NMS-P715 is a selective, ATP-competitive inhibitor of MPS1, with an IC₅₀ of 182 nM. IC50 & Target: IC50: 182 nM (MPS1)^[1] In Vitro: NMS-P715 is a selective inhibitor of MPS1, with an IC₅₀ of 182 nM. NMS-P715 is highly specific for MPS1, with no other kinases inhibited below an IC₅₀ value of 5 μM and only 3 kinases inhibited below 10 μM (CK2, MELK, and NEK6). NMS-P715 promotes massive spindle assembly checkpoint (SAC) override with an EC₅₀ of 65 nM. NMS-P715 (1 μM) causes mitotic acceleration in U2OS cells overexpressing YFP-α-tubulin, induces aneuploidy and inhibits the proliferation of HCT116 cells. NMS-P715 (0.5, 1 μM) affects mitotic checkpoint complex (MCC) stability and cdc20 ubiquitylation^[1]. NMS-P715 (1 μM) exhibits bypass of the spindle assembly checkpoint and apoptosis in pancreatic ductal adenocarcinoma (PDAC) cell lines. NMS-P715 (0-25 μM) also selectively inhibits growth of PDAC cells^[2]. In Vivo: NMS-P715 (10 mg/kg) exhibits an oral bioavailability of 37% and good pharmacokinetic properties in nude mice bearing subcutaneous implanted human tumor cell xenografts. NMS-P715 (90 mg/kg, p.o.) is well tolerated and cuases no signs of body weight loss or other overt toxicities in an A2780 ovary carcinoma xenograft model. NMS-P715 (100 mg/kg, p.o.) inhibits the tumor growth by appr 43% in the A375 melanoma xenograft model^[1].