levels, decreases the expression of ER alpha-target genes and halts ER-mediated signaling. This results in an inhibition of proliferation in ER alpha-overexpressing tumor cells. In addition, the degradation of the ER alpha protein releases the ARV-471 and can bind to additional ER alpha target proteins. ER alpha is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation.

SYN

https://chemistry-europe.onlinelibrary.wiley.com/doi/10.1002/slct.202405939

PAT

Step 11: Preparation of 3-[5-[4-[[1-[4-[(1R, 2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl]-4-piperidyl]methyl]piperazin-1-yl]-1-oxo-isoindolin-2-yl]piperidine-2,6-dione (Compound (I-b))

To a solution of 3-(1-oxo-5-piperazin-1-yl-isoindolin-2-yl)piperidine-2,6-dione hydrochloride (319 mg, 0.87 mmol, prepared in Step 17 described for Exemplary Compound 62) in methanol (4 mL) and dichloromethane (4 mL) was added sodium acetate (120 mg, 1.46 mmol, 2 eq). The mixture was stirred at 20° C. for 0.5 h, then to the mixture was added 1-[4-[(1R,2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl]piperidine-4-carbaldehyde (300 mg, 0.73 mmol, 1 eq) and sodium cyanoborohydride (137 mg, 2.19 mmol, 3 eq). The mixture was stirred at 20° C. for 12 h. LC-MS showed the starting material was consumed completely and one main peak with desired MW was detected. The reaction mixture was concentrated under reduced pressure. The residue was purified by prep-HPLC (Phenomenex luna C 18 column, 250×50 mm, 10 um; mobile phase: [water (0.05% HCl)-acetonitrile]; B %: acetonitrile 10%-40% in 30 min). The desired compound 3-[5-[4-[[1-[4-[(1R, 2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl]-4-piperidyl]methyl]piperazin-1-yl]-1-oxo-isoindolin-2-yl]piperidine-2,6-dione (288.4 mg, 0.37 mmol, 51% yield) was obtained as a white solid of hydrochloride salt. LC-MS (ESI) m/z: 724.4 [M+1] +; 1H NMR (400 MHz, DMSO-d 6) δ 10.97 (s, 1H), 10.83 (s, 0.9H, HCl), 7.60 (d, J=8.5 Hz, 1H), 7.40 (br s, 2H), 7.22-7.11 (m, 5H), 6.83 (d, J=6.0 Hz, 2H), 6.69-6.63 (m, 2H), 6.58-6.47 (m, 3H), 5.07 (dd, J=5.2, 13.2 Hz, 1H), 4.41-4.30 (m, 2H), 4.28-4.21 (m, 1H), 4.00 (d, J=12.7 Hz, 2H), 3.61 (d, J=11.0 Hz, 2H), 3.54-3.36 (m, 6H), 3.16 (br s, 4H), 3.06-2.84 (m, 3H), 2.76-2.53 (m, 1H), 2.43-2.33 (m, 1H), 2.27 (br s, 1H), 2.16-2.04 (m, 3H), 2.02-1.69 (m, 5H).

Synthesis of (3S)-3-[5-[4-[[1-[4-[(1R, 2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl]-4-piperidyl]methyl]piperazin-1-yl]-1-oxo-isoindolin-2-yl]piperidine-2,6-dione (Compound (I-c))

   To a mixture of (3 S)-3-(1-oxo-5-piperazin-1-yl-isoindolin-2-yl)piperidine-2,6-dione (1.30 g, 3.47 mmol, 1 eq, benzene sulfonate) in dichloromethane (8 mL) and methanol (32 mL) was added sodium acetate (854 mg, 10.41 mmol, 3 eq) in one portion at 20° C. The mixture was stirred at 20° C. for 10 minutes. Then 1-[4-[(1R, 2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl] piperidine-4-carbaldehyde (1 g, 2.43 mmol, 0.7 eq, prepared as described above in the synthesis of Compound (I-b)) was added. The mixture was stirred at 20° C. for 10 minutes. After that, acetic acid (0.2 mL) and sodium cyanoborohydride (436 mg, 6.94 mmol, 2 eq) was added in one portion. The mixture was stirred at 20° C. for 40 minutes. The mixture was concentrated in vacuum, and 50 mL of tetrahydrofuran and 20 mL of water were added. The mixture was stirred for 20 minutes. Saturated aqueous sodium bicarbonate solution was added to adjust the pH to 8-9. The aqueous phase was extracted with ethyl acetate and tetrahydrofuran (v:v=2:1, 60 mL×3). The combined organic phase was washed with brine (60 mL×1), dried with anhydrous sodium sulfate, filtered and concentrated in vacuum. The residue was purified by preparative reverse phase HPLC (column: Phenomenex luna C18 250×50 mm, 10 micron; mobile phase: [water (0.225% formic acid)-acetonitrile]; B %: 20%-50% in 30 min). The product (3S)-3-[5-[4-[[1-[4-[(1R,2S)-6-hydroxy-2-phenyl-tetralin-1-yl]phenyl]-4-piperidyl]methyl] piperazin-1-yl]-1-oxo-isoindolin-2-yl]piperidine-2,6-dione (964 mg, 1.23 mmol, 35% yield, 98% purity, formate) was obtained as a white solid of formic acid salt after lyophilization. Chiral purity was analyzed by chiral SFC (Chiralcel OJ-3 50×4.6 mm, 3 micron; mobile phase: 50% ethanol (0.05% DEA) in CO 2; flow rate: 3 mL/min, wavelength: 220 nm) and observed t p=2.89 min with de over 95%. [α D=−267.5 (c=0.2 in DMF, 25° C.). LC-MS (ESI) m/z: 724.2 [M+1] +. 1H NMR (400 MHz, DMSO-d 6) δ 10.94 (s, 1H), 8.16 (s, 1H, formate), 7.51 (d, J=8.8 Hz, 1H), 7.21-6.98 (m, 5H), 6.83 (d, J=6.4 Hz, 2H), 6.68-6.57 (m, 2H), 6.56-6.44 (m, 3H), 6.20 (d, J=8.8 Hz, 2H), 5.04 (dd, J=5.2, 13.2 Hz, 1H), 4.32 (d, J=16.8 Hz, 1H), 4.19 (d, J=17.2 Hz, 1H), 4.12 (d, J=4.8 Hz, 1H), 3.51 (br d, J=10.0 Hz, 4H), 3.27 (br s, 8H), 3.03-2.82 (m, 3H), 2.63-2.54 (m, 1H), 2.43-2.28 (m, 2H), 2.19 (d, J=6.8 Hz, 2H), 2.15-2.02 (m, 1H), 2.01-1.89 (m, 1H), 1.83-1.51 (m, 4H), 1.28-1.04 (m, 2H).
       1H-NMR of the free non-salt form: (400 MHz, DMSO-d 6) δ 10.93 (s, 1H), 9.09 (s, 1H), 7.51 (d, J=8.8 Hz, 1H), 7.18-7.09 (m, 3H), 7.08-7.02 (m, 2H), 6.83 (d, J=6.4 Hz, 2H), 6.64 (d, J=8.4 Hz, 1H), 6.60 (d, J=2.0 Hz, 1H), 6.53 (d, J=8.8 Hz, 2H), 6.48 (dd, J=2.4, 8.4 Hz, 1H), 6.20 (d, J=8.8 Hz, 2H), 5.04 (dd, J=5.2, 13.2 Hz, 1H), 4.39-4.27 (m, 1H), 4.24-4.15 (m, 1H), 4.12 (d, J=4.8 Hz, 1H), 3.51 (d, J=9.6 Hz, 2H), 3.29-3.24 (m, 5H), 3.03-2.83 (m, 3H), 2.62-2.54 (m, 4H), 2.52 (s, 3H), 2.41-2.36 (m, 1H), 2.19 (d, J=7.2 Hz, 2H), 2.15-2.08 (m, 1H), 2.00-1.89 (m, 1H), 1.81-1.58 (m, 4H), 1.22-1.06 (m, 2H).

PAT

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References

References

  1.  Iwata, H.; Naito, Y.; Hattori, M.; Yoshimura, A.; Yonemori, K.; Aizawa, M.; et al. (November 2023). “58P Safety and pharmacokinetics (PK) of vepdegestrant in Japanese patients with estrogen receptor (ER)+/human epidermal growth factor receptor 2 (HER2)- advanced breast cancer: Results from a Japanese phase I study”. Annals of Oncology. 34: S1488–S1489. doi:10.1016/j.annonc.2023.10.193. S2CID 265657144.
  2.  Iwata, H.; Hamilton, E.P.; Ma, C.X.; De Laurentiis, M.; Hurvitz, S.A.; Wander, S.A.; et al. (November 2023). “73TiP Global phase III studies evaluating vepdegestrant in estrogen receptor (ER)+/human epidermal growth factor receptor 2 (HER2)- advanced breast cancer: VERITAC-2 and VERITAC-3”. Annals of Oncology. 34: S1493. doi:10.1016/j.annonc.2023.10.207. S2CID 265654990.
  3.  “Arvinas, Pfizer reworking partnership on ‘Protac’ cancer drug | BioPharma Dive”. http://www.biopharmadive.com. Retrieved 17 September 2025.
  4.  “Estrogen Receptor”. Arvinas. Retrieved 17 September 2025.
  5.  Sakamoto, Kathryn M.; Kim, Kwon B.; Kumagai, Ayumu; Mercurio, Frank; Crews, Craig M.; Deshaies, Raymond J. (18 January 2022). “PROTAC targeted protein degraders: the past is prologue”. Nature Reviews Drug Discovery. 21 (3): 181–200. doi:10.1038/s41573-021-00371-6. PMC 8765495. PMID 35046570.
  6.  “Vepdegestrant (ARV-471) PROTAC ER Degrader”. MedChemExpress. Retrieved 17 September 2025.
  7.  Hamilton, Erika P.; Ma, Cynthia; De Laurentiis, Michelino; Iwata, Hiroji; Hurvitz, Sara A.; Wander, Seth A.; et al. (2024). “VERITAC-2: a Phase III study of vepdegestrant, a PROTAC ER degrader, versus fulvestrant in ER+/HER2- advanced breast cancer”. Future Oncology (London, England). 20 (32): 2447–2455. doi:10.1080/14796694.2024.2377530. ISSN 1744-8301. PMC 11524203. PMID 39072356.
  8.  “A Study to Compare the Efficacy and Safety of Vepdegestrant (ARV-471) Versus Fulvestrant in Participants With Estrogen Receptor-positive, HER2-negative Advanced Breast Cancer (VERITAC-2)”. ClinicalTrials.gov. 30 June 2025. Retrieved 17 September 2025.
  9.  “Arvinas and Pfizer Announce Positive Topline Results from Phase 3 VERITAC-2 Clinical Trial”. Arvinas. Retrieved 17 September 2025.
  10.  “VERITAC-2 Trial Shows Vepdegestrant Significantly Improves Survival in ESR1-Mutant Breast Cancer”. Applied Clinical Trials Online. 24 March 2025. Retrieved 17 September 2025.
  11.  “Arvinas Announces Results from the VERITAC-2 Trial Selected as Late-Breaking Oral Presentation at the 2025 ASCO Annual Meeting”. Arvinas. 23 April 2025. Retrieved 17 September 2025.
  12.  Gough, Sheryl M.; Flanagan, John J.; Teh, Jimmy (15 August 2024). “Oral Estrogen Receptor PROTAC Vepdegestrant (ARV-471) Is Highly Efficacious as Monotherapy and in Combination with CDK4/6 or PI3K/mTOR Pathway Inhibitors in Preclinical ER+ Breast Cancer Models”. Clinical Cancer Research. 30 (16): 3549–3562. doi:10.1158/1078-0432.CCR-23-3465. PMC 11325148. PMID 38819400.
  13.  “FDA Grants Fast Track Status to Vepdegestrant for ER+/HER2– Metastatic Breast Cancer”. Oncology Live. 6 February 2024. Retrieved 17 September 2025.
  14.  “Vepdegestrant Gains FDA Fast Track Designation in ER+/HER2- Breast Cancer”. Targeted Oncology. 6 February 2024. Retrieved 17 September 2025.
  15.  “Arvinas Announces Submission of New Drug Application to U.S. FDA for Vepdegestrant for Patients with ESR1-Mutated ER+/HER2- Advanced or Metastatic Breast Cancer” (Press release). Arvinas. 24 June 2025. Retrieved 17 September 2025.

External links

Clinical data
Pronunciation/ˌvɛpdəˈdʒɛstrənt/
VEP-də-JES-trənt
Other namesARV-471
Legal status
Legal statusInvestigational
Identifiers
IUPAC name
CAS Number2229711-68-4
PubChem CID134562533
ChemSpider114935295
UNIIWC1U3R1YMI
ChEMBLChEMBL5095210
Chemical and physical data
FormulaC45H49N5O4
Molar mass723.918 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

////////////vepdegestrant, anax lab, approvals 2026, fda 2026, Veppanu, FDA 2026, APROVALS 2026, Veppanu, ARV 471, WC1U3R1YMI, PF 07850327

#vepdegestrant, #anax lab, #approvals 2026, #fda 2026, #Veppanu, #FDA 2026, #APROVALS 2026, #Veppanu, #ARV 471, #WC1U3R1YMI, #PF 07850327

Daraxonrasib


Daraxonrasib

CAS 2765081-21-6

8/26/2026, FDA APPROVED 2026, FDA 2026, Rasonque

MFC44H58N8O5S MW811.0 g/mol

trans-(1S,2S)-N-[(7S,13S)-21-ethyl-20-[2-[(1S)-1-methoxyethyl]-5-(4-methylpiperazin-1-yl)-3-pyridinyl]-17,17-dimethyl-8,14-dioxo-15-oxa-4-thia-9,21,27,28-tetrazapentacyclo[17.5.2.12,5.19,13.022,26]octacosa-1(25),2,5(28),19,22(26),23-hexaen-7-yl]-2-methylcyclopropane-1-carboxamide

Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2,

To treat metastatic pancreatic cancer

Daraxonrasib (formerly RMC-6236) is an investigational, orally administered “molecular glue” RAS inhibitor developed by Revolution Medicines for treating advanced solid tumors with RAS mutations, particularly metastatic pancreatic cancer. April 2026 Phase 3 trials showed it significantly improves survival, demonstrating high potential as a first-line treatment. 

Key Clinical Findings and Updates (as of April 2026):

  • Mechanism: It acts as a RAS(ON) inhibitor, targeting mutated and wild-type RAS proteins () to disrupt cancer signaling.
  • Breakthrough Results: Data from the RASolute 302 trial showed a substantial survival benefit in patients with previously treated metastatic pancreatic ductal adenocarcinoma (PDAC).
  • High Response Rates: In trials, daraxonrasib combined with chemotherapy showed a 58% confirmed objective response rate (ORR) and 84% progression-free survival (PFS) at 6 months in untreated RAS-mutant metastatic pancreatic cancer.
  • Safety Profile: Generally well-tolerated, with side effects including rash, diarrhea, stomatitis, and nausea.
  • Recognition: Named the “2025 Molecule of the Year” by Drug Hunter for its, novel mechanism and clinical potential. 

Daraxonrasib is currently being studied in the Phase 3 RASolute 303 trial for first-line treatment of pancreatic cancer.

Daraxonrasib (RMC-6236) is a RAS inhibitor drug. It is undergoing testing by Revolution Medicines to treat advanced solid tumors with RAS mutations, especially metastatic pancreatic ductal adenocarcinoma (PDAC) containing KRAS G12X mutations.[1] It received a breakthrough therapy designation from the U.S. Food and Drug Administration.[2]

Daraxonrasib is orally active and multi-selective RAS inhibitor. It uses a tri-complex mechanism to target the active, GTP-bound form of RAS proteins, including mutant and wild-type forms. Unlike conventional RAS inhibitors, it first binds to the chaperone-like protein cyclophilin A to form a complex, which then attaches to active RAS. This interaction blocks downstream effector binding and inhibits oncogenic signaling.[3]

In 2026, Daraxonrasib clinical trial completed a phase 3 clinical trial (RASolute 302) to assess efficacy compared to standard-of-care chemotherapy.[4] The trial met all primary and key secondary endpoints, including progression-free survival (PFS). The company reported median survival of 13.2 months with daraxonrasib vs. 6.7 months with standard chemotherapy. The hazard ratio for death was 0.40 (a 60% reduction in risk of death; p < 0.0001). Daraxonrasib was generally well tolerated with a manageable safety profile and no new safety signals.[5]

PAT

PAT

PATENT ATTORNEY DOCKET: 51432-038WO2 Part 4 – Purification of Compound A – (1S,2S)-N-[(7S,13S)-21-ethyl-20-{2-[(1S)-1- methoxyethyl]-5-(4-

1.0equiv) at 25°C. The resulting suspension was stirred until solids were completely dissolved. The resulting methanol solution was filtered through microporous filter and transferred to another reactor. Then the reactor temperature was maintained at 25°C and slowly water (2.41kg, 1.0 V) water was added over a period of 30 minutes. The resulting cloudy solution was stirred for another 30 minutes at 25°C. Then a solution of methanol and water (3.42kg, 1:2, v/v) slowly over 1 hour. The resulting suspension was stirred for 2 hours at 25°C. Again, to the suspension additional water (2.48kg) slowly added over 1 hour. The final, suspension was stirred for additional 1 hour. Water (9.29kg, 3.75 V) was added to the suspension slowly over 2 hours and the mixture was stirred for at least for 16 hours at 25°C. The resulting suspension was filtered and washed with mixed solvent water: MeOH (3:2, v/v) twice (2x 2.2 kg), followed by water (4.91kg) washing. The wet cake was dried under reduced pressure and controlled humidity (temperature: 25 ± 5 ˚C, vacuum ≥ -0.085 MPa, humidity: 10%~20%) for 37 hours to afford Compound A as a white solid (2.68 kg, 99.4% a/a purity, 93.0% w/w assay, KF: 6.7%, 3.07 mol, 92% yield, Table 27).

PAT

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References

References

  1.  Cregg J, Edwards AV, Chang S, Lee BJ, Knox JE, Tomlinson AC, et al. (March 2025). “Discovery of Daraxonrasib (RMC-6236), a Potent and Orally Bioavailable RAS(ON) Multi-selective, Noncovalent Tri-complex Inhibitor for the Treatment of Patients with Multiple RAS-Addicted Cancers”. Journal of Medicinal Chemistry. 68 (6): 6064–6083. doi:10.1021/acs.jmedchem.4c02314. PMID 40056080.
  2.  Sava J (July 1, 2025). “Daraxonrasib Earns FDA Breakthrough Status in Pancreatic Cancer”. Targeted Oncology. Retrieved October 12, 2025.
  3.  Jiang J, Jiang L, Maldonato BJ, Wang Y, Holderfield M, Aronchik I, et al. (June 2024). “Translational and Therapeutic Evaluation of RAS-GTP Inhibition by RMC-6236 in RAS-Driven Cancers”. Cancer Discovery. 14 (6): 994–1017. doi:10.1158/2159-8290.CD-24-0027. PMC 11149917. PMID 38593348.
  4.  Clinical trial number NCT05379985 at ClinicalTrials.gov
  5.  Mast J (2026-04-13). “Revolution Medicines touts ‘unprecedented’ data for pancreatic cancer pill”. STAT. Retrieved 2026-04-13.
Clinical data
Other namesRMC-6236
Identifiers
IUPAC name
CAS Number2765081-21-6
PubChem CID164726578
IUPHAR/BPS13368
ChemSpider115275938
UNIIB6T47Y2UAP
KEGGD13265
ChEBICHEBI:746946
Chemical and physical data
FormulaC44H58N8O5S
Molar mass811.06 g·mol−1
3D model (JSmol)Interactive image
SMILES
InChI

//////////daraxonrasib, anax labs, Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2, FDA APPROVED 2026, FDA 2026, Rasonque

#daraxonrasib, #anax labs, #Kirsten rat sarcoma viral oncogene homolog inhibitor, #antineoplastic, #RMC-6236, #RMC 6236, B6T47Y2UAP, #RAS-IN-2, #APPROVALS 2026, #FDA 2026, #Rasonque

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