[{"from": "human", "value": "Could you give me a brief overview of this molecule? [C][N][C][C][N][Branch1][Branch1][C][C][Ring1][=Branch1][C][=C][Branch2][Ring2][=N][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][N][C][=N][C][=C][Branch1][=Branch1][C][=C][N][Ring1][Branch1][C][=Branch1][Ring2][=N][Ring1][=Branch2][O][C][=C][C][=C][C][=Branch1][Ring2][=C][Ring1][=Branch1][N][C][=Branch1][C][=O][C][=C][F].[C][=Branch1][#Branch1][=C][\\C][=Branch1][C][=O][O][\\C][=Branch1][C][=O][O]"}, {"from": "gpt", "value": "The molecule is the maleate salt form of abivertinib, an orally available, irreversible, epidermal growth factor receptor (EGFR) mutant-selective inhibitor, with potential antineoplastic activity. Upon oral administration, abivertinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the drug-resistant T790M EGFR mutant, which prevents signaling mediated by mutant forms of EGFR. This may both induce cell death and inhibit tumor growth in EGFR-mutated tumor cells. EGFR, a receptor tyrosine kinase that is mutated in a variety of cancers, plays a key role in tumor cell proliferation and tumor vascularization. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors, which also inhibit wild-type EGFR."}]