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TAS-117 hydrochloride
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
TAS-117 hydrochloride图片
规格:98%
分子量:460.96
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议

产品介绍
TAS-117 hydrochloride 是一种有效、选择性、具有口服活性的别构 Akt 抑制剂 (对 Akt1、2 和 3 的 IC50 分别为 4.8、1.6 和 44 nM)。TAS-117 hydrochloride 激发抗骨髓瘤活性并增强蛋白酶体抑制诱导的致命内质网应激。TAS-117 hydrochloride 诱导细胞凋亡 (apoptosis) 和自噬 (autophagy)。
货号:ajcx34104
CAS:N/A
分子式:C26H25ClN4O2
分子量:460.96
溶解度:DMSO : 62.5 mg/mL (135.59 mM; ultrasonic and warming and heat to 60°C)
纯度:98%
存储:Store at -20°C
库存:现货

Background:

TAS-117 hydrochloride is a potent, selective, orally active allosteric Akt inhibitor (with IC50s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). TAS-117 hydrochloride triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. TAS-117 hydrochloride induces apoptosis and autophagy[1].

TAS-117 (1 μM; 6 hours) blocks basal phosphorylation of Akt and downstream p-FKHR/FKHRL1 in MM cells with high baseline p-Akt[1].TAS-117 (0-10 μM; 72 hours) selectively inhibits Akt and induces cytotoxicity in MM cells with high baseline phosphorylation of Akt[1].TAS-117 abrogates the cytoprotective effect of the bone marrow microenvironment associated with Akt inhibition in both MM cells and BMSCs. TAS-117 enhances Carfilzomib-induced cytotoxicity and fatal ER stress in MM cells. TAS-117 (0.5, 1 μM) triggers G0/G1 arrest followed by apoptosis, associated with induction of autophagy and endoplasmic reticulum stress response[1].TAS-117 enhances bortezomib-induced cytotoxicity, associated with increased CHOP (a fatal ER-stress marker) and PARP cleavage and blockade of bortezomib-induced p-Akt, suggesting that TAS-117 augments Bortezomib-induced ER stress and apoptotic signaling[1].

TAS-117 (12-16 mg/kg; p.o.; daily for 5 days a week, 21 days) inhibits tumor growth in murine xenograft models of human MM[1].TAS-117 enhances bortezomib-induced MM cytotoxicity in vivo[1].

[1]. Mimura N, et al. Selective and potent Akt inhibition triggers anti-myeloma activities and enhances fatal endoplasmic reticulum stress induced by proteasome inhibition. Cancer Res. 2014;74(16):4458-4469.