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技术文章
SKF-96365 hydrochloride前沿研究进展
点击次数:707 发布时间:2017/11/17 13:48:16
产品名称"> :目录号: HY-100001
SKF-96365是SOCE的抑制剂, 能够在结直肠癌细胞里通过引起细胞周期阻滞和凋亡,表现抗肿瘤活性。
所属研究领域:Membrane Transporter/Ion ChannelAutophagy,所属靶点TRP ChannelAutophagy
产品生物活性:Description
SKF-96365 hydrochloride, an SOCE inhibitor, exhibits potent anti-neoplastic activity by inducing cell-cycle arrest and apoptosis in colorectal cancer cells.
In Vitro
SKF-96365 exhibits potent anti-neoplastic activity by inducing cell-cycle arrest and apoptosis in colorectal cancer cells. SKF-96365 inhibits hERG current in a concentration-dependent manner[1]. SKF-96365 can induces cytoprotective autophagy to delay apoptosis by preventing the release of cytochrome c (cyt c) from the mitochondria into the cytoplasm. Mechanistically, SKF-96365 treatment inhibits the calcium/calmodulin-dependent protein kinase IIγ (CaMKIIγ)/AKT signaling cascade. Overexpression of CaMKIIγ or AKT abolishes the effects of SKF-96365 on cancer cells, suggesting a critical role of the CaMKIIγ/AKT signaling pathway in SFK-96365-induced biological effects[2].
In Vivo
SKF-96365 inhibits CRC cell growth in vivo. SKF-96365 treatment results in a decrease of p-CaMKII and p-AKT as well as an increase in LC3-II, cleaved PARP, caspase-3, and caspase-9 in mice[2].
References
[1]. Liu H, et al. SKF-96365 blocks human ether-à-go-go-related gene potassium channels stably expressed in HEK 293 cells. Pharmacological Research. Pharmacol Res, 2016 Feb, 104:61-9.
[2]. Jing Z, et al. SKF-96365 activates cytoprotective autophagy to delay apoptosis in colorectal cancer cells through inhibition of the calcium/CaMKIIγ/AKT-mediated pathway. Cancer Lett, 2016 Mar 28, 372(2):226-38.