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Silevertinib


Silevertinib
CAS 2607829-38-7
MF C30H30ClFN6O2 MW561.0 g/mol
(E)-N-[4-(3-chloro-2-fluoroanilino)-7-[2-[(1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl]quinazolin-6-yl]-4-morpholin-4-ylbut-2-enamide
(2E)-N-[4-(3-chloro-2-fluoroanilino)-7-{[(1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl]ethynyl}quinazolin-6-yl]-4-(morpholin-4-yl)but-2-enamide
epidermal growth factor receptor tyrosine kinase inhibitor, antineoplastic, BDTX-1535, BDTX 1535, CANCER, Glioblastoma, Black Diamond Therapeutics, RP9F537KVY
Silevertinib is an investigational new drug that is being evaluated by Black Diamond Therapeutics for the treatment of glioblastoma and non-small cell lung cancer.[1] It is a EGFR protein tyrosine kinase inhibitor.[1][2]
Silevertinib (formerly known as BDTX-1535) is an investigational, orally bioavailable, fourth-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) developed by Black Diamond Therapeutics. It is specifically engineered to be brain-penetrant and to target a broad spectrum of both classical and non-classical EGFR mutations, as well as resistance mutations, while sparing wild-type EGFR to reduce side effects.
Silevertinib is an orally bioavailable, brain penetrating, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, silevertinib selectively targets, irreversibly binds to, and inhibits the activity of various EGFR alterations and mutations, including certain intrinsic and acquired resistance mutations. This prevents EGFR-mediated signaling in susceptible tumor cells. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
Mechanism of Action
Silevertinib works by selectively and irreversibly binding to mutated EGFR receptors. EGFR is a receptor tyrosine kinase that, when mutated, triggers uncontrolled cell division and tumor vascularization. By shutting down this signaling cascade, silevertinib induces tumor cell death and inhibits further growth.
A major clinical advantage of the drug is its ability to cross the blood-brain barrier, allowing it to target central nervous system (CNS) tumors and brain metastases that many traditional therapies fail to reach.
Target Indications & Clinical Data
Silevertinib is primarily being studied for two aggressive types of cancer:
- Non-Small Cell Lung Cancer (NSCLC): It targets frontline patients with classical and over 50 non-classical EGFR driver mutations, as well as patients who have developed the acquired C797S resistance mutation from prior treatments. Phase 2 clinical trial data presented at the American Society of Clinical Oncology (ASCO) 2026 Annual Meeting showcased robust efficacy:
- Objective Response Rate (ORR): 60% in treatment-naïve patients.
- CNS Response Rate: An impressive 86% intracranial ORR in patients presenting with brain metastases.
- Disease Control Rate (DCR): 91%.
- Glioblastoma Multiforme (GBM): In May 2026, a randomized Phase 2 trial was initiated for newly diagnosed patients with EGFRvIII-positive, MGMT-negative glioblastoma, evaluating silevertinib in combination with temozolomide.
Safety Profile & Side Effects
The adverse events of silevertinib are consistent with the broader class of EGFR inhibitors. The most frequently reported treatment-related adverse events (TRAEs) include:
- Rash
- Diarrhea
- Stomatitis (mouth sores)
- Paronychia (nail bed inflammation)
While a high percentage of patients (up to 77–84%) require dose reductions to manage these side effects, data shows that 86% of responding patients maintained or deepened their clinical response even after dropping to a lower dose. The treatment discontinuation rate remains low at roughly 9–14%, indicating the drug is manageable for long-term therapy.
Regulatory Status
As an investigational drug, silevertinib is not yet approved for commercial use by global regulatory agencies. However, the manufacturer anticipates regulatory feedback from the US FDA regarding its registration pathway for first-line NSCLC therapy.
- OriginatorBlack Diamond Therapeutics
- Class2 ring heterocyclic compounds; Amides; Amines; Aniline compounds; Antineoplastics; Halogenated hydrocarbons; Morpholines; Quinazolines; Small molecules
- Mechanism of ActionErbB receptor antagonists
- Phase IIGlioblastoma
- Phase I/IINon-small cell lung cancer
- Phase 0Glioma
- 06 Aug 2026Black Diamond Therapeutics anticipates regulatory feedback from the US FDA on registration path of silevertinib for Non-small cell lung cancer (First-line therapy) in the fourth quarter of 2026 (Black Diamond pipeline, May 2026)
- 02 Jun 2026Efficcay and adverse event data from phase I/II trial in Non-small cell lung cancer presented at the 62nd Annual Meeting of the American Society of Clinical Oncology (ASCO-2026)
- 21 May 2026Efficacy and adverse events data from a phase I/II trial in Non small cell lung cancer released by Black Diamond Therapeutics
SYN
- BDTX-1535 Goes after Osimertinib ResistancePublication Name:Cancer DiscoveryPublication Date:2021-12-01PMID:34702733DOI:10.1158/2159-8290.cd-nb2021-0395
- Further characterization of a DNA polymerase activity in mouse sperm nucleiPublication Name:Biochimica et Biophysica Acta (BBA) – Nucleic Acids and Protein SynthesisPublication Date:1976-10-04PMID:10003DOI:10.1016/0005-2787(76)90342-7
PAT
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2021030711&_cid=P21-MU6CBO-49598-1
Example 33. Synthesis of Compound No. 37 ((E)-N-(4-((3-chloro-2-fluorophenyl)amino)-7-(((1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl)ethynyl)quinazolin-6-yl)-4-morpholinobut-2-enamide)

PAT
WO2026064728

PAT
US20220298120
https://patentscope.wipo.int/search/en/detail.jsf?docId=US375116378&_cid=P21-MU6C60-41372-1
Example 33. Synthesis of Compound No. 37 ((E)-N-(4-((3-chloro-2-fluorophenyl)amino)-7-(((1R,5S)-3-methyl-3-azabicyclo[3.1.0]hexan-1-yl)ethynyl)quinazolin-6-yl)-4-morpholinobut-2-enamide)

| Step 1. To a solution of (E)-4-bromobut-2-enoic acid (5.00 g, 30.3 mmol) and dimethylformamide (22.2 mg, 303 umol) in dichloromethane (20 mL) was added (COCl) 2 (3.85 g, 30.3 mmol) dropwise at 0° C. under N 2. The mixture was stirred at 0-25° C. for 4 h. On completion, the reaction mixture was concentrated in vacuo to give (E)-4-bromobut-2-enoyl chloride (5.8 g, crude) as a yellow oil. |
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References
- “Silevertinib”. AdisInsight. Springer Nature Switzerland AG. Retrieved 5 July 2026.
- Joshi H, Sheikh MS (August 2025). “Cell Death, Molecular Targeted Therapies, and Metabolic Reprogramming in EGFR-Mutant Lung Cancer”. Cancers. 17 (17). Basel: 2791. doi:10.3390/cancers17172791. PMC 12427363. PMID 40940888.
PAT
- Polymorphs as erbb inhibitorsPublication Number:EP-4405350-A1Priority Date:2021-09-21
- Polymorphs as erbb inhibitorsPublication Number:US-2024425492-A1Priority Date:2021-09-21
- Polymorphs as erbb inhibitorsPublication Number:WO-2023049168-A1Priority Date:2021-09-21
- Method of treating cancers with alkyne substituted quinazoline derivativesPublication Number:WO-2022094464-A1Priority Date:2020-11-02
- Alkynyl quinazoline compoundsPublication Number:EP-4013749-A1Priority Date:2019-08-15
- Alkynyl quinazoline compoundsPublication Number:US-2022298120-A1Priority Date:2019-08-15
- Alkynyl quinazoline compoundsPublication Number:US-2026049063-A1Priority Date:2019-08-15
- Alkynyl quinazoline compoundsPublication Number:US-12435046-B2Priority Date:2019-08-15Grant Date:2025-10-07
- Alkynyl quinazoline compoundsPublication Number:EP-4013749-B1Priority Date:2019-08-15Grant Date:2026-03-11
- Alkynyl quinazoline compoundsPublication Number:WO-2021030711-A1Priority Date:2019-08-15
| Clinical data | |
|---|---|
| Other names | RVU-120 |
| Identifiers | |
| IUPAC name | |
| CAS Number | 2607829-38-7 |
| PubChem CID | 156071569 |
| IUPHAR/BPS | 13371 |
| UNII | RP9F537KVY |
| KEGG | D13300 |
| Chemical and physical data | |
| Formula | C30H30ClFN6O2 |
| Molar mass | 561.06 g·mol−1 |
| 3D model (JSmol) | Interactive image |
| SMILES | |
| InChI | |
///////////silevertinib, anax labs, epidermal growth factor receptor tyrosine kinase inhibitor, antineoplastic, BDTX-1535, BDTX 1535, CANCER, Glioblastoma, Black Diamond Therapeutics, RP9F537KVY
#silevertinib, #anax labs, #epidermal growth factor receptor tyrosine kinase inhibitor, #antineoplastic, #BDTX-1535, #BDTX 1535, #CANCER, #Glioblastoma, #Black Diamond Therapeutics, #RP9F537KVY
Floretyrosine F 18


Floretyrosine F 18
CAS 178433-03-9
FormulaC₁₁H₁₄[¹⁸F]NO₃
Molecular Weight226.23 g/mol
FDA UNII1326R5J1IA
FDA 2026, APPROVALS 2026, Pixclara, TELIX PHARMACEUTICALS, GLIOMA, CANCER, TLX101-CDx, TLX101-Px, 1326R5J1IA, L-(18F)FET, O-(2-((18)F)fluoroethyl)-L-tyrosine
(2S)-2-amino-3-[4-(2-[¹⁸F]fluoroethoxy)phenyl]propanoic acid, (2S)-2-amino-3-[4-(2-(18F)fluoroethoxy)phenyl]propanoic acid
To use with positron emission tomography to differentiate recurrent or progressive glioma from treatment-related change in conjunction with other diagnostic evaluations
Floretyrosine F 18 (brand name Pixclara®, also known as 18F-FET) is a newly FDA-approved radiopharmaceutical imaging drug used in positron emission tomography (PET) scans for patients with glioma (brain cancer). Developed by Telix Pharmaceuticals, it received formal U.S. Food and Drug Administration (FDA) approval on September 14, 2026, making it the first and only approved FET-PET diagnostic tracer for brain tumors in the United States.
Primary Clinical Indication
Pixclara is indicated for use in both adult and pediatric patients (1 month of age and older).
Its primary clinical purpose is to differentiate recurrent or progressive glioma from treatment-related changes (such as radiation necrosis or inflammation). Following chemotherapy or radiation, traditional MRI scans often show areas that “light up,” making it incredibly difficult for neuro-oncologists to tell whether a tumor is growing back or if the brain is simply healing from harsh treatments. Pixclara solves this diagnostic dilemma by providing metabolic clarity.
How It Works (Mechanism of Action)
- Targeted Delivery: Floretyrosine F 18 is a synthetic amino acid analogue labeled with the radioactive isotope fluorine-18. [1, 2]
- Cellular Uptake: Once injected intravenously, it specifically targets and binds to L-type amino acid transporters 1 and 2 (LAT1 and LAT2). These transporters are heavily overexpressed on the membranes of active glioma cells compared to healthy brain tissue.
- PET Detection: The tumor cells rapidly absorb the tracer, and the energy emissions from the fluorine-18 isotope are captured by a PET scanner, creating a highly accurate metabolic map of the tumor.
Strategic & Future Impact
The approval aligns U.S. practice with international clinical guidelines—such as the National Comprehensive Cancer Network (NCCN) Guidelines®—which already recommend FET-PET imaging for brain tumor management. Furthermore, Telix Pharmaceuticals is currently conducting a Phase 3 registrational study to expand Pixclara’s indication to include the diagnosis and characterization of brain metastases (cancers that have spread to the brain from other parts of the body)
Fluoroethyl-l-tyrosine (18F), commonly known as [18F]FET, is a radiopharmaceutical tracer used in positron emission tomography (PET) imaging. This synthetic amino acid, labeled with the radioactive isotope fluorine-18, is a valuable radiopharmaceutical tracer for use in neuro-oncology for diagnosing, planning treatment, and following up on brain tumors such as gliomas. The tracer’s ability to provide detailed metabolic imaging of tumors makes it an essential tool in the clinical management of brain cancer patients. Continued advancements in PET imaging technology and the development of more efficient synthesis methods are expected to further enhance the clinical utility of [18F]FET.[2]
Radiosynthesis
There are two common pathways for the radiosynthesis of [18F]FET. The first one utilizes a nucleophilic 18F-fluorination of ethyleneglycol-1,2-ditosylate with a subsequent 18F-fluoroethylation of a precursor di-sodium salt of L-tyrosine. This sequence requires two purification steps, two different precursors and a dual-reactor synthesis module which is not widely available in research or commercial centers.[3][4][5] The schematic for this pathway is:[6]

The second route of radiosynthesis is a direct nucleophilic 18F-fluorination a TET (O-(2-tosyloxy-ethyl)-N-trityl-L-tyrosine tert-butyl ester) protected precursor followed by acidic hydrolysis of protecting groups.[3][4][7] The schematic for this pathway is:[6]
REF
- Fluorinated phenylalanines: synthesis and pharmaceutical applicationsPublication Name:Beilstein Journal of Organic ChemistryPublication Date:2020-05-15PMCID:PMC7237815PMID:32509033DOI:10.3762/bjoc.16.91
- Solid-Phase Synthesis of O-(2-[18F]-Fluoro-ethyl)-l-tyrosinePublication Name:SynfactsPublication Date:2013-03-15DOI:10.1055/s-0032-1318420
- Investigations into the synthesis, radiofluorination and conjugation of a new [18F]fluorocyclobutyl prosthetic group and its in vitro stability using a tyrosine model systemPublication Name:Bioorganic & Medicinal ChemistryPublication Date:2013-02-01PMID:23290251DOI:10.1016/j.bmc.2012.11.049
- Microfluidic technology: An economical and versatile approach for the synthesis of O-(2-[18F]fluoroethyl)-l-tyrosine ([18F]FET)Publication Name:Bioorganic & Medicinal Chemistry LettersPublication Date:2012-03-15PMID:22342141DOI:10.1016/j.bmcl.2012.01.083
- Synthesis and biological evaluation of novel F-18 labeled pyrazolo[1,5-a]pyrimidine derivatives: Potential PET imaging agents for tumor detectionPublication Name:Bioorganic & Medicinal Chemistry LettersPublication Date:2011-08-15PMID:21752641DOI:10.1016/j.bmcl.2011.06.072
- (18)F Labeled benzimidazole derivatives as potential radiotracer for positron emission tomography (PET) tumor imagingPublication Name:Bioorganic & Medicinal ChemistryPublication Date:2010-04-01PMID:20303769DOI:10.1016/j.bmc.2010.02.060
- No carrier added synthesis of O-(2′-[18F]fluoroethyl)-l-tyrosine via a novel type of chiral enantiomerically pure precursor, NiII complex of a (S)-tyrosine Schiff basePublication Name:Bioorganic & Medicinal ChemistryPublication Date:2008-05-01PMID:18378460DOI:10.1016/j.bmc.2008.03.040
- Solid-Phase Synthesis of O-(2-[18F]-Fluoro-ethyl)-l-tyrosine, DOI:10.1055/s-0032-1318420, Publication Date:2013, Publication Name:Synfacts
SYN
US20190223814/US249082034

PAT
US20120189546
https://patentscope.wipo.int/search/en/detail.jsf?docId=US73636763&_cid=P11-MU3HO5-37901-1
PAT
US20140235861
https://patentscope.wipo.int/search/en/detail.jsf?docId=US107206441&_cid=P11-MU3HO5-37901-1
Another example of an 18F-fluoroalkylation reaction to obtain a PET tracer is the reaction described by Wang et al (2006 J Radioanalyt Nuc Chem; 270(2): 439-43) used to obtain the 18F-labeled amino acid O-(2-[ 18F]fluoroethyl)-L-tyrosine ([ 18F]FET):

[ 18F]Fluoroethyl tosylate was prepared in step (i) by displacement of a tosyl group from 1,2-bistosyloxyethane by reaction with K 18F/Kryptofix 2.2.2 in acetonitrile at 90° C. for 10 minutes. The purified [ 18F]fluoroethyl tosylate was then reacted in step (ii) with a solution of L-tyrosine and 10% aqueous NaOH in DMSO (or di-Na-salt of L-tyrosine in DMSO) 20 minutes at 90° C. to obtain [ 18F]FET. In contrast to the method for preparation of 18F-labelled S-fluoroalkyl diarylguanidines as reported by Robins et al (supra), this method for preparation of [ 18F]FET uses a soluble base in the alkylation reaction. However, the reaction is still not ideal for carrying out on an automated synthesis device that uses a cassette due to the fact that and additional vial is required for the base used for the subsequent fluoroalkylation step.
PAT
Radiation radiation detector with position tracking system and its use in medical systems and proceduresPublication Number:
JP-2004512502-APriority Date:2000-08-21
- Novel imaging agents and precursors and methods of preparation thereofPublication Number:CN-1234680-CPriority Date:2001-06-04Grant Date:2006-01-04
- Radioactive emission detector equipped with a position tracking system and utilization thereof with medical systems and in medical proceduresPublication Number:US-2005055174-A1Priority Date:2000-08-21
- Radioactive emission detector equipped with a position tracking system and utilization thereof with medical systems and in medical proceduresPublication Number:US-7826889-B2Priority Date:2000-08-21Grant Date:2010-11-02
- Radioactive emission detector equipped with a position tracking system and utilization thereof with medical systems and in medical proceduresPublication Number:US-2004015075-A1Priority Date:2000-08-21
- Radioactive emission detector equipped with a position tracking systemPublication Number:US-2014249402-A1Priority Date:2000-08-21
- Tumor imaging compoundsPublication Number:CA-2479514-CPriority Date:2002-04-30Grant Date:2011-07-26
- Protected tyrosine derivatives, method for the production thereof and use of the same for producing o-(2-[18f]-fluoroethyl)-l-tyrosinePublication Number:WO-02102765-A3Priority Date:2001-06-05
- Protected tyrosine derivatives, method for the production thereof and use of the same for producing o-(2-[18f]-fluoroethyl)-l-tyrosinePublication Number:US-2004192954-A1Priority Date:2001-06-05
- PROTECTED TYROSINE DERIVATIVES, METHOD FOR THE PRODUCTION THEREOF AND THEIR USE FOR THE PRODUCTION OF O-(2-?18 F)-FLUORETHYL)-L-TYROSINEPublication Number:AT-E289992-T1Priority Date:2001-06-05Grant Date:2005-03-15
- Imaging agents, precursors thereof and methods of manufacturePublication Number:US-2003124059-A1Priority Date:2001-06-04
- Radioactively labelled amino acid analogues, their preparation and usePublication Number:US-2006127306-A1Priority Date:2002-08-02
- Radioactively labelled amino acid analogues, their preparation and usePublication Number:EP-1539250-A1Priority Date:2002-08-02
- Tumor imaging compoundsPublication Number:US-7989649-B2Priority Date:2002-04-30Grant Date:2011-08-02
- Tumor imaging compoundsPublication Number:US-2009240041-A1Priority Date:2002-04-30
- Tumor imaging compoundsPublication Number:US-7544715-B2Priority Date:2002-04-30Grant Date:2009-06-09
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References
- CID 54255856 from PubChem
- Treglia G, Muoio B, Giovanella L (2020). “18F-FET”. In Calabria F, Schillaci O (eds.). Radiopharmaceuticals: A Guide to PET/CT and PET/MRI. Cham: Springer International Publishing. pp. 83–88. doi:10.1007/978-3-030-27779-6_4. ISBN 978-3-030-27778-9.
- Bourdier T, Greguric I, Roselt P, Jackson T, Faragalla J, Katsifis A (July 2011). “Fully automated one-pot radiosynthesis of O-(2-[18F]fluoroethyl)-L-tyrosine on the TracerLab FX(FN) module”. Nuclear Medicine and Biology. 38 (5): 645–651. doi:10.1016/j.nucmedbio.2011.01.001. PMID 21718939.
- Siddiq IS, Atwa ST, Shama SA, Eltaoudy MH, Omar WM (March 2018). “Radiosynthesis and modified quality control of O-(2-[18F]fluoroethyl)-L-tyrosine ([18F]FET) for brain tumor imaging”. Applied Radiation and Isotopes. 133: 38–44. Bibcode:2018AppRI.133…38S. doi:10.1016/j.apradiso.2017.12.011. PMID 29275040.
- Wester HJ, Herz M, Weber W, Heiss P, Senekowitsch-Schmidtke R, Schwaiger M, et al. (January 1999). “Synthesis and radiopharmacology of O-(2-[18F]fluoroethyl)-L-tyrosine for tumor imaging”. Journal of Nuclear Medicine. 40 (1): 205–212. PMID 9935078.
- Wang M, Glick-Wilson BE, Zheng QH (December 2019). “Facile fully automated radiosynthesis and quality control of O-(2-[18F]fluoroethyl)-l-tyrosine ([18F]FET) for human brain tumor imaging”. Applied Radiation and Isotopes. 154 108852. Bibcode:2019AppRI.15408852W. doi:10.1016/j.apradiso.2019.108852. PMID 31442794.
- Mueller D, Klette I, Kalb F, Baum RP (July 2011). “Synthesis of O-(2-[18F]fluoroethyl)-L-tyrosine based on a cartridge purification method”. Nuclear Medicine and Biology. 38 (5): 653–658. doi:10.1016/j.nucmedbio.2011.01.006. PMID 21718940.
- Muoio B, Giovanella L, Treglia G (2018-09-04). “Recent Developments of 18F-FET PET in Neuro-oncology”. Current Medicinal Chemistry. 25 (26): 3061–3073. doi:10.2174/0929867325666171123202644. PMID 29173147.
- Wang L, Lieberman BP, Ploessl K, Kung HF (January 2014). “Synthesis and evaluation of ¹⁸F labeled FET prodrugs for tumor imaging”. Nuclear Medicine and Biology. 41 (1): 58–67. doi:10.1016/j.nucmedbio.2013.09.011. PMC 3895945. PMID 24183614.
- Lee TS, Ahn SH, Moon BS, Chun KS, Kang JH, Cheon GJ, et al. (August 2009). “Comparison of 18F-FDG, 18F-FET and 18F-FLT for differentiation between tumor and inflammation in rats”. Nuclear Medicine and Biology. 36 (6): 681–686. doi:10.1016/j.nucmedbio.2009.03.009. PMID 19647174.
- Leung K (2004), “O-(2-[18F]Fluoroethyl)-L-tyrosine”, Molecular Imaging and Contrast Agent Database (MICAD), Bethesda (MD): National Center for Biotechnology Information (US), PMID 20641653, retrieved 2024-07-10
- Heiss P, Mayer S, Herz M, Wester HJ, Schwaiger M, Senekowitsch-Schmidtke R (August 1999). “Investigation of transport mechanism and uptake kinetics of O-(2-[18F]fluoroethyl)-L-tyrosine in vitro and in vivo”. Journal of Nuclear Medicine. 40 (8): 1367–1373. PMID 10450690.
- Wang HE, Wu SY, Chang CW, Liu RS, Hwang LC, Lee TW, et al. (May 2005). “Evaluation of F-18-labeled amino acid derivatives and [18F]FDG as PET probes in a brain tumor-bearing animal model”. Nuclear Medicine and Biology. 32 (4): 367–375. doi:10.1016/j.nucmedbio.2005.01.005. PMID 15878506.
- Rau FC, Weber WA, Wester HJ, Herz M, Becker I, Krüger A, et al. (August 2002). “O-(2-[(18)F]Fluoroethyl)- L-tyrosine (FET): a tracer for differentiation of tumour from inflammation in murine lymph nodes”. European Journal of Nuclear Medicine and Molecular Imaging. 29 (8): 1039–1046. doi:10.1007/s00259-002-0821-6. PMID 12173018.
- Holzgreve A, Brendel M, Gu S, Carlsen J, Mille E, Böning G, et al. (2016-06-14). “Monitoring of Tumor Growth with [(18)F]-FET PET in a Mouse Model of Glioblastoma: SUV Measurements and Volumetric Approaches”. Frontiers in Neuroscience. 10: 260. doi:10.3389/fnins.2016.00260. PMC 4906232. PMID 27378835.
- “Product Characteristic of IASOglio©” (PDF). synektik.com.pl. 28 June 2024. Retrieved 28 June 2024.
- Pauleit D, Floeth F, Herzog H, Hamacher K, Tellmann L, Müller HW, et al. (April 2003). “Whole-body distribution and dosimetry of O-(2-[18F]fluoroethyl)-L-tyrosine”. European Journal of Nuclear Medicine and Molecular Imaging. 30 (4): 519–524. doi:10.1007/s00259-003-1118-0. PMID 12589478.
- Tang G, Tang X, Wang M, Luo L, Gan M (January 2004). “Radiation dosimetry of O-(3-[18F]fluoropropyl)-L-tyrosine as oncologic PET tracer based on the mice distribution data”. Applied Radiation and Isotopes. 60 (1): 27–32. doi:10.1016/j.apradiso.2003.10.005. PMID 14687633.
- Mattsson S, Johansson L, Leide Svegborn S, Liniecki J, Noßke D, Riklund KÅ, et al. (July 2015). “Radiation Dose to Patients from Radiopharmaceuticals: a Compendium of Current Information Related to Frequently Used Substances” (PDF). Annals of the ICRP. 44 (2 Suppl): 7–321. doi:10.1177/0146645314558019. PMID 26069086.
- “IASOglio”. Curium Pharma. Retrieved 2024-07-10.
| Clinical data | |
|---|---|
| Other names | 18F-FET; O-(2-(18F)fluoroethyl)-l-tyrosine, O-(2-Fluorethyl)-l-thyrosine, l-(18F)FET[1] |
| Routes of administration | Intravenous |
| ATC code | V09IX10 (WHO) |
| Identifiers | |
| IUPAC name | |
| CAS Number | 178433-03-9 |
| PubChem CID | 9834479 |
| ChemSpider | 8010200 |
| UNII | 1326R5J1IA |
| CompTox Dashboard (EPA) | DTXSID601045942 |
| Chemical and physical data | |
| Formula | C11H14FNO3 |
| Molar mass | 227.235 g·mol−1 |
| 3D model (JSmol) | Interactive image |
| SMILES | |
| InChI | |
///////////floretyrosine F 18, anax labs, FDA 2026, APPROVALS 2026, Pixclara, TELIX PHARMACEUTICALS, GLIOMA, CANCER, TLX101-CDx, TLX101-Px, 1326R5J1IA, L-(18F)FET, O-(2-((18)F)fluoroethyl)-L-tyrosine
#floretyrosine F 18, #anax labs, #FDA 2026, #APPROVALS 2026, #Pixclara, #TELIX PHARMACEUTICALS, #GLIOMA, #CANCER, #TLX101-CDx, #TLX101-Px, #1326R5J1IA, #L-(18F)FET, #O-(2-((18)F)fluoroethyl)-L-tyrosine
Prifetrastat



Prifetrastat
CAS 2569008-99-5
MFC19H18N4O5S MW414.4 g/mol
N-(6-((1H-Pyrazol-1-yl)methyl)-4-methoxybenzo[d]isoxazol-3-yl)-2-methoxybenzenesulfonamide
2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide
antineoplastic, PF-07248144, PF 07248144, Solid tumours, CANCER, KAT6-IN-1, GN6DU4ZE30
Prifetrastat is an inhibitor of MYST histone acetyltransferase (HAT) KAT6, with potential antineoplastic activity. Upon administration, prifetrastat targets and binds to KAT6, and inhibits the acetylation of histones and other nonhistone substrates. This may disrupt gene expression and inhibit the proliferation of tumors that overexpress KAT6. KAT6A (MOZ; MYST3) and KAT6B (MORF; MOZ2; MYST4), commonly amplified genes in solid tumors, play key roles in cell cycle regulation and in tumorigenesis.
Prifetrastat (also known as PF-07248144) is an investigational, first-in-class small molecule drug that acts as a selective inhibitor of the epigenetic modifiers KAT6A and KAT6B. It is primarily studied as an antineoplastic agent for hormone receptor-positive (ER+/HER2–) advanced or metastatic breast cancer.
Mechanism of Action
- Inhibits KAT6A and KAT6B histone acetyltransferases to block abnormal tumor cell growth.
- Suppresses lineage-specific gene expression tied to estrogen receptor signaling and drug resistance.
- Induces cell cycle arrest and tumor senescence.
Clinical Development
- Evaluated in clinical trials (such as phase 1/2 and phase 3 evaluations) for patients whose breast cancer progressed after prior endocrine therapy and CDK4/6 inhibitors.
- Commonly tested in combination regimens alongside anti-estrogen therapies like fulvestrant
Prifetrastat (also known as PF-07248144) is an investigational, first-in-class small molecule drug that acts as a selective inhibitor of the epigenetic modifiers KAT6A and KAT6B. It is primarily studied as an antineoplastic agent for hormone receptor-positive (ER+/HER2–) advanced or metastatic breast cancer.
Mechanism of Action
- Inhibits KAT6A and KAT6B histone acetyltransferases to block abnormal tumor cell growth.
- Suppresses lineage-specific gene expression tied to estrogen receptor signaling and drug resistance.
- Induces cell cycle arrest and tumor senescence.
Clinical Development
- Evaluated in clinical trials (such as phase 1/2 and phase 3 evaluations) for patients whose breast cancer progressed after prior endocrine therapy and CDK4/6 inhibitors.
- Commonly tested in combination regimens alongside anti-estrogen therapies like fulvestrant
- Phase IIIHER2 negative breast cancer
- Phase IISolid tumours
- No development reportedBreast cancer
- 07 Aug 2026Prifetrastat is still in phase II development in Solid-tumours (Combination therapy, Late-stage disease, Metastatic disease, Second-line therapy or greater) in USA, Australia, Japan, China, South Korea (PO, Tablet) (NCT04606446)
- 07 Aug 2026Prifetrastat is still in phase II development in Solid-tumours (Monotherapy, Late-stage disease, Metastatic disease, Second-line therapy or greater) in USA, Australia, Japan, China, South Korea (PO, Tablet) (NCT04606446)
- 28 Jul 2026No recent reports of development identified for phase-I development in Breast-cancer(Metastatic disease) in USA (PO)
PAT
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2020254946&_cid=P12-MSO1IP-41527-1
Example 45: Preparation of 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide according to Scheme C (Route A).

To a suspension of 4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-amine (A-2) (2.5 g, 10 mmol) in pyridine (8.0 mL) was added 2-methoxybenzene-1-sulfonyl chloride (3.17 g, 15.4 mmol). The reaction was stirred at 120 °C for 1.5 h. The mixture was cooled to room temperature and diluted with MeOH. The resulting suspension was filtered. and the filter cake was washed with MeOH (30 mL). The solids were dissolved in DCM (50 mL) and MeOH (30 mL) was added. The DCM was removed under vacuum
and the precipitate was collected by filtration. The filter cake was dried by lyophilization to provide 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (2.5 g, 59% yield) as a white solid. 1 H NMR (400 MHz, DMSO-d6) d 10.18 (s, 1H), 7.87 (d, J= 2.0 Hz, 1H), 7.80 (dd, J=1.6, 7.9 Hz, 1H), 7.66– 7.59 (m, 1H), 7.49 (d, J=1.5 Hz, 1H), 7.19 (d, J=8.3 Hz, 1H), 7.09 (t, J=7.7 Hz, 1H), 6.83 (s, 1H), 6.74 (s, 1H), 6.30 (t, J=2.0 Hz, 1H), 5.44 (s, 2H), 3.82 (s, 3H), 3.78 (s, 3H); m/z (ESI+) 415.0 (M+H) + .
Example 45: Alternative preparation of 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide according to Scheme D.

A 100 mL reactor equipped with an overhead stirrer was charged with 4-methoxy-6-(1H-pyrazol-1-ylmethyl)-1,2-benzoxazol-3-amine (A-2) (10.00 g, 40.94 mmol), 2-methoxybenzenesulfonyl chloride (10.15 g, 49.13 mmol), and acetonitrile (100 mL). The resulting suspension was stirred at 25 °C for 55 minutes. Via pipette, dimethylsulfoxide (0.36 mL, 4.09 mmol) was added in one portion. Via syringe, 3,5-lutidine (14.8 mL, 122.82 mmol) was added dropwise over 15 minutes. The resulting light-yellow suspension was stirred at 25 °C for 18 hours to reach >98% conversion as judged by LCMS. The reaction mixture was acidified with 1 M aq. HCl (100 mL), then
concentrated to ~80 mL (rotary evaporator, 40 °C, 85 mbar). The slurry was treated with additional 1 M aq. HCl (40 mL) to rinse down the walls of the vessel, then stirred at 20 °C for 2.5 hours. The resulting precipitate was collected by suction filtration. The filter cake was washed with water (2 x 50 mL), then dried under vacuum at 35 °C for 48 hours, affording crude 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (15.2 g, 90% yield, 98% purity by LCMS) as a solid. m/z 415.1 (M+H) + .
To purify the crude product, a suspension of crude 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (14.00 g, 33.78 mmol) in dichloromethane (210 mL) was heated in a 40 °C bath until a clear solution was obtained (10 minutes). The mixture was filtered, and the filtrate returned to a clean reaction vessel, using additional dichloromethane (70 mL) to quantitate the transfer. Ethyl acetate (140 mL) was added to the solution over 2 minutes, then the mixture stirred for 2.5 hours. No crystallization was observed, so the solution was concentrated under reduced pressure (200 mbar) to remove dichloromethane (volume was reduced by about 70 mL). More ethyl acetate (140 mL) was added to the residue, and the mixture stirred at room temperature for 21 hours. The resulting suspension was concentrated under reduced pressure (40 °C, 200 mbar) to about 280 mL, then stirred at room temperature for 3 hours. The solids were collected by filtration, with additional ethyl acetate (70 mL) used to rinse the reaction vessel and filter cake. The filter cake was dried in a vacuum oven at 35 °C for 23 hours, affording 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (12.0 g, 85% yield, 97.9% purity by UPLC, no single impurity larger than 0.5%) as a solid. m/z 415.1 (M+H) + .
To purify further, a suspension of 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (2.0 g, 4.73 mmol) in acetone (80 mL) was heated to reflux (bath temperature 55 °C) with stirring for 2 hours. While the mixture was still heated, ethyl acetate (30 mL) was added slowly, so that the internal temperature remained above 45 °C. The resulting slurry was concentrated to about 30 mL under mild vacuum (bath temp 65 °C), then cooled slowly at a rate of 1 °C/min to 20 °C (~31 minutes). The resulting precipitate was collected by suction filtration. The filter cake dried under vacuum at 50 °C for 22 hours, yielding 2-methoxy-N-{4-methoxy-6-[(1H-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamide (Example 45) (1.825 g, 93% yield, 99.5% purity by UPLC) as a crystalline solid. 1 hour
NMR (400 MHz, CHLOROFORM-d) d 8.14 (dd, J=1.7, 7.8 Hz, 1H), 8.04 (s, 1H), 7.59 -7.51 (m, 2H), 7.44 (d, J=2.2 Hz, 1H), 7.14 – 7.06 (m, 1H), 6.95 (d, J=8.3 Hz, 1H), 6.78 (d, J=0.6 Hz, 1H), 6.45 (s, 1H), 6.32 (t, J=2.1 Hz, 1H), 5.38 (s, 2H), 3.97 (s, 3H), 3.91 (s, 3H).
PAT
PAT
Scheme 1
Step 2







In an inerted reactor were added 6-((1 H-pyrazol-1-yl)methyl)-4-methoxybenzo[d]isoxazol-3-amine (lnt-4, 27.5 Kg, 112.6 mol, 1 equiv.), 2-methoxybenzenesulfonyl chloride (lnt-5, 33.9 Kg, 168.9 mol, 1.5 equiv.) and THF (248 L, 9-L/Kg). A solution of sodium te/Y-butoxide in THF (2 M, 197 L, 394.1 mol, 3.5 eq.) was added to the stirred mixture at 20 °C over 4 h. At the end of the addition the line was rinsed with THF (27.5 L, 1 L/Kg) and the mixture stirred for a further 1 h. Following reaction completion water (413 L, 15 L/Kg) was added at once followed by slow addition of aq. HCI (2 M, 197 L, 394.1 mol, 3.5 equiv.). The mixture was left stirring overnight, then the slurry was filtered, washed twice with CH3OH (82.5 L, 3 L/Kg) and dried to afford the title compound as a white solid (42.32 Kg, 90.6% yield).
1H NMR (400 MHz, DMSO) 5 10.09 (s, 1 H), 7.87 (dd, J = 2.3, 0.7 Hz, 1 H), 7.81 (dd, J = 7.8, 1.7 Hz, 1 H), 7.63 (ddd, J = 8.4, 7.4, 1.7 Hz, 1 H), 7.50 (dd, J = 1.8, 0.7 Hz, 1 H), 7.10 (td, J = 7.6, 1 .0 Hz, 1 H), 6.84 (d, J = 1 .0 Hz, 1 H), 6.30 (t, J = 2.1 Hz, 1 H), 5.44 (s, 2H), 3.83 (s, 3H), 3.79 (s, 3H). 13C NMR (101 MHz, DMSO) 5 164.82, 156.92, 154.39, 151.76, 144.13, 139.80, 135.73, 131.03, 130.43, 127.66, 120.52, 113.34, 106.25, 106.17, 104.42, 101.33, 56.51, 56.42, 55.01. HRMS: Ci9Hi8N4O5S+ [M+1 ]+ calculated:
415.1072; measured: 415.1071.
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References
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- Benzisoxazole sulfonamide derivativesPublication Number:EP-4299135-B1Priority Date:2019-06-18Grant Date:2025-08-06
- Benzisoxazole sulfonamide derivativesPublication Number:AU-2020296361-A1Priority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:EP-4299135-A2Priority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:TW-202115048-APriority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:CN-114364672-BPriority Date:2019-06-18Grant Date:2024-09-06
- Benzisoxazole sulfonamide derivativesPublication Number:EP-3986890-A1Priority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:US-11492346-B2Priority Date:2019-06-18Grant Date:2022-11-08
- Benzisoxazole sulfonamide derivativesPublication Number:CA-3143666-A1Priority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:CN-114364672-APriority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:EP-3986890-B1Priority Date:2019-06-18Grant Date:2023-11-15
- Benzisoxazole sulfonamide derivativesPublication Number:WO-2020254946-A1Priority Date:2019-06-18
- Kat6 inhibitor and combinations for breast cancer treatmentPublication Number:EP-4181920-B1Priority Date:2020-07-15Grant Date:2025-09-10
- Benzisoxazole sulfonamide derivativesPublication Number:KR-20220024671-APriority Date:2019-06-18
- Benzisoxazole Sulfonamide DerivativesPublication Number:US-2023174522-A1Priority Date:2019-06-18
- Benzisoxazole Sulfonamide DerivativesPublication Number:US-2020399258-A1Priority Date:2019-06-18
- Benzisoxazole sulfonamide derivativesPublication Number:CA-3143666-CPriority Date:2019-06-18Grant Date:2024-06-11
- Dosing regimens comprising a kat6 inhibitor for the treatment of cancerPublication Number:WO-2024023703-A1Priority Date:2022-07-29
- Dosing regimens comprising a kat6 inhibitor for the treatment of cancerPublication Number:EP-4561571-A1Priority Date:2022-07-29
- Kat6 inhibitor methods and combinations for cancer treatmentPublication Number:EP-4181920-A1Priority Date:2020-07-15
- Kat6 inhibitor methods and combinations for cancer treatmentPublication Number:WO-2022013369-A1Priority Date:2020-07-15
- KAT6 inhibitor methods and combinations for cancer treatmentPublication Number:CN-116113407-APriority Date:2020-07-15
- Crystalline form of 2-methoxy-n-{4-methoxy-6-[(1h-pyrazol-1-yl)methyl]-1,2-benzoxazol-3-yl}benzene-1-sulfonamidePublication Number:WO-2025141469-A1Priority Date:2023-12-26
- Sulfonamide compound and use thereofPublication Number:WO-2025098417-A1Priority Date:2023-11-08
- MYST InhibitorsPublication Number:US-2025122182-A1Priority Date:2023-09-27
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///////////prifetrastat, anax labs, antineoplastic, PF-07248144, PF 07248144, Solid tumours, CANCER, KAT6-IN-1, GN6DU4ZE30
#prifetrastat, #anax labs, #antineoplastic, #PF-07248144, #PF 07248144, #Solid tumours, #CANCER, #KAT6-IN-1, #GN6DU4ZE30
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
- (14R)-7-ethyl-16-fluoro-2,14-dihydro-2,14-dimethyl-7H-8,12-Metheno-4H-pyrazolo[3,4-h]-1,2,3-triazolo[4,5-k][2,5]benzoxaazacyclotetradecin-11-a mine
- (14R)-7-Ethyl-16-fluoro-2,14-dihydro-2,14-dimethyl-7H-8,12-metheno-4H-pyrazolo[3,4-h]-1,2,3-triazolo[4,5-k][2,5]benzoxaazacyclotetradecin-11-amine
- (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
- 7H-8,12-Metheno-4H-pyrazolo[3,4-h]-1,2,3-triazolo[4,5-k][2,5]benzoxaazacyclotetradecin-11-amine, 7-ethyl-16-fluoro-2,14-dihydro-2,14-dimethyl-, (14R)-
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
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
- “JIDEYTRO™ (zidesamtinib) for Patients”. Jideytro. 2026-02-05. Retrieved 2026-07-23.
- “Jideytro: Uses, Dosage, Side Effects & Warnings”. Drugs.com. Retrieved 2026-07-23.
- “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.
- 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.
- “New FDA Drug Approvals for 2026”. Drugs.com. Retrieved 2026-07-23.
- Center for Drug Evaluation and Research (2026-07-22). “Novel Drug Approvals for 2026”. FDA.
- Zidesamtinib Selective Targeting of Diverse ROS1 Drug-Resistant MutationsPublication Name:Molecular Cancer TherapeuticsPublication Date:2025-05-09PMCID:PMC12214885PMID:40299789DOI:10.1158/1535-7163.mct-25-0025
- Targeting Solvent-Front Mutations for Kinase Drug Discovery: From Structural Basis to Design StrategiesPublication Name:Journal of Medicinal ChemistryPublication Date:2024-08-15PMID:39143914DOI:10.1021/acs.jmedchem.4c00361
- NVL-520 Is a Selective, TRK-Sparing, and Brain-Penetrant Inhibitor of ROS1 Fusions and Secondary Resistance MutationsPublication Name:Cancer DiscoveryPublication Date:2022-12-13PMCID:PMC9975673PMID:36511802DOI:10.1158/2159-8290.cd-22-0968
- Electron transport by C-type cytochromes. I. The reaction of horse heart cytochrome c with anionic reductantsPublication Name:Biophysics of structure and mechanismPublication Date:1975-02-19PMID:10021DOI:10.1007/bf00539772
PAT
- Solid forms, pharmaceutical compositions and preparation of heteroaromatic macrocyclic ether compoundsPublication Number:WO-2023056405-A1Priority Date:2021-10-01
- Solid forms, pharmaceutical compositions and preparation of heteroaromatic macrocyclic ether compoundsPublication Number:US-12043626-B2Priority Date:2021-10-01Grant Date:2024-07-23
- Methods of treating solid tumor using heteroaromatic macrocyclic ether compoundsPublication Number:US-2024398768-A1Priority Date:2021-10-01
- Heteroaromatic macrocyclic ether chemotherapeutic agentsPublication Number:US-12054498-B2Priority Date:2020-05-05Grant Date:2024-08-06
- Heteroaromatic macrocyclic ether chemotherapeutic agentsPublication Number:US-2023107663-A1Priority Date:2020-05-05
- Heteroaromatic macrocyclic ether chemotherapeutic agentsPublication Number:US-11542278-B1Priority Date:2020-05-05Grant Date:2023-01-03
- Heteroaromatic macrocyclic ether chemotherapeutic agentsPublication Number:WO-2021226208-A2Priority Date:2020-05-05
- Heteroaromatic macrocyclic ether chemotherapeutic agentsPublication Number:US-2024352037-A1Priority Date:2020-05-05
| Clinical data | |
|---|---|
| Pronunciation | jih-DAY-troh[1][2] |
| Trade names | Jideytro |
| Other names | NUV-520; NVL 520 |
| AHFS/Drugs.com | jideytro |
| Routes of administration | By mouth |
| Drug class | Tyrosine kinase inhibitor |
| Legal status | |
| Legal status | US: ℞-only |
| Identifiers | |
| IUPAC name | |
| CAS Number | 2739829-00-4 |
| PubChem CID | 166560233 |
| IUPHAR/BPS | 12392 |
| DrugBank | DB21623 |
| ChemSpider | 128922073 |
| UNII | MX5KQV5XHC |
| KEGG | D12899 |
| ChEBI | CHEBI:747901 |
| ChEMBL | ChEMBL5314497 |
| Chemical and physical data | |
| Formula | C22H22FN7O |
| Molar mass | 419.464 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
Lonitoclax


Lonitoclax
CAS 2952589-57-8
MF C43H45ClN4O5 MW733.3 g/mol
5-[5-chloro-2-[(3S)-3-(morpholin-4-ylmethyl)-3,4-dihydro-1H-isoquinoline-2-carbonyl]phenyl]-N-(4-hydroxyphenyl)-N-[(3-methoxy-2-methylphenyl)methyl]-1,2-dimethylpyrrole-3-carboxamide
- 1H-Pyrrole-3-carboxamide, 5-[5-chloro-2-[[(3S)-3,4-dihydro-3-(4-morpholinylmethyl)-2(1H)-isoquinolinyl]carbonyl]phenyl]-N-(4-hydroxyphenyl)-N-[(3-methoxy-2-methylphenyl)methyl]-1,2-dimethyl-
- 5-(5-Chloro-2-(((3S)-3-(morpholin-4-ylmethyl)-3,4-dihydroisoquinolin-2-(1-H)-yl)carbonyl)phenyl)-N-4-hydroxyphenyl)-N-(3-methoxy-2-methylbenzyl)-1,2-dimethyl-1H-pyrrole-3-carboxamide
- 5-[5-chloro-2-[(3S)-3-(morpholinomethyl)- 3,4-dihydro-1H-isoquinoline-2- carbonyl]phenyl]-N-(4-hydroxyphenyl)-N- [(3-methoxy-2-methyl-phenyl)methyl]-1,2- dimethyl-pyrrole-3-carboxamide
- 5-{5-Chloro-2-[(3S)-3-[(morpholin-4-yl)methyl]-3,4-dihydroisoquinoline-2(1H)-carbonyl]phenyl}-N-(4-hydroxyphenyl)-N-[(3-methoxy-2-methylphenyl)methyl]-1,2-dimethyl-1H-pyrrole-3-carboxamide
5-(5-chloro-2-{(3S)-3-[(morpholin-4-yl)methyl]-3,4-dihydroisoquinoline-2(1H)-carbonyl}phenyl)-N-(4-
hydroxyphenyl)-N-[(3-methoxy-2-methylphenyl)methyl]-1,2-dimethyl-1H-pyrrole-3-carboxamide
B-cell lymphoma 2 (Bcl-2) inhibitor, antineoplastic, ZE50-0134, ZE50 0134, Lomond Therapeutics, CANCER, 76NBC3X6A3
Lonitoclax (also known as ZE50-0134) is an investigational, next-generation, orally administered B-cell lymphoma 2 (Bcl-2) inhibitor being developed for the treatment of hematologic malignancies like Acute Myeloid Leukemia (AML) and Chronic Lymphocytic Leukemia (CLL). Developed by Lomond Therapeutics, the drug is engineered as a highly selective option to improve upon existing first-generation Bcl-2 inhibitors like venetoclax.
Mechanism and Advantages Over Venetoclax
Unlike earlier therapies, lonitoclax features a unique binding mode and a structurally distinct chemotype. Its design yields several pharmacology advantages:
- Higher Selectivity: It binds tightly to Bcl-2 while demonstrating exceptional selectivity over Bcl-xL, which helps lower hematologic toxicities.
- Limited Immune Suppression: In preclinical data, lonitoclax spared healthy non-malignant immune cells (B cells, CD8 T cells, and NK cells), a major shift from the immunosuppressive profile of venetoclax.
- Reduced Drug Interaction & Accumulation: It features a shorter half-life (~9–10 hours) and minimal CYP3A4 (P4503A4) inhibition. This prevents the drug from building up dangerously and mitigates the risk of Tumor Lysis Syndrome (TLS), potentially enabling safer outpatient treatments.
Clinical Development Status
Lonitoclax is currently advancing through early-phase clinical trials:
- IND Clearances: The U.S. FDA cleared Investigational New Drug (IND) applications evaluating lonitoclax for CLL/SLL and as a combination treatment for relapsed or refractory AML.
- Healthy Volunteer Studies: Phase 1 single ascending dose (SAD) studies in healthy adults confirmed that the drug is well tolerated with linear pharmacokinetics and no significant safety issues. Target engagement was confirmed through plasma apoptosis assays.
- Combination Trials: Active Phase 1b multicenter trials are underway evaluating the safety, efficacy, and synergy of lonitoclax when combined with hypomethylating agents like azacitidine in AML patients.
SYN
PAT
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2023129553&_cid=P11-MQVQMH-93381-1



ADVERISEMENT
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Can’t Find? Let’s Connect

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References
- Bcl-2 inhibitorsPublication Number: WO-2023129553-A1Priority Date: 2021-12-29
- BCL-2 InhibitorsPublication Number: US-2025115577-A1Priority Date: 2021-12-29
- Bcl-2 inhibitorsPublication Number: EP-4457223-A1Priority Date: 2021-12-29
///////Lonitoclax, ANAX LABS, B-cell lymphoma 2 (Bcl-2) inhibitor, antineoplastic, ZE50-0134, ZE50 0134, Lomond Therapeutics, CANCER, 76NBC3X6A3
#Lonitoclax, #ANAX LABS, #B-cell lymphoma 2 (Bcl-2) inhibitor, #antineoplastic, #ZE50-0134, #ZE50 0134, #Lomond Therapeutics, #CANCER, #76NBC3X6A3
Imlunestrant



Imlunestrant
CAS 2408840-26-4
as tosylate: 2408840-41-3
(5R)-5-[4-[2-[3-(fluoromethyl)azetidin-1-yl]ethoxy]phenyl]-8-(trifluoromethyl)-5H-chromeno[4,3-c]quinolin-2-ol
- (5r)-5-(4-(2-(3-(fluoromethyl)azetidin-1-yl)ethoxy)phenyl)-8-(trifluoromethyl)-5h-(1)benzopyrano(4,3-c)quinolin-2-ol
- 5h-(1)benzopyrano(4,3-c)quinolin-2-ol, 5-(4-(2-(3-(fluoromethyl)-1-azetidinyl)ethoxy)phenyl)-8-(trifluoromethyl)-, (5r)-
MF C29H24F4N2O3 MW 524.516
FDA 9/25/2025, Inluriyo, LY3484356, LY-3484356, To treat estrogen receptor-positive, human epidermal growth factor receptor 2-negative, estrogen receptor-1-mutated advanced or metastatic breast cancer with disease progression following at least one line of endocrine therapy
Imlunestrant, sold under the brand name Inluriyo, is an anti-cancer medication used for the treatment of breast cancer.[1] It is an is an estrogen receptor antagonist.[1] It is used as the salt, imlunestrant tosylate.[2] It is taken by mouth.[1] It was developed by Eli Lilly and Company.[2]
The most common adverse events and laboratory abnormalities include decreased hemoglobin, musculoskeletal pain, decreased calcium, decreased neutrophils, increased AST, fatigue, diarrhea, increased ALT, increased triglycerides, nausea, decreased platelets, constipation, increased cholesterol, and abdominal pain.[2]
Imlunestrant was approved for medical use in the United States in September 2025.[2]
SYN
- Imlunestrant with or without Abemaciclib in Advanced Breast CancerPublication Name: The New England journal of medicinePublication Date: 2025-03-27PMID: 39660834DOI: 10.1056/nejmoa2410858
- Targeting the Estrogen Receptor for the Treatment of Breast Cancer: Recent Advances and ChallengesPublication Name: Journal of Medicinal ChemistryPublication Date: 2023-06-28PMID: 37377342DOI: 10.1021/acs.jmedchem.3c00136
- Novel endocrine therapies: What is next in estrogen receptor positive, HER2 negative breast cancer?Publication Name: Cancer Treatment ReviewsPublication Date: 2023-06PMID: 37146385DOI: 10.1016/j.ctrv.2023.102569
- Oral Selective Estrogen Receptor Degraders (SERDs) as a Novel Breast Cancer Therapy: Present and Future from a Clinical PerspectivePublication Name: International Journal of Molecular SciencesPublication Date: 2021-07-22PMCID: PMC8345926PMID: 34360578DOI: 10.3390/ijms22157812
PAT
https://patentscope.wipo.int/search/en/detail.jsf?docId=US281655517&_cid=P12-MG7DCV-14904-1
Example 1A
5-(4-{2-[3-(Fluoromethyl)azetidin-1-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H-[1]benzopyrano[4,3-c]quinolin-2-ol, Isomer 1Separate the two enantiomers of 5-(4-{2-[3-(fluoromethyl)azetidin-1-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H-[1]benzopyrano[4,3-c]quinolin-2-ol by chiral SFC with the following conditions: Column: LUX® Cellulose-1, 5×25 cm; eluting with a mobile phase of 30% iPrOH (with 0.5% DMEA) in CO 2; column temperature: 40° C.; flow rate: 300 g/minute; UV detection wavelength: 270 nm to give Example 1A as the first eluting enantiomer (Isomer 1). ES/MS (m/z): 525.2 (M+H). Confirm enantiomeric enrichment of Isomer 1 by chiral analytical SFC, >99% ee, t (R): 1.30 minutes; column: CHIRALCEL® OD-H, 4.6×150 mm; eluting with a mobile phase of 30% MeOH (0.2% IPA) in CO 2; column temperature: 40° C.; flow rate: 5 mL/minute; UV detection wavelength: 225 nm. Isolate the title compound of Example 1B to give the second eluting enantiomer (Isomer 2). ES/MS (m/z): 525.2 (M+H). Confirm enantiomeric enrichment of Isomer 2 by chiral analytical SFC, 98% ee, t (R): 2.03 minutes; column: CHIRALCEL® OD-H, 4.6×150 mm; eluting with a mobile phase of 30% MeOH (0.2% IPA) in CO 2; column temperature: 40° C.; flow rate: 5 mL/minute; UV detection wavelength: 225 nm.
Alternate Preparation Example 1B
Crystalline 5-(4-{2-[3-(Fluoromethyl)azetidin-1-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H-[1]benzopyrano[4,3-c]quinolin-2-ol, Isomer 2
PAT
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2020014435&_cid=P12-MG7DHN-18354-1


EXAMPLE 1
Racemic 5-(4-{2-[3-(Fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H- [ 1 ]benzopyrano[4,3 -c]quinolin-2-ol

Cool a solution of (4-{2-[3-(fluoromethyl)azetidin-l-yl]ethoxy}phenyl){3-[2-fluoro-4-(trifluoromethyl)phenyl]-7-hydroxyquinolin-4-yl}methanone (5.27 g, 9.71 mmol) in 1,4-dioxane (100 mL) to 5 °C. Add lithium triethylborohydride (1 M in THF, 30.0 mL, 30.0 mmol). Remove the cooling bath and stir for 1.5 hours at room temperature. Quench the mixture with water. Add saturated NH4Cl solution and EtOAc. Separate the layers and extract the aqueous layer with EtOAc. Combine the organic extracts, dry over anhydrous MgS04, filter, and concentrate the filtrate. Dissolve the crude residue in THF (100 mL).
Add sodium hydride (60% in mineral oil, 1.94 g, 48.5 mmol). Reflux the solution for 1.5 hours. Add additional sodium hydride (60% in mineral oil, 1.94 g, 48.5 mmol), then reflux for an additional 30 minutes. Cool the solution to room temperature and quench with water. Add EtOAc and saturated NH4Cl solution. Separate the layers and extract the aqueous layer with EtOAc. Combine the organic extract, dry over anhydrous MgS04, filter, and concentrate the filtrate. Purify the residue by silica gel column chromatography eluting with a gradient of 5-7% MeOH in DCM to give the title compound (3.70 g, 72%) as a light yellow foam. ES/MS (m/z): 525.2 (M+H).
Prepare the following compounds in a manner essentially analogous to the method of Example 1, with the following variations in procedure. For the reduction, use 3 to 5 equivalents of lithium triethylborohydride with reaction times from 30 minutes to one hour and drying of the organic layers over magnesium sulfate or sodium sulfate. ETse the crude residue directly or purify by silica gel column chromatography eluting with a gradient of 0-5-7.5-10% MeOH in DCM before cyclization. Complete the cyclization by refluxing in THF for up to 16 hours, or in DMF, from 2 hours at room temperature for Ex 2, to 2 hours at 85 °C for Ex 8. Extract with DCM or EtOAc and dry organic layers over magnesium sulfate or sodium sulfate. Purify by silica gel column chromatography using up to 10% (MeOH or 7 M ammoniated MeOH) in DCM (Ex 2: gradient 0-10% MeOH in DCM; Ex 5: gradient 4-10% 7 M ammoniated MeOH in DCM; Ex 8: gradient 5-7.5% 7 M ammoniated MeOH in DCM) or by high pH reversed phase HPLC as noted.
EXAMPLE 1A
-(4-{2-[3-(Fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H- [l]benzopyrano[4,3-c]quinolin-2-ol, Isomer 1
and
EXAMPLE 1B
5-(4-{2-[3-(Fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H- [l]benzopyrano[4,3-c]quinolin-2-ol, Isomer 2

Separate the two enantiomers of 5-(4-{2-[3-(fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H-[l]benzopyrano[4,3-c]quinolin-2-ol by chiral SFC with the following conditions: Column: LUX® Cellulose-l, 5 x 25 cm; eluting with a mobile phase of 30% iPrOH (with 0.5% DMEA) in C02; column temperature: 40 °C; flow rate: 300 g/minute; UV detection wavelength: 270 nm to give Example 1 A as the first eluting enantiomer (Isomer 1). ES/MS (m/z): 525.2 (M+H). Confirm enantiomeric enrichment of Isomer 1 by chiral analytical SFC, >99% ee, /(R>: 1.30 minutes; column: CHFRALCEL® OD-H, 4.6 x 150 mm; eluting with a mobile phase of 30% MeOH (0.2% IP A) in C02; column temperature: 40 °C; flow rate: 5 mL/minute; UV detection wavelength: 225 nm. Isolate the title compound of Example 1B to give the second eluting enantiomer (Isomer 2). ES/MS (m/z): 525.2 (M+H). Confirm enantiomeric enrichment of Isomer 2 by chiral analytical SFC, 98% ee, /(R>: 2.03 minutes; column: CHIRALCEL® OD-H, 4.6 x 150 mm; eluting with a mobile phase of 30% MeOH (0.2% IP A) in C02; column temperature: 40 °C; flow rate: 5 mL/minute; UV detection wavelength: 225 nm.
Alternate Preparation EXAMPLE 1B
Crystalline 5-(4-{2-[3-(Fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H- [l]benzopyrano[4,3-c]quinolin-2-ol, Isomer 2
Stir 5-(4-{2-[3-(fluoromethyl)azetidin-l-yl]ethoxy}phenyl)-8-(trifluoromethyl)-5H-[l]benzopyrano[4,3-c]quinolin-2-ol, 4-methylbenzenesulfonic acid, Isomer 2 (23.8 g, 0.034 mol) in water (250 mL) at 1000 rpm. Add NaOH (76 pL) and stir the solution for 2 hours. Add DCM (600 mL). Separate the mixture, dry the DCM extract with magnesium sulfate, filter the material through a syringe filter (0.45 pm), and concentrate to dryness. Allow the material to sit under a N2 stream over a weekend. Add 1 : 1 EtOH/water (80 mL) and stir the mixture with sonication. Collect a tan solid by filtration on a nylon membrane to give the title compound (10.47 g, 0.02 mol, 59%).
PAT
- Selective estrogen receptor degradersPublication Number: US-2023234960-A1Priority Date: 2018-07-12
- Selective estrogen receptor degraderPublication Number: CN-112424205-BPriority Date: 2018-07-12Grant Date: 2023-10-31
- selective estrogen receptor degraderPublication Number: CN-117379428-APriority Date: 2018-07-12
- Selective estrogen receptor degradersPublication Number: US-11993608-B2Priority Date: 2018-07-12Grant Date: 2024-05-28
- Selective estrogen receptor degradersPublication Number: US-12128040-B2Priority Date: 2018-07-12Grant Date: 2024-10-29
PAT
https://patents.google.com/patent/US11926634B2/en
Selective estrogen receptor degraders (SERDs) bind to the estrogen receptor (ER) and downregulate ER-mediated transcriptional activity. The degradation and downregulation caused by SERDs can be useful in the treatment of various proliferative immune mediated disorders, cell proliferation disorders, including cancers such as breast cancer, ovarian cancer, endometrial cancer, prostate cancer, uterine cancer, gastric cancer, and lung cancer as well as mutations due to emerging resistance. Some small molecule examples of SERDs have been disclosed in the literature (see, e.g., WO2005073204, WO2014205136, and WO2016097071). Nonetheless, there is a need for new SERDs to treat ER-positive cancers, such as breast cancer, gastric cancer, and/or lung cancer.
As described in U.S. Pat. No. 10,654,866 (the ‘866 patent) a series of SERDs of the following formula have been discovered, along with pharmaceutically acceptable salts thereof:

wherein one of R1 and R2 are independently Cl, F, —CF3, or —CH3, and the other is H.





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……
| Clinical data | |
|---|---|
| Trade names | Inluriyo |
| Other names | LY3484356, LY-3484356 |
| AHFS/Drugs.com | Inluriyo |
| License data | US DailyMed: Imlunestrant |
| Routes of administration | By mouth |
| Drug class | Estrogen receptor antagonist |
| ATC code | None |
| Legal status | |
| Legal status | US: ℞-only[1] |
| Identifiers | |
| IUPAC name | |
| CAS Number | 2408840-26-4as tosylate: 2408840-41-3 |
| PubChem CID | 146603228 |
| DrugBank | DB19043 |
| ChemSpider | 115010421 |
| UNII | 9CXQ3PF69Uas tosylate: F7UDT90EW5 |
| KEGG | D12216as tosylate: D12217 |
| ChEMBL | ChEMBL5095183 |
| Chemical and physical data | |
| Formula | C29H24F4N2O3 |
| Molar mass | 524.516 g·mol−1 |
| 3D model (JSmol) | Interactive image |
| SMILES | |
| InChI | |
References
- https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/218881s000lbl.pdf
- “FDA approves imlunestrant for ER-positive, HER2-negative, ESR1-mutated advanced or metastatic breast cancer”. U.S. Food and Drug Administration (FDA). 25 September 2025. Retrieved 27 September 2025.
This article incorporates text from this source, which is in the public domain. - “U.S. FDA approves Inluriyo (imlunestrant) for adults with ER+, HER2-, ESR1-mutated advanced or metastatic breast cancer” (Press release). Eli Lilly. 25 September 2025. Retrieved 27 September 2025 – via PR Newswire.
- World Health Organization (2022). “International nonproprietary names for pharmaceutical substances (INN): recommended INN: list 88”. WHO Drug Information. 36 (3). hdl:10665/363551.
Further reading
- Jhaveri, Komal L.; Jeselsohn, Rinath; Lim, Elgene; Hamilton, Erika P.; Yonemori, Kan; Beck, J. Thaddeus; et al. (June 2022). “A phase 1a/b trial of imlunestrant (LY3484356), an oral selective estrogen receptor degrader (SERD) in ER-positive (ER+) advanced breast cancer (aBC) and endometrial endometrioid cancer (EEC): Monotherapy results from EMBER”. Journal of Clinical Oncology. 40 (16_suppl): 1021. doi:10.1200/JCO.2022.40.16_suppl.1021. S2CID 249445691.
- Jhaveri, Komal; O’Shaughnessy, Joyce; Andre, Fabrice; Goetz, Matthew P.; Harbeck, Nadia; Martín, Miguel; et al. (March 2023). “Abstract OT1-01-02: EMBER-4: A phase 3 adjuvant trial of imlunestrant vs standard endocrine therapy (ET) in patients with ER+, HER2- early breast cancer (EBC) with an increased risk of recurrence who have previously received 2 to 5 years of adjuvant ET”. Cancer Research. 83 (5_Supplement): OT1–01–02-OT1-01–02. doi:10.1158/1538-7445.SABCS22-OT1-01-02.
- Neven, P.; Stahl, N.; Losada, M.J. Vidal; Jimenez, M. Martin; Kaufman, P.A.; Harbeck, N.; et al. (October 2023). “273P A preoperative window-of-opportunity (WOO) study of imlunestrant in ER+, HER2- early breast cancer (EBC): Final analysis from EMBER-2”. Annals of Oncology. 34: S292 – S293. doi:10.1016/j.annonc.2023.09.470. S2CID 264385454.
External links
- Clinical trial number NCT04975308 for “A Study of Imlunestrant, Investigator’s Choice of Endocrine Therapy, and Imlunestrant Plus Abemaciclib in Participants With ER+, HER2- Advanced Breast Cancer (EMBER-3)” at ClinicalTrials.gov
/////////Imlunestrant, FDA 2025, APPROVALS 2025, Inluriyo, CANCER, LY3484356, LY 3484356, 9CXQ3PF69U
Envonalkib

Envonalkib
- CAS 1621519-26-3
- QB7KTQ7VW9
- 5-((1R)-1-(2,6-Dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((2S)-2-methyl-1-piperazinyl)(3,3′-bipyridin)-6-amine
- 506.4 g/mol, C24H26Cl2FN5O2
TQ-B3139, Chia Tai Tianqing, Anluoqing, cancer
ENVONALKIB is a small molecule drug with a maximum clinical trial phase of II and has 1 investigational indication.
SYN
https://patentscope.wipo.int/search/en/WO2014117718
Example 27: 5-[(2,6-dichloro-3-fluorophenyl)ethoxy-4′-methoxy-6′ …

Step 1: 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methyl-4-tert-butoxycarbonylpiperazin-1-yl)-3,3′-bipyridin-6-amine
To dioxane (10 mL) and water (1.5 mL) were added tert-butyl (S)-4-(5-bromo-4-methoxypyridin-2-yl)-3-methylpiperidin-1-carboxylate (106 mg, 0.275 mmol), (R)-3-(1-(2,6-dichloro-3-fluorophenyl)ethoxy)-5-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)-2-aminopyridine (140 mg, 0.33 mmol), tetrakis(triphenylphosphine)palladium (32 mg, 0.0275 mmol) and cesium carbonate (179 mg, 0.55 mmol), the atmosphere was replaced with nitrogen, and the reaction was carried out at 100 ° C. overnight. After cooling, the mixture was separated by silica gel column chromatography to give 5-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6-(5-(2-methyl-4-tert-butoxycarbonylpiperidin-1-yl)-3,3′-bipyridin-6-amine) (70 mg) in a yield of 42%. MS m/z [ESI]: 606.2 [M+1].
Step 2: 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methylpiperazin-1-yl)-3,3′-bipyridin-6-amine
To a stirred dichloromethane solution (10 mL) of 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methyl-4-tert-butoxycarbonylpiperidin-1-yl)-3,3′-bipyridin-6-amine (67 mg, 0.11 mmol) was added trifluoroacetic acid (1 mL) and stirred for 1 hour. The pH was adjusted to greater than 13 with sodium hydroxide solution, and the mixture was extracted with dichloromethane. The organic phase was dried over anhydrous sodium sulfate, filtered, and the filtrate was concentrated. The product was separated and purified by column chromatography (with dichloromethane:methanol = 8:1 as eluent) to give 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methylpiperidin-1-yl)-3,3′-bipyridin-6-amine (30 mg). Yield: 55%, MS m/z [ESI]: 506.1[M+1]. 1H-NM (400 MHz, CDC1 3 ):5= 7.94(1H, s), 7.71(1H, s), 7.28-7.32(lH, m), 7.07(1H, t, J=8.4Hz), 6.97(1H, s), 6.04-6.13(2H, m), 4.86 (2H : s), 4.57-4.59(lH, m), 4.03 (1H, d, J=14Hz), 3.76(3H, s), 3.07-3.33(4H, m), 2.88-3.00(lH, m), 1.84(3H, d, J=6.8Hz), 1.34 (3H, d, J=6.8Hz).
SYN
CN107949560
SYN
https://patentscope.wipo.int/search/en/detail.jsf?docId=US154015806&_cid=P11-MEF9W1-27198-1
Example 27: 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methylpiperazin-1-yl)-[3,3′-bipyridin]-6-amine
General Synthetic Methods:

Step 1: (S)-tert-butyl 4-(6′-amino-5′-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4-methoxy-[3,3′-bipyridin]-6-yl)-3-methylpiperazine-1-carboxylate
Step 2: 5-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-4′-methoxy-6′-((S)-2-methylpiperazin-1-yl)-[3,3′-bipyridin]-6-amine
SYN
European Journal of Medicinal Chemistry 291 (2025) 117643
Envonalkib, also known as TQ-B3139, is a novel small-molecule TKI, developed by Chia Tai Tianqing Pharmaceutical Group. It targets ALK, ROS1, and c-Met kinases, exhibiting potent antitumor activity against cancers harboring these genetic alterations. In 2024, the NMPA approved Envonalkib under the brand name Anluoqing for the treatment of adult patients with ALK-positive locally advanced or metastatic NSCLC who have not received prior ALK inhibitor therapy [24]. Envonalkib exerts its therapeutic effects through selective inhibition of the kinase activities of ALK, ROS1, and c-Met, thereby interrupting the downstream signaling pathways that are crucial for tumor cell proliferation and survival [25]. The inhibition of these targets results in cell cycle arrest and apoptosis in cancer cells。The clinical efficacy of Envonalkib was evidenced in a Phase III randomized, open-label, multicenter clinical trial (NCT04009317), which compared Envonalkib with crizotinib in treatment-naïve patients with ALK-positive advanced NSCLC [25,26]. In the reported study, Envonalkib demonstrated a me dian PFS of 24.87 months, which was markedly superior to the 11.60 months achieved with crizotinib (hazard ratio [HR] = 0.47, p < 0.0001). Notably, in patients harboring brain metastases, Envonalkib exhibited a
central nervous system objective response rate (CNS-ORR) of 78.95 %, a substantial improvement over the 23.81 % observed with crizotinib. In terms of safety profile, Envonalkib was generally well-tolerated. Treat ment-related adverse events (TRAEs) of Grade ≥3 were noted in 55.73 % of patients receiving Envonalkib, contrasting with the 42.86 % incidence in the crizotinib cohort. The predominant TRAEs encompassed elevated liver enzymes, neutropenia, and gastrointestinal symptoms, all of which
were amenable to effective management through appropriate support ive care measures. The regulatory approval of Envonalkib thus in troduces a novel therapeutic modality for patients with ALK-positive NSCLC, effectively addressing a significant unmet medical need within this patient population [25].
The synthesis of Envonalkib, illustrated in Scheme 6, initiates with Mitsunobu coupling of Envo-001 and Envo-002, affording Envo-003 [27]. Sequential reduction and NBS-bromination converts Envo-003 to
Envo-005 via Envo-004. Miyaura borylation of Envo-005 constructs Envo-006, which undergoes Suzuki-Miyaura cross-coupling with Envo-007 followed by deprotection to deliver Envonalkib. In parallel,
Envo-009 reacts with Envo-010 through Buchwald-Hartwig cross coupling to form Envo-011. This intermediate is brominated to produce Envo-007, which is used in the Suzuki-Miyaura coupling with Envo-006
[24] X. Li, Y. Xia, C. Wang, S. Huang, Q. Chu, Efficacy of ALK inhibitors in Asian
patients with ALK inhibitor-naïve advanced ALK-Positive non-small cell lung
cancer: a systematic review and network meta-analysis, Transl. Lung Cancer Res.
13 (2024) 2015–2022.
[25] Y. Yang, J. Min, N. Yang, Q. Yu, Y. Cheng, Y. Zhao, M. Li, H. Chen, S. Ren, J. Zhou,
W. Zhuang, X. Qin, L. Cao, Y. Yu, J. Zhang, J. He, J. Feng, H. Yu, L. Zhang, W. Fang,
Envonalkib versus crizotinib for treatment-naive ALK-Positive non-small cell lung
cancer: a randomized, multicenter, open-label, phase III trial, Signal Transduct
Target Ther 8 (2023) 301.
[26] R. Garcia-Carbonero, A. Carnero, L. Paz-Ares, Inhibition of HSP90 molecular
chaperones: moving into the clinic, Lancet Oncol. 14 (2013) e358–e369.
[27] F. Gong, X. Li, R. Zhao, X. Zhang, X. Xu, X. Liu, D. Xiao, Y. Han, Process for
Preparation of Pyridine Substituted 2-aminopyridine Protein Kinase Inhibitor
Crystal, 2017. CN107949560B.




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……
- New drugs approved by the NMPA in 2024: Synthesis and clinical applicationsPublication Name: European Journal of Medicinal ChemistryPublication Date: 2025-07-05PMID: 40262297DOI: 10.1016/j.ejmech.2025.117643
- Efficacy of ALK inhibitors in Asian patients with ALK inhibitor-naïve advanced ALK-positive non-small cell lung cancer: a systematic review and network meta-analysisPublication Name: Translational Lung Cancer ResearchPublication Date: 2024-08-31PMCID: PMC11384493PMID: 39263024DOI: 10.21037/tlcr-24-604
- Envonalkib versus crizotinib for treatment-naive ALK-positive non-small cell lung cancer: a randomized, multicenter, open-label, phase III trialPublication Name: Signal Transduction and Targeted TherapyPublication Date: 2023-08-14PMCID: PMC10423717PMID: 37574511DOI: 10.1038/s41392-023-01538-w
- Pharmacokinetic, pharmacodynamic, and behavioural studies of deschloroketamine in Wistar ratsPublication Name: British Journal of PharmacologyPublication Date: 2021-10-31PMID: 34519023DOI: 10.1111/bph.15680
//////////Envonalkib, china 2024, approvals 2024, TQ-B3139, TQ B3139, Chia Tai Tianqing, Anluoqing, cancer, QB7KTQ7VW9
Befotertinib



Befotertinib
D-0316, 0XT2CPR891
CAS No. : 1835667-63-4, MESYLATE CAS No. 2226167-02-6
- 2-propenamide, n-(2-((2-(dimethylamino)ethyl)methylamino)-4-methoxy-5-((4-(1-(2,2,2-trifluoroethyl)-1h-indol-3-yl)-2-pyrimidinyl)amino)phenyl)-
- N-(2-((2-(dimethylamino)ethyl)(methyl)amino)-4-methoxy-5-((4-(1-(2,2,2-trifluoroethyl)-1h-indol-3-yl)pyrimidin-2-yl)amino)phenyl)prop-2-enamide
- N-[2-[2-(dimethylamino)ethyl-methylamino]-4-methoxy-5-[[4-[1-(2,2,2-trifluoroethyl)indol-3-yl]pyrimidin-2-yl]amino]phenyl]prop-2-enamide
| Molecular Weight | 567.61 |
|---|---|
| Formula | C29H32F3N7O2 |
Befotertinib (D-0316) is an orally active EGFR tyrosine kinase inhibitor. Befotertinib can inhibit the proliferation of tumor cells. Befotertinib can be used in the research of EGFR T790M-positive non-small cell lung cancer (NSCLC).
Befotertinib is an orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. Upon administration, befotertinib specifically binds to and inhibits EGFR T790M, a secondarily acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR T790M-expressing tumor cells. Compared to some other EGFR inhibitors, befotertinib may have therapeutic benefits in tumors with T790M-mediated drug resistance. EGFR, a receptor tyrosine kinase that is mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
PAPER
J. Med. Chem. 2017, 60, 6480−6515.
PATENT
WO 2019218987
https://patentscope.wipo.int/search/en/WO2019218987
[0054]
U.S. Publication No. 2017/0355696 A1 describes a method of preparing Compound 4 and various pharmaceutically acceptable salts thereof. The exemplified synthetic process in U. S. Publication No. 2017/0355696 A1 includes a two-step conversion from the aniline compound, corresponding to Compound 1 of this disclosure, into the bismesylate of Compound 4, which has a low yield.
[0055]
As shown herein, representative methods of preparation of Compound 4, or a pharmaceutically acceptable salt, (or alternatively referred to as synthetic methods) , can provide the desired Compound 4, or a pharmaceutically acceptable salt, in improved yield and high purity and can be adapted for large-scale manufacture.
[0056]
In various embodiments, the present invention provides a novel method of preparing Compound 4, or a pharmaceutically acceptable salt thereof. The method typically includes converting a compound of Formula III, or a salt thereof, into compound 4, typically under an elimination reaction condition:

Syn
https://doi.org/10.1021/acs.jmedchem.4c02079
J. Med. Chem. 2025, 68, 2147−2182
Befotertinib (Surmana). Befotertinib (17), an oral, highly selective, third generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) developed by Betta Pharmaceuticals and InventisBio, was approved in China in May 2023 for the second-line treatment of patients
with locally advanced or metastatic nonsmall cell lung cancer (NSCLC) with positive EGFR T790 M mutation who have disease progression on previous EGFR TKI therapy. 140 139 NSCLC
has a high incidence and disease burden in China, which has spurred the development of multiple EGFR TKIs by Chinese companies.
Achromatography-free process route to befotertinib (17) has been reported in the patent literature by researchers at InventisBio (Scheme 29), although details about scale and yields were not provided.
141 142 The reaction sequence closely follows that of osimertinib, a third generation EGFR inhibitor
that was first approved in 2015 and was covered in our previous review.
Osimertinib and befotertinib share a common backbone, differing only in N-substitution on the indole ring.
Friedel−Crafts arylation of 1H-indole with 2,4-dichloropyrimidine (17.1) gave the 3-pyrimidinyl indole 17.2. The trifluoroethyl moiety in indole 17.4 was introduced via Nalkylation of 17.2 with triflate 17.3. This was followed by an SAr reaction with nitroaniline 17.5 to provide amino pyrimidine 17.6. Next, N,N,N′-trimethylethylenediamine (17.7) displaced the electrophilic aryl fluoride in an SNArreaction to generate intermediate 17.8. The acrylamide moiety was installed using a three-step sequence: hydrogenolytic
reduction of the nitro group to the corresponding aniline, acylation with 3-chloropropanoyl chloride, and immediate elimination to the acrylamide. Mesylate salt formation and crystallization furnished befotertinib mesylate (17) in eight steps from 17.1.
(139) Blair, H. A. Befotertinib: first approval. Drugs 2023, 83, 1433−
1437.
(140) Lau, S. C. M.; Ou, S.-H. I. And still they come over troubled
waters: can Asia’s third-generation EGFR tyrosine kinase inhibitors
(Furmonertinib, Aumolertinib, Rezivertinib, Limertinib, Befotertinib,
SH-1028, and Lazertinib) affect global treatment of EGFR+ NSCLC. J.
Thorac. Oncol. 2022, 17, 1144−1154.
(141) Dai, X.; Jiang, Y. Preparation of pyrimidine derivative and its
pharmaceutical salt as EGFR inhibitors for the treatment of cancer and
other diseases. WO 2019218987, 2019.
(142) Flick, A. C.; Ding, H. X.; Leverett, C. A.; Kyne, R. E.; Liu, K. K.
C.; Fink, S. J.; O’Donnell, C. J. Synthetic approaches to the new drugs
approved during 2015. J. Med. Chem. 2017, 60, 6480−6515.




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……
- [1]. Nagasaka M, et, al. Beyond Osimertinib: The Development of Third-Generation EGFR Tyrosine Kinase Inhibitors For Advanced EGFR+ NSCLC. J Thorac Oncol. 2021 May;16(5):740-763. [Content Brief][2]. Blair HA. Befotertinib: First Approval. Drugs. 2023 Oct;83(15):1433-1437. [Content Brief]
/////////Befotertinib, APPROVALS 2023, CHINA 2023, Betta Pharmaceuticals, InventisBio, CANCER, D-0316, D 0316, 0XT2CPR891
Olverembatinib



Olverembatinib
1257628-77-5- 3-((1H-pyrazolo[3,4-b]pyridin-5-yl)ethynyl)-4-methyl-N-(4-((4-methylpiperazin-1-yl)methyl)-3-(trifluoromethyl)phenyl)benzamide
- HQP1351
- 4-methyl-N-[4-[(4-methylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl]-3-[2-(1H-pyrazolo[3,4-b]pyridin-5-yl)ethynyl]benzamide
- HQP1351 is under investigation in clinical trial NCT03883100 (A Pivotal Study of HQP1351 in Patients of Chronic Myeloid Leukemia in Accelerated Phase With T315I Mutation).
- 4-methyl-N-[4-[(4-methylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl]-3-[2-(1H-pyrazolo[3,4-b]pyridin-5-yl)ethynyl]benzamide
- D-824
- GZD824
WeightAverage: 532.571
Monoisotopic: 532.219844002, Chemical FormulaC29H27F3N6O

| Molecular Weight | 724.77 |
|---|---|
| Formula | C31H35F3N6O7S2 |
Olverembatinib (GZD824) dimesylate is a potent and orally active pan-Bcr-Abl inhibitor. Olverembatinib dimesylate potently inhibits a broad spectrum of Bcr-Abl mutants. Olverembatinib dimesylate strongly inhibits native Bcr-Abl and Bcr-AblT315I with IC50s of 0.34 nM and 0.68 nM, respectively. Olverembatinib dimesylate has antitumor activity. Olverembatinib (dimesylate) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Olverembatinib is a BCR-ABL1 tyrosine kinase inhibitor developed by Ascentage Pharma. In 2021, it was approved in China “for the treatment of adult patients with TKI-resistant chronic-phase CML (CML-CP) or accelerated-phase CML (CML-AP) harbouring the T315I mutation”.[1][2][3]
SYN
Ren, Xiaomei;Pan, Xiaofen;Zhang, Zhang;Wang, Deping;Lu, Xiaoyun;Li, Yupeng;Wen, Donghai;Long, Huoyou;Luo, Jinfeng;Feng, Yubing;Zhuang, Xiaoxi;Zhang, Fengxiang;Liu, Jianqi;Leng, Fang;Lang, Xingfen;Bai, Yang;She, Miaoqin;Tu, Zhengchao;Pan, Jingxuan;Ding, Ke [Journal of Medicinal Chemistry,2013,vol. 56,# 3,p. 879 – 894]
https://pubs.acs.org/doi/10.1021/jm301581y



PATENT
CN 114163434
https://patentscope.wipo.int/search/en/detail.jsf?docId=CN355399053&_cid=P10-MDPKRT-75688-1
| Example |
| The following examples further illustrate but do not limit the present invention. It should be noted that those skilled in the art can make various modifications and improvements without departing from the inventive concept of the present invention, all of which are included in the scope of protection of the present invention. |
| The specific conditions not disclosed in the experimental methods of the following examples can be selected according to conventional methods and conditions, or according to the product instructions. |
| Unless otherwise specified, “room temperature” in the following examples refers to 20°C to 25°C. The term “h” used herein refers to hours. |
| Example 1 |
| Step 1: |
| |
| Under nitrogen, N-methylpyrrolidone (137.6 g) was heated to 30-35°C to obtain the compound of Formula 1 (14.4 g, 1.3 eq) and the compound of Formula 2 (19.14 g, 1 eq). Bis(triphenylphosphate)palladium dichloride (0.46 g, 0.01 eq) and cuprous iodide (0.113 g, 0.01 eq) were added sequentially. Triethylamine (9.45 g, 1.5 eq) was then added under nitrogen. The reaction mixture was heated to 65-75°C and maintained at this temperature for 2 hours. The reaction process was monitored by liquid chromatography-mass spectrometry. The reaction was terminated when the content of the compound of Formula 2 was ≤0.1%. After completion of the reaction, the reaction solution was cooled to 35-45°C and N-acetyl-L-cysteine (1 g, 0.1 eq) was added directly. The reaction was stirred for 4-5 hours. The resulting product was cooled to room temperature, precipitated with water, centrifuged, and washed with pure water to obtain a crude filter cake. The crude filter cake was vacuum-dried and then slurried with a mixture of ethyl acetate and n-heptane (5 mL of the mixed solvent, wherein the volume ratio of ethyl acetate to n-heptane was 1:1) at a rate of 5 mL per gram of crude filter cake. The resulting slurry was vacuum-dried to yield the compound of Formula 3 with a yield of 85.97% and a purity of 98.2%. |
| The NMR data for the compound of Formula 3 are as follows : 1 H NMR (400 MHz, d-DMSO): δ ppm: 8.93 (1H, d, J = 2.0 Hz); 8.63 (1H, d, J = 2.0 Hz); 8.49 (1H, s); 8.11 (1H, d, J = 2.0 Hz); 7.92 (1H, dd, J = 1.6 Hz; J = 8.0 Hz); 7.52 (1H, d, J = 8.0 Hz); 3.88 (3H, s); 2.59 (3H, s); 1.65 (9H, s). |
| Step 2: |
| |
| Under nitrogen, methanol (160 g) and water (50 g) were sequentially added to the compound of formula 3 (20 g, 1.0 eq). The reaction system was stirred at reflux for 18 hours with process control. The resulting product was cooled to room temperature and filtered to obtain a filter cake (no drying required). Recrystallization was performed by adding 10 times the mass of the filter cake in methanol. The resulting mixture was stirred at 60-70°C for 8-10 hours, then cooled to 40-50°C and subjected to a gradient cooling process at a cooling rate of 5°C per 1 to 1.5 hours to slowly form a solid precipitate. The resulting mixture was filtered, the filter cake was washed with methanol, and vacuum dried to obtain the compound of formula 4 in a 91% yield and 99.7% purity. |
| The NMR data for the compound of Formula 4 are as follows : 1 H NMR (400 MHz, d-DMSO): δ ppm: 8.73 (1H, d, J = 2.0 Hz); 8.52 (1H, t, J = 2.0 Hz); 8.21 (1H, d, J = 2.0 Hz); 8.06 (1H, s); 7.86 (1H, dd, J1 = 2.0 Hz; J2 = 8.0 Hz); 7.49 (1H, dd, J1 = 1.6 Hz; J2 = 7.6 Hz); 3.86 (3H, s); 2.56 (3H, s). |
| Step 3: |
| |
| Under nitrogen, THF (448 mL), compound of formula 4 (29.1 g, 1 eq), and compound of formula 5 (24.6 g, 0.9 eq) were added, stirred, and cooled to -65°C to -60°C. At this temperature, potassium tert-butoxide (19 g x 3) was added in batches every 0.5 h. The reaction process was controlled by liquid phase detection. After 2 hours, the reaction temperature was raised to -5 to 0°C. The reaction solution was washed with purified water, stirred for 0.5-1 hour, washed with brine, and separated to obtain an organic phase. N-acetyl-L-cysteine (11.41 g, 0.7 eq) was added to the organic phase, stirred, washed with brine, neutralized, and concentrated under reduced pressure. The resulting filter cake was washed with purified water and made into a slurry. The resulting product was washed again with purified water and dried under vacuum to obtain compound of formula 6 with a yield of 88.2% and a purity of 98.6%. |
| The NMR data for the compound of formula 6 are as follows : 1 H NMR (400 MHz, d-DMSO): δ ppm: 10.53 (1H, s); 8.75 (d, J = 2.0); 8.53 (d, J = 2.4); 8.24 (1H, s); 8.23 (d, J = 2.4); 8.21 (d, J = 1.6); 8.09 (dd, J1 = 1.6; J2 = 8.4); 7.94 (dd, J1 = 2.0; J2 = 8.0); 7.71 (d, J = 8.8); 7.53 (d, J = 8.0); 3.56 (2H, s); 2.59 (3H, s); 2.34-2.35 (8H, m), 2.16 (3H, s). |
| Its carbon spectrum data are 13 C NMR (100 MHz, d-DMSO): δ ppm: 20.38, 45.65, 52.64, 54.67, 57.41, 88.26, 91.86, 111.76, 113.98, 117.19, 122.14, 123.43, 127.35 (q), 124.30 (q), 128.10, 129.89, 130.49, 131.15, 132.02, 132.13, 132.93, 133.66, 138.15, 143.65, 150.55, 164.64. |
PATENT
CN 101885722
https://patentscope.wipo.int/search/en/detail.jsf?docId=CN84081329&_cid=P10-MDPKML-68458-1
| Example 23 |
| 3-((1H-pyrazolo[3,4-b]pyridine-5-substituted)ethynyl)-4-methyl-N-(4-((4-methylpiperazine-1-substituted)methyl)3-(trifluoromethyl)phenyl)benzamide (D824) |
| (3-((1H-pyrazolo[3,4-b]pyridin-5-yl)ethynyl)-4-methyl-N-(4-((4-methylpiperazin-1-yl)m ethyl)-3-(trifluoromethyl)phenyl)benzamide) |

| The synthesis method is the same as in Example 1. |
| 1 HNMR (400MHz, d-DMSO), δ13.92 (s, 1H), 10.55 (s, 1H), 8.72 (d, J=2.0Hz, 1H), 8.52 (d, J=2.0Hz, 1H), 8.17 (m, 3H), 8.10 (d, J=8.0Hz, 1H), 7.92 (dd, J=8.0, 2.0Hz, 1H), 7.70 (d, J=8.8Hz, 1H), 7.53 (d, J=8.0Hz, 1H), 3.80 (s, 2H), 3.10 (brs, 8H), 2.71 (s, 3H), 2.57 (s, 3H). |
| MS(ESI), m/z: 533, (M + +H + ). |
SYN
Olverembatinib(24) wasdeveloped by Ascentage Pharma as anorally available, third-generation
tyrosinekinase inhibitor (TKI) for the treatment of chronic myeloid leukemia (CML), acute myeloid leukemia, acute lymphoblastic leukemia (ALL), and solid tumors.167 It received its first approval inChina inNovember 2021 and was approved for use in adults with TKI-resistant CML chronicphaseandCML-acceleratephaseharboringtheT315I “gatekeeper” mutation.168 The current mainstay of CML
treatmentiscenteredaroundTKIs;however,resistancetoTKItherapy, often through BCR-ABL1 kinase domain point mutations, remains a challenge for early generation therapies.169Olverembatinibretainsitsefficacybyfunctioningasan ATP-bindingsiteinhibitorofwild-typeBCR-ABL1kinaseand broadly relatedmutants including T315I, which otherwise confers resistance against all first and second generation TKIs.168
Thesynthesisofolverembatinibhasbeenreportedinseveral patents,170−172 aswell as a journal article173 that details the divergentapproachtorelatedanalogues. Inarecentpatent,170 the synthesis of olverembatinib began with a Sonogashira coupling of commercially available alkyne 24.1 with
bromopyridine24.2toaffordester24.3in98%yield(Scheme43). Cleavage of the N-Boc group was accomplished by refluxingcarbamate24.3inaMeOHandwatermixturetogive pyrazole24.4 in91%yield. AfinalKOtBumediatedamide formation with aniline 24.5 resulted in the isolation of
olverembatinib(24) in88%yield.
(167) Dhillon, S. Olverembatinib: First approval. Drugs 2022, 82,
469−475.
(168) Braun, T. P.; Eide, C. A.; Druker, B. J. Response and resistance
to BCR-ABL1-targeted therapies. Cancer Cell 2020, 37, 530−542.
(169) Shoukier, M.; Kubiak, M.; Cortes, J. Review of new-generation
tyrosine kinase inhibitors for chronic myeloid leukemia. Curr. Oncol.
Rep. 2021, 23, 91.
(170) Wen, J.; Feng, J.; Wu, T.; Cai, M.; Teng, S. Preparation
method of alkynyl containing compound and its intermediate. China
Patent CN 114163434, 2022.
(171) Guo, M.; Wen, J.; Teng, S.; Wu, T.; Feng, J. Preparation of
(trifluoromethylphenyl)(pyrazolo[3,4-b]pyridinylethynyl)benzamide
derivative. China Patent CN 113292556, 2021.
(172) Ding, K.; Wang, D.; Pei, D.; Zhang, Z.; Shen, M.; Luo, K.;
Feng, Y. Heterocyclic alkynylbenzene derivatives as cancer cell line
inhibitors and their preparation, pharmaceutical compositions and use
in the treatment of cancer. China Patent CN 101885722, 2010.
(173) Ren, X.; Pan, X.; Zhang, Z.; Wang, D.; Lu, X.; Li, Y.; Wen, D.;
Long, H.; Luo, J.; Feng, Y.; et al. Identification of GZD824 as an
orally bioavailable inhibitor that targets phosphorylated and non
phosphorylated breakpoint cluster region−abelson (Bcr-Abl) kinase
and overcomes clinically acquired mutation-induced resistance against
imatinib. J. Med. Chem. 2013, 56, 879−894.




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References
- Dhillon, Sohita (March 2022). “Olverembatinib: First Approval”. Drugs. 82 (4): 469–475. doi:10.1007/s40265-022-01680-9. PMID 35195876. S2CID 247027755.
- Jiang, Qian; Li, Zongru; Qin, Yazhen; Li, Weiming; Xu, Na; Liu, Bingcheng; Zhang, Yanli; Meng, Li; Zhu, Huanling; Du, Xin; Chen, Suning; Liang, Yang; Hu, Yu; Liu, Xiaoli; Song, Yongping; Men, Lichuang; Chen, Zi; Niu, Qian; Wang, Hengbang; Lu, Ming; Yang, Dajun; Zhai, Yifan; Huang, Xiaojun (18 August 2022). “Olverembatinib (HQP1351), a well-tolerated and effective tyrosine kinase inhibitor for patients with T315I-mutated chronic myeloid leukemia: results of an open-label, multicenter phase 1/2 trial”. Journal of Hematology & Oncology. 15 (1): 113. doi:10.1186/s13045-022-01334-z. PMC 9389804. PMID 35982483.
- Jiang, Qian; Huang, Xiaojun; Chen, Zi; Niu, Qian; Shi, Dayu; Li, Zongru; Hou, Yue; Hu, Yu; Li, Weiming; Liu, Xiaoli; Xu, Na; Song, Yongping; Zhang, Yanli; Meng, Li; Hong, Zhenya; Liu, Bingcheng; Zeng, Shan; Men, Lichuang; Li, Yan; Chen, Suning; Xue, Mengxing; Zhu, Huanling; Li, He; Du, Xin; Lou, Jin; Zhang, Xiaohan; Liang, Yang; Dai, Yujun; Lu, Ming; Wang, Hengbang; Ji, Jiao; Yue, Changai; Yang, Dajun; Zhai, Yifan (5 November 2020). “Novel BCR-ABL1 Tyrosine Kinase Inhibitor (TKI) HQP1351 (Olverembatinib) Is Efficacious and Well Tolerated in Patients with T315I-Mutated Chronic Myeloid Leukemia (CML): Results of Pivotal (Phase II) Trials”. Blood. 136 (Supplement 1): 50–51. doi:10.1182/blood-2020-142142. S2CID 228875477.
| Clinical data | |
|---|---|
| Other names | GZD-824; GZD824 |
| Legal status | |
| Legal status | Investigational |
| Identifiers | |
| IUPAC name | |
| CAS Number | 1257628-77-5 |
| PubChem CID | 51038269 |
| IUPHAR/BPS | 10630 |
| DrugBank | DB16185 |
| ChemSpider | 29395146 |
| UNII | KV1M7Q3CBP |
| ChEMBL | ChEMBL2316582 |
| CompTox Dashboard (EPA) | DTXSID301352011 |
| Chemical and physical data | |
| Formula | C29H27F3N6O |
| Molar mass | 532.571 g·mol−1 |
| 3D model (JSmol) | Interactive image |
| SMILES | |
| InChI | |
[1]. Ren X, Pan X, Zhang Z, Identification of GZD824 as an orally bioavailable inhibitor that targets phosphorylated and nonphosphorylated breakpoint cluster region-Abelson (Bcr-Abl) kinase and overcomes clinically acquired mutation-induced resistance against imatinib. J Med Chem. 2013 Feb 14;56(3):879-94. [Content Brief]
//////////Olverembatinib, approvals 2021, china 2021, Ascentage Pharma, cancer, HQP1351, HQP 1351, D-824, D 824, KV1M7Q3CBP, GZD824
Sontigidomide



Sontigidomide
CAS 2560577-69-5
| Molecular Weight | 513.47 |
|---|---|
| Formula | C26H22F3N3O5 |
N-[[2-(2,6-Dioxo-3-piperidinyl)-2,3-dihydro-1-oxo-1H-isoindol-5-yl]methyl]-α-oxo-4-[1-(trifluoromethyl)cyclopropyl]benzeneacetamide
enzeneacetamide, N-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1-oxo-1H-isoindol-5-yl]methyl]-α-oxo-4-[1-(trifluoromethyl)cyclopropyl]-
FDD2NVW84X, Sontigidomida
Sontigidomide (Compound 5) is an antineoplastic compound. Sontigidomide inhibits MOLM-13 cell proliferation more than 80% at 1 μM (3 days).
SCHEME
COUPLER………….

MAIN……….

PATENTS
WO2023070120 BioTheryX, Inc.
PATENT
US20200369679
https://patentscope.wipo.int/search/en/detail.jsf?docId=US311579044&_cid=P20-MD87Y5-18242-1
Example 5
Compound I-5: N-((2-(2,6-Dioxopiperidin-3-yl)-1-oxoisoindolin-5-yl)methyl)-2-oxo-2-(4-(1-(trifluoromethyl)cyclopropyl)phenyl)acetamide

Compound I-5 was synthesized as shown in Scheme 5.

To a solution of 3-(5-(aminomethyl)-1-oxoisoindolin-2-yl)piperidine-2,6-dione 8 (80 mg, 0.258 mmol) in DCM (4 mL) at 0° C. was added TEA (52.2 mg, 0.516 mmol). After stirring for 2 min, 2-oxo-2-(4-(1-(trifluoromethyl)cyclopropyl)phenyl)acetyl chloride 13 (71.3 mg, 0.258 mmol) was added and the mixture was stirred at RT for 2 h. After concentration, the residue was purified using prep-HPLC eluting with ACN/H 2O (0.1% TFA) from 10% to 95% to afford compound I-5 (16.1 mg) in 12% yield. MS (ESI) m/z: 514.0 [M+H] +; 1H NMR (400 MHz, DMSO-d 6) δ 10.98 (s, 1H), 9.57 (t, J=6.0 Hz, 1H), 8.03-8.01 (m, 2H), 7.74-7.48 (m, 7H), 5.13-5.09 (m, 1H), 4.59-4.57 (m, 2H), 4.49-4.31 (m, 2H), 2.95-2.87 (m, 1H), 2.63-2.58 (m, 1H), 2.45-2.38 (m, 1H), 2.03-1.99 (m, 1H), 1.43-1.40 (m, 2H), 1.24-1.21 (m, 2H).
- Ketoamides for treating malignancyPublication Number: WO-2023070120-A1Priority Date: 2021-10-22
- Protein-targeting compounds and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: US-2020369679-A1Priority Date: 2019-05-24
- Compounds targeting proteins and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: WO-2020242960-A1Priority Date: 2019-05-24
- Compounds targeting proteins and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: AU-2020283744-A1Priority Date: 2019-05-24
- Targeted protein compound, its pharmaceutical composition and therapeutic applicationPublication Number: CN-114502543-APriority Date: 2019-05-24
- Compounds targeting proteins and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: EP-3976623-A1Priority Date: 2019-05-24
- Protein targeting compounds, pharmaceutical compositions thereof and therapeutic applications thereofPublication Number: KR-20220023343-APriority Date: 2019-05-24
- Protein-targeting compounds and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: US-11345712-B2Priority Date: 2019-05-24Grant Date: 2022-05-31
- Protein-targeting compounds and pharmaceutical compositions thereof, and their therapeutic applicationsPublication Number: US-2022298172-A1Priority Date: 2019-05-24
////////Sontigidomide, FDD2NVW84X, CANCER, Sontigidomida
..



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DRUG APPROVALS BY DR ANTHONY MELVIN CRASTO
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