COH-17

COH-17 (1.56-100 μg/mL; 24 h) potently inhibits the viability of MCF-7, MDA-MB-231, C6, MG-63, and A549 cancer cells with IC₅₀ values ranging from 15.56 to 17.35 μg/mL, and exhibits selective cytotoxicity toward cancer cells relative to normal MCF-10A breast epithelial cells^[1].
COH-17 (5-25 μg/mL) dose-dependently reduces mTOR protein levels in MCF-7 cells, with the greatest suppression observed at the 25 μg/mL dose and an 86% reduction at the IC₅₀ dose of 15 μg/mL^[1].
COH-17 (5-25 μg/mL) dose-dependently disrupts cell membrane integrity in MCF-7 cells, resulting in high cytotoxicity at 25 μg/mL, moderate cytotoxicity at 10 μg/mL, and low cytotoxicity at 5 μg/mL^[1].
COH-17 (15.56 μg/mL) treatment of MCF-7 cells upregulates tumor suppressor and pro-apoptotic genes (BRCA1, BRCA2, PTEN, TP53, Caspase-3, BRAD1) and downregulates anti-apoptotic and PI3K/Akt pathway genes (BCL-2, PI3K, AKT) at its IC₅₀ dose^[1].
COH-17 (15.56 μg/mL) treatment of MCF-7 cells increases pro-apoptotic BAX and tumor suppressor p53 protein levels, decreases anti-apoptotic BCL-2 protein levels, and does not alter caspase-3 protein levels^[1].
COH-17 (10-20 μg/mL) treatment of MCF-7 cells induces chromatin decondensation, indicating altered nuclear morphology and increased transcriptional activity at doses of 10, 15, and 20 μg/mL^[1].
COH-17 (10-25 μg/mL) dose-dependently induces apoptosis and reduces viability in MCF-7 cells, with the highest apoptotic activity observed at the 25 μg/mL dose^[1].
COH-17 arrests MCF-7 cells in the G0/G1 phase of the cell cycle, with 83.7% of cells accumulating in this growth-preparatory phase^[1].

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