[{"from": "human", "value": "Please give me some details about this molecule. [C][=C][C][=Branch1][C][=O][N][C][=C][Branch2][Ring2][#Branch2][C][=C][C][=Branch1][Ring2][=C][Ring1][=Branch1][C][=Branch1][=Branch1][=N][C][=N][Ring1][#Branch1][N][C][=C][C][=Branch2][Ring1][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][O][C][C][=C][C][=C][C][=N][Ring1][=Branch1][Cl][O][C][C][N][C][C][O][C][C][Ring1][=Branch1]"}, {"from": "gpt", "value": "The molecule is an orally bioavailable, irreversible, selective, small-molecule inhibitor of certain oncogenic driver, allosteric mutations of the ErbB receptor tyrosine kinases epidermal growth factor receptor (EGFR/ErbB1) and human epidermal growth factor receptor 2 (HER2/neu or ErbB2), including extracellular domain allosteric mutations of HER2, and EGFR and HER2 exon 20 insertion mutations, with potential antineoplastic activity. Upon oral administration, tuxobertinib selectively binds to and inhibits these allosteric ErbB mutants while sparing wild-type EGFR, which may result in the selective inhibition of cellular proliferation and angiogenesis in tumor cells and tumors expressing these allosteric ErbB mutations. EGFR and HER2, ErbB receptor tyrosine kinases mutated or overexpressed in many tumor cell types, play a key role in tumor cell proliferation and tumor vascularization."}]