[{"from": "human", "value": "Provide a brief overview of this molecule. [C][C][Branch1][C][C][Branch2][Branch1][N][C][O][C][=C][N][C][=Branch1][#Branch2][=C][Branch1][Branch1][C][=N][Ring1][Branch1][C][#N][C][=Branch1][Ring2][=C][Ring1][O][C][=C][N][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][N][C][C][C][C][Branch1][Ring2][C][Ring1][=Branch1][N][Ring1][Branch1][C][C][=C][N][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][O][C][O]"}, {"from": "gpt", "value": "The molecule is an orally bioavailable selective inhibitor of wild-type, mutant and fusion products involving the proto-oncogene receptor tyrosine kinase rearranged during transfection (RET), with potential antineoplastic activity. Upon oral administration, selpercatinib selectively binds to and targets wild-type RET as well as various RET mutants and RET-containing fusion products. This results in an inhibition of cell growth of tumors cells that exhibit increased RET activity. In addition, selpercatinib targets, binds to and inhibits vascular endothelial growth factor receptor 1 (VEGFR1) and 3 (VEGFR3), and fibroblast growth factor receptor 1 (FGFR1), 2 (FGFR2), and 3 (FGFR3). RET overexpression, activating mutations, and fusions result in the upregulation and/or overactivation of RET tyrosine kinase activity in various cancer cell types; dysregulation of RET activity plays a key role in the development and progression of these cancers."}]