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Y15 is a **small molecule inhibitor** specifically targeting **focal adhesion kinase (FAK) autophosphorylation at the Y397 site**. It exerts anti-tumor effects by inhibiting FAK-mediated signaling pathways critical for cancer cell survival, migration, and proliferation. Y15 has demonstrated efficacy in preclinical models by reducing cell viability, clonogenicity, and tumor growth in various cancers, including non-small cell lung cancer, neuroblastoma, breast, pancreatic, and thyroid cancers. Mechanistically, Y15 blocks FAK Y397 autophosphorylation, induces apoptosis partly through downregulation of anti-apoptotic proteins Bcl-2 and Mcl-1, and impacts multiple genes involved in apoptosis, cell cycle, and stemness. Y15 has shown strong synergism with other targeted therapeutics like Cabozantinib, Sorafenib, Pazopanib, Sunitinib, and PF-04554878 (Defactinib). Preclinical toxicology studies indicate that Y15 is well tolerated in mice via oral and intraperitoneal routes and caused no significant toxicity[1][3][5].
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