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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
Iodofalan (131I)



Iodofalan (131I)
CAS 76641-05-9
MFC9H10131INO2
Molecular FormulaC9H10INO2
Molecular Weight295.09
4-(131I)iodo-L-phenylalanine
(2S)-2-amino-3-(4-iodophenyl)propanoic acid
radiopharmaceutical, antineoplastic, Phase 2, Glioblastoma, 606VTF676Y, 131I-TLX-101, ACD 101
- 4-Iodophenylalanine I-131
- 4-(131I)Iodo-L-phenylalanine
- 4-Iodo-L-phenylalanine-131I
- ACD-101
- L-Phenylalanine, 4-(iodo-131I)-
- OriginatorTherapeia
- DeveloperTelix Pharmaceuticals; Therapeia
- ClassAmino acids; Antineoplastics; Radioisotopes; Radiopharmaceutical diagnostics; Radiopharmaceuticals; Small molecules
- Mechanism of ActionApoptosis stimulants; Positron-emission tomography enhancers
- Orphan Drug StatusYes – Glioblastoma
- Phase IIGlioblastoma
- 14 Oct 2025Telix Pharmaceuticals receives IND approval for TLX 101 in Glioblastoma
- 27 Jul 2025Telix Pharmaceuticals plans a phase III IPAX BrIGHT trial for Glioblastoma (Monotherapy, Combination therapy, Recurrent, Second-line therapy or greater) in Australia(IV) (NCT07100730)(EudraCT2025-521785-10) in September 2025
- 16 Apr 2025Telix has submitted for ethics approval a registration-enabling study of TLX101 in recurrent glioblastoma.
Iodofalan (131I) is a radiopharmaceutical that has garnered significant attention in oncological research due to its targeted therapeutic potential. This compound, which includes the radioactive isotope Iodine-131, has been explored for its efficacy in treating certain types of cancers, particularly those associated with the thyroid. Various research institutions worldwide have been studying Iodofalan (131I) to better understand its clinical benefits, optimize its usage, and minimize potential side effects. As a drug type, Iodofalan (131I) is categorized as a targeted radiopharmaceutical therapy, which leverages the properties of radioactive isotopes to destroy cancer cells with precision. Currently, its primary indications include differentiated thyroid cancer and non-resectable metastatic thyroid cancer, among other investigational uses.
Iodofalan (131I) Mechanism of Action
The mechanism of action for Iodofalan (131I) centers on the properties of Iodine-131, a beta-emitting isotope. When administered, Iodofalan (131I) is selectively absorbed by thyroid cells. This selectivity is due to the thyroid gland’s natural ability to uptake iodine, a key element required for the production of thyroid hormones. Cancerous thyroid tissues retain this ability, making them ideal targets for Iodofalan (131I) therapy.
Once absorbed by the thyroid cancer cells, the radioactive decay of Iodine-131 begins. This decay process emits beta particles, which possess sufficient energy to destroy nearby cells. The radiation from these beta particles causes direct DNA damage, leading to cell death. Additionally, the gamma radiation emitted by Iodine-131 can be used diagnostically to track the distribution and uptake of the compound in the body via imaging techniques such as SPECT (Single Photon Emission Computed Tomography).
The dual role of Iodofalan (131I) in both treatment and diagnostic contexts underscores its importance in managing thyroid cancers. By delivering a localized radiation dose to thyroid cancer cells, Iodofalan (131I) minimizes damage to surrounding healthy tissues, which is a significant advantage over traditional external beam radiotherapy.
What is the indication of Iodofalan (131I)?
The primary indication for Iodofalan (131I) is the treatment of differentiated thyroid cancer, a category that includes papillary and follicular thyroid cancers. These subtypes are characterized by their ability to absorb iodine, making them particularly amenable to radioiodine therapy. Iodofalan (131I) is typically used in cases where the thyroid cancer is not amenable to surgical removal or has metastasized to other parts of the body. In such scenarios, the radiopharmaceutical offers a non-invasive therapeutic option that can target and destroy cancer cells even in distant metastatic sites.
SYN
https://patentscope.wipo.int/search/en/detail.jsf?docId=US42129729&_cid=P21-MHE8B5-15309-1
EXAMPLE 1

EXAMPLE 2
General synthesis of 3,4-[124I]iodo-L-phenylalanine (m, p-IPA-124), 3,4-[125I]iodo-L-phenylalanine (m,p-IPA-125) and 3,4-[131I]iodo-L-phenylalanine (m,p-IPA-131) by non-isotopic radioiodo-debromination
PAT
- Pharmaceutical combinations and uses thereofPublication Number: US-2024197715-A1Priority Date: 2022-11-18
- Pharmaceutical combinations and uses thereofPublication Number: WO-2024105610-A1Priority Date: 2022-11-18
- Iodine-labeled homoglutamic acid and glutamic acid derivativesPublication Number: US-2013034497-A1Priority Date: 2009-11-17
- MALIGNAS NEOPLASIAS THERAPY.Publication Number: ES-2341575-T3Priority Date: 2005-11-25Grant Date: 2010-06-22
- Therapy of malignant neoplasiasPublication Number: US-2007128108-A1Priority Date: 2005-11-18
- Therapy of malignant neoplasias
- Publication Number: US-9682158-B2
- Priority Date: 2005-11-18
- Grant Date: 2017-06-20



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//////////Iodofalan (131I), radiopharmaceutical, antineoplastic, Phase 2, Glioblastoma, 606VTF676Y, 131I-TLX-101, ACD 101
BQ-788
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BQ-788
- Molecular FormulaC34H50N5NaO7
- Average mass663.780 Da
SP ROT +3.8 ° Conc: 1.032 g/100mL; methanol; Wavlenght: 589.3 nm, Development of an efficient strategy for the synthesis of the ETB receptor antagonist BQ-788 and some related analogues
Peptides (New York, NY, United States) (2005), 26, (8), 1441-1453., https://doi.org/10.1016/j.peptides.2005.03.022
FOR FREE FORM +19.6 °, Conc: 0.998 g/100mL; : N,N-dimethylformamide; 589.3 nm
BQ-788 is a selective ETB antagonist.[1]
presumed to be under license from Banyu , was investigating BQ-788, a selective endothelin receptor B (ETRB) antagonist, for treating metastatic melanoma. By December 2009, the drug was in validation.
Also claimed is their use as an ETBR antagonist and for treating cancers, such as brain cancer, pancreas cancer, colon cancer, breast cancer, ovary cancer, prostate cancer, glioblastoma, solid tumor, melanoma and squamous cell carcinoma. Represent a first filing from ENB Therapeutics Inc and the inventors on these deuterated forms of BQ-788. Melcure SarL ,

SYN
By Brosseau, Jean-Philippe et alFrom Peptides (New York, NY, United States), 26(8), 1441-1453; 2005

CONTD…………

PAPER
https://pubs.acs.org/doi/pdf/10.1021/jo00130a028

N-(cw-2,6-Dimethylpiperidinocarbonyl)-y-methylleucylD-l-(methoxycarbonyl)tryptophanyl-D-norleucine Sodium Salt (1, BQ-788). To a solution of 15 (3.5 g, 5.5 mmol) in methanol (50 mL) was slowly added 5% aqueous NaHCOs (300 mL) over a period of 30 min. The solution was stirred until clarity was achieved (30 min, 23 °C). The solution was diluted with water (200 mL), and the resulting solution was passed through a C18 (60 mL) cartridge preequilbrated in water. BQ-788 (1) was eluted with methanol (2 x 50 mL), concentrated under reduced pressure, resuspended in water (50 mL), and lyophilized to quantitatively yield compound 1 as a white powder:
HPLC £r = 16.4 (gradient A, > 99%);
NMR (400 MHz, DMSO-d6) ó 0.80 (s, 9H), 0.74-0.85 (m, 3H), 1.00 (d, 3H), 1.02 (d, 3H), 1.10-1.25 (m, 6H), 1.30-1.55 (m, 6H), 1.60-1.75 (m, 2H), 2.92 (dd, 1H), 3.12 (dd, 1H), 3.78 (m, 1H), 3.95 (s, 3H), 4.08 (m, 1H), 4.13 (m, 1H), 4.29 (m, 1H), 4.50 (m, 1H), 5.98 (d, 1H), 7.22 (t, 1H), 7.32 (t, 1H), 7.50 (s, 1H), 7.58 (br d, 1H), 7.65 (d, 1H), 8.05 (d, 1H), 8.15 (br d, 1H) ESMS m/z 640.6 (M).
PATENT
WO-2019140324
Novel deuterated analogs of a substituted heterocyclic compound, particularly BQ-788 , processes for their preparation and compositions and combinations comprising them are claimed.
PAPER
https://www.sciencedirect.com/science/article/abs/pii/S0196978105001415

PAPER
By He, John X.; Cody, Wayne L.; Doherty, Annette M., From Journal of Organic Chemistry (1995), 60(25), 8262-6
Journal of medicinal chemistry (1996), 39(12), 2313-30.
References
| Names | |
|---|---|
| Systematic IUPAC name
Sodium N-{[(2R,6S)-2,6-dimethyl-1-piperidinyl]carbonyl}-4-methyl-L-leucyl-N-[(1R)-1-carboxylatopentyl]-1-(methoxycarbonyl)-D-tryptophanamide
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3D model (JSmol)
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PubChem CID
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CompTox Dashboard (EPA)
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| Properties | |
| C34H50N5NaO7 | |
| Molar mass | 663.792 g·mol−1 |
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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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///////////BQ-788, BQ 788, BQ788, ETBR antagonist, cancers, brain cancer, pancreas cancer, colon cancer, breast cancer, ovary cancer, prostate cancer, glioblastoma, solid tumor, melanoma, squamous cell carcinoma, PEPTIDE
CCCC[C@H](C(=O)O)NC(=O)[C@@H](Cc1cn(c2c1cccc2)C(=O)OC)NC(=O)[C@H](CC(C)(C)C)NC(=O)N3[C@@H](CCC[C@@H]3C)C
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