PI3K/Akt/mTOR-IN-7

PI3K/Akt/mTOR-IN-7 (DG23) (10 μM; 24 h) shows no significant cytotoxicity toward BV2 microglial cells at 10 μM^[1].
PI3K/Akt/mTOR-IN-7 (10 μM; 24 h) inhibits nitric oxide production in LPS (HY-D1056)-stimulated BV2 microglial cells by 51.62% at 10 μM^[1].
PI3K/Akt/mTOR-IN-7 (10 μM; 24 h) shows no obvious cytotoxicity toward SH-SY5Y human neuroblastoma cells at 10 μM^[1].
PI3K/Akt/mTOR-IN-7 (10 μM; 26 h) confers neuroprotection against H₂O₂-induced oxidative damage in SH-SY5Y human neuroblastoma cells with a 42.68% cell viability rescue rate at 10 μM, and exhibits a concentration-dependent protective effect^[1].
PI3K/Akt/mTOR-IN-7 (10 μM; 8 h) most potently inhibits H₂O₂-induced upregulation of pro-apoptotic Bcl-2/Bax and Caspase-3 mRNA expression in SH-SY5Y human neuroblastoma cells^[1].
PI3K/Akt/mTOR-IN-7 (2.5-10 μM; 8 h) dose-dependently inhibits H₂O₂-induced reactive oxygen species accumulation in SH-SY5Y human neuroblastoma cells, with significant effects observed at 5 μM and 10 μM^[1].
PI3K/Akt/mTOR-IN-7 (2.5-10 μM; 8 h) dose-dependently reduces H₂O₂-induced Caspase-3 protein expression and restores p-Akt, p-mTOR, and p-STAT3 protein expression in SH-SY5Y human neuroblastoma cells at 2.5-10 μM, with greater potency than diosgenin^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.