In Vitro |
CDK1-IN-7 (compound 7a) (10 µM, 48 hours) has the high antiproliferative activity with a mean percentage of growth inhibition of 48.5 % over NCI cancer cell lines, and caused more than 40% growth inhibition in 36 cancer cell lines from different cancer subtypes[1]. CDK1-IN-7 (0.1-100 μM, 48 hours) has better selectivity for cancer cells over normal cell lines (IC50 of 17.7 and 6.28 μM in WI-38 and HCT-116 cells, respectively; SI=2.8)[1]. CDK1-IN-7 (17.7 μM in WI-38 and 6.28 μM in HCT-116; 48 hours) has a superior activity on cancerous cells than normal cells in inducing apoptosis and arresting the cell cycle at the G2/M phase[1]. CDK1-IN-7 (17.7 μM in WI-38 and 6.28 μM in HCT-116; 48 hours) can cause cell death mainly through apoptosis rather than necrosis and confirmed that its activity is more selective to cancerous cells than normal cells[1]. CDK1-IN-7 (6.28 μM; 48 hours) induce apoptosis in p53 dependent manner through the intrinsic apoptotic pathway in HCT-116 cells[1]. Cell Proliferation Assay Cell Line: 60 human cancer cell lines (LOX IMVI, IGROV1, A498, COLO205 et al.)[1] Concentration: 10 µM Incubation Time: 48 hours Result: Had the high antiproliferative activity with a mean percentage of growth inhibition of 48.5 % over NCI cancer cell lines, and caused more than 40% growth inhibition in 36 cancer cell lines from different cancer subtypes. Cell Cytotoxicity Assay Cell Line: HCT-116 and WI-38 cells[1] Concentration: 0.1-100 μM Incubation Time: 48 hours Result: Had better selectivity for cancer cells over normal cell lines (IC50 of 17.7 and 6.28 μM in WI-38 and HCT-116 cells, respectively; SI=2.8). Cell Cycle Analysis Cell Line: HCT-116 and WI-38 cells[1] Concentration: 17.7 μM in WI-38 and 6.28 μM in HCT-116 Incubation Time: 48 hours Result: Exerted a superior activity on cancerous cells than normal cells in inducing apoptosis and arresting the cell cycle at the G2/M phase.
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