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Pifusertib hydrochloride
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Pifusertib hydrochloride
CAS No. : 2930090-28-9
MCE 站:Pifusertib hydrochloride
产品活性:Pifusertib (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)。Pifusertib 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。Pifusertib hydrochloride 诱导细胞凋亡 (apoptosis) 和自噬 (autophagy)。
研究领域:PI3K/Akt/mTOR | Apoptosis | Autophagy
作用靶点:Akt | Apoptosis | Autophagy
In Vitro: Pifusertib (1 μM; 6 hours) blocks basal phosphorylation of Akt and downstream p-FKHR/FKHRL1 in MM cells with high baseline p-Akt.
Pifusertib (0-10 μM; 72 hours) selectively inhibits Akt and induces cytotoxicity in MM cells with high baseline phosphorylation of Akt.
Pifusertib abrogates the cytoprotective effect of the bone marrow microenvironment associated with Akt inhibition in both MM cells and BMSCs. Pifusertib enhances Carfilzomib-induced cytotoxicity and fatal ER stress in MM cells. Pifusertib (0.5, 1 μM) triggers G0/G1 arrest followed by apoptosis, associated with induction of autophagy and endoplasmic reticulum stress response.
Pifusertib 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 Pifusertib augments Bortezomib-induced ER stress and apoptotic signaling.
In Vivo: Pifusertib (12-16 mg/kg; p.o.; daily for 5 days a week, 21 days) inhibits tumor growth in murine xenograft models of human MM.
Pifusertib enhances bortezomib-induced MM cytotoxicity in vivo.
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热门标签:TAS-117 hydrochloride