ICSN3250 hydrochloride

ICSN3250 (10 μM) hydrochloride weakly inhibits mTOR kinase activity in vitro, but shows no effect on PI3K, AKT1, EGFR, or other kinases^[1].
ICSN3250 (5-100 nM, 24 h) hydrochloride specifically inhibits mTORC1 pathway by reducing phosphorylation of S6K, S6, and 4EBP1 in HCT116 cells^[1].
ICSN3250 (5-100 nM, 8-24 h) hydrochloride induces autophagy in HCT116 and U2OS cancer cells, as evidenced by increased LC3-II levels, decreased p62, and GFP-LC3 puncta accumulation^[1].
ICSN3250 (10-30 nM, 24 h) hydrochloride causes G0-G1 cell-cycle arrest in HCT116 cells^[1].
ICSN3250 (25-100 nM, 24 h) hydrochloride completely inhibits mTORC1 and induces autophagy in TSC2⁺/⁺ MEFs, but fails to do so in TSC2⁻/⁻ MEFs^[1].
ICSN3250 (100 nM, 24 h) hydrochloride loses its ability to inhibit mTORC1 in HCT116 and U2OS cells when TSC2 is knocked down by siRNA^[1].
ICSN3250 (10 μM, 24 h) hydrochloride directly binds to mTOR's FRB domain (confirmed by SPR) and displaces phosphatidic acid (PA), reversing mTORC1 activation in HCT116 cells^[1].
ICSN3250 (100 nM, 24-72 h) hydrochloride shows 10-100 fold higher cytotoxicity in cancer cells (HCT116, U2OS, U87, K562) than in non-cancer cells (NHDF, HUVEC, HFDPC)^[1].
ICSN3250 (100 nM, 72 h) hydrochloride selectively reduces viability of primary colorectal cancer cells but not patient-derived fibroblasts^[1].
ICSN3250 (100 nM, 72 h) hydrochloride decreases GFP-positive cancer cell population in co-cultures of GFP-labeled HCT116/U2OS with non-cancer cells (HUVEC/NHDF)^[1].

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