[{"from": "human", "value": "What can you tell me about this molecule? [C][C][C][Ring1][Ring1][C][=Branch1][C][=O][N][C][=N][C][=C][C][=Branch1][Ring2][=C][Ring1][=Branch1][O][C][=C][Branch2][Ring2][Branch2][C][=C][Branch1][Branch2][C][=Branch1][Ring2][=C][Ring1][=Branch1][F][N][C][=Branch1][C][=O][C][Branch1][Branch1][C][C][Ring1][Ring1][C][=Branch1][C][=O][N][C][=C][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][F][F]"}, {"from": "gpt", "value": "The molecule is an orally bioavailable inhibitor of c-Met/hepatocyte growth factor receptor (HGFR), vascular endothelial growth factor receptor type 2 (VEGFR2), Tie2 receptor tyrosine kinase (TIE2), and tropomyosin receptor kinase (Trk), with potential antiangiogenic and antineoplastic activities. Upon administration, altiratinib selectively binds to c-Met, VEGFR2, Tie2 and Trk tyrosine kinases, which may lead to the inhibition of endothelial cell migration, proliferation and survival. This also results in both an inhibition of tumor cell proliferation and increased tumor cell death in c-Met/VEGFR2/Tie2/Trk-expressing cells. These receptor tyrosine kinases (RTKs), frequently overexpressed or mutated by a variety of tumor cell types, play crucial roles in the regulation of angiogenesis, tumor cell growth and survival."}]