https://www.selleckchem.com/products/OSI-906.html
SAR131675 significantly inhibited cell viability and induced apoptosis in HUVECs in a dose-dependent manner. Moreover, SAR131675 induced mitochondrial dysfunction, ROS generation, Bcl-2 down-regulation, Bax up-regulation, cytochrome c release, and caspase-3 activation, which displays features of the mitochondria-dependent apoptosis signaling pathway. Our present data demonstrated that SAR131675-induced cytotoxicity in HUVECs is associated with the mitochondria apoptotic pathway. These results suggest that further studies are required to
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