1835667-63-4
Chemical Structure
Befotertinib
Synonym(s): D-0316
- CAS No.: 1835667-63-4
- Formula:C29H32F3N7O2
- Molecular Weight:567.61
IUPAC Name: 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)acrylamide
InChIKey: USOCZVZOXKTJTI-UHFFFAOYSA-N
SMILES: O=C(NC1=CC(NC2=NC(C3=CN(CC(F)(F)F)C4=C3C=CC=C4)=CC=N2)=C(C=C1N(CCN(C)C)C)OC)C=C
Biological Activity: Befotertinib (D-0316) is an orally active EGFR inhibitor and ABCB1 inhibitor. Befotertinib selectively targets EGFR mutations including EGFRT790M, EGFRL858R and delE746-A750, forms covalent bonds with EGFRC797, inhibits oncogenic signaling pathways, and exerts antiproliferative effects. Befotertinib inhibits ABCB1-mediated drug efflux, activates the ATPase activity of ABCB1, acts as a chemosensitizer and apoptosis enhancer, and restores the sensitivity of multidrug-resistant cancer cells. Befotertinib can be used in research related to multidrug-resistant cancers and non-small cell lung cancer[1][2].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Befotertinib | 99.77% | Befotertinib (D-0316) is an orally active EGFR inhibitor and ABCB1 inhibitor. Befotertinib selectively targets EGFR mutations including EGFRT790M, EGFRL858R and delE746-A750, forms covalent bonds with EGFRC797, inhibits oncogenic signaling pathways, and exerts antiproliferative effects. Befotertinib inhibits ABCB1-mediated drug efflux, activates the ATPase activity of ABCB1, acts as a chemosensitizer and apoptosis enhancer, and restores the sensitivity of multidrug-resistant cancer cells. Befotertinib can be used in research related to multidrug-resistant cancers and non-small cell lung cancer. | ||||||||||||||||||||
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References
- [1]. Li YC, et al. Befotertinib restored chemosensitivity to multidrug-resistant cancer cells by inhibiting the drug efflux activity of ABCB1. J Pharm Pharmacol. 2026;78(3):rgag020. [Content Brief]
- [2]. Damghani T, et al. Profiling and Optimizing Targeted Covalent Inhibitors through EGFR-Guided Studies. J Med Chem. 2025;68(16):17917-17932. [Content Brief]
