PI3K/Akt/mTOR-IN-2 是一种有效的 PI3K/AKT/mTOR 抑制剂。PI3K/Akt/mTOR-IN-2 具有抗癌作用，并对 MDA-MB-231 细胞具有选择性，IC₅₀ 为 2.29 μM。PI3K/Akt/mTOR-IN-2 可诱导癌细胞周期阻滞和细胞凋亡 (apoptosis)。

PI3K/Akt/mTOR-IN-2 is a PI3K/AKT/mTOR pathway inhibitor. PI3K/Akt/mTOR-IN-2 possess anti-cancer effects and selectivity against MDA-MB-231 cells with IC 50 value of 2.29 μM. PI3K/Akt/mTOR-IN-2 can induce cancer cell cycle arrest and apoptosis.

Solid

IC50: 2.29 μM (PI3K/AKT/mTOR) in MDA-MB-231

PI3K/Akt/mTOR-IN-2 (compound 23) (0.5 - 100 μM; 72 hours) exhibits effective anti-cancer activity with IC50s of 2.29 - 24.63 μM, of which, IC50 in MDA-MB-231 is 2.29 μM.
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces growth inhibition of MDA-MB-231 cells by cell cycle arrest at G0/G1.
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24, 48 and 72 hours) induces apoptosis in MDA-MB-231 cells with both dose- and time-dependent manners.
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 48 hours) increases the expression of Bax, and decreases the expression of Bcl-2 in MDA-MB-231 cells.
PI3K/Akt/mTOR-IN-2 (1 μM, 2 μM and 4 μM; 24 hours) induces mitochondria-dependent apoptosis in MDA-MB-231 cells through disruption of MMP, accumulation of ROS, depletion of GSH and elevation of intracellular Ca.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Qin J, Sun X, Ma Y, et al. Design, synthesis and biological evaluation of novel 1,3,4,9-tetrahydropyrano[3,4-b]indoles as potential treatment of triple negative breast cancer by suppressing PI3K/AKT/mTOR pathway [published online ahead of print, 2021 Dec

In Vitro: DMSO : ≥ 100 mg/mL (350.52 mM)配制储备液