In vitro | Obatoclax (GX15-070) shows inhibition of BCL-2, BCL-XL, MCL-1, BCL-w, A1, and BCL-b with Ki values≈1-7 μM [2]. Obatoclax (50-200 nM; 24-72 hours) induces a dose- and time-dependent reduction of cell numbers in all human colorectal cancer cell lines. In particular, the IC 50 of cell proliferation at 72 h are 25.85, 40.69, and 40.01 nM for HCT116, HT-29, and LoVo cells, respectively [1]. Obatoclax (400 nM; for 24 hours) induces autophagy in OSCC cells [3]. Obatoclax (50-200 nM; for 24 hours) provokes a dose-dependent increase in the G1-phase cell populations [1]. Obatoclax (25-200 nM; for 24 hours) indicates a marked drop in cyclin D1 levels as low as 50 nM [1]. Obatoclax induces T286 phosphorylation-dependent or -independent cyclin D1 degradation. in HCT116 and LoVo cells, the steady-state levels of p-Cyclin D (T286) began to decline once exposed to obatoclax (200 nM; 1, 3, 6, 12, 24 hours). Obatoclax inhibits GSK3β but activates p38 MAPK, while barely affecting ERK1/2 activity in HT-29 cells [1]. Obatoclax (50, 100, 150, 200, 250, 300, 350, 400, 450 nM) potently inhibits the clonogenic potential of oral cancer cells [1]. Cell Proliferation Assay [1] Cell Line: human colorectal cancer HCT116, HT-29 and LoVo cells Concentration: 50, 100, 200 nM Incubation Time: 24, 48, and 72 hours Result: Induced a dose- and time-dependent reduction of cell numbers. Cell Autophagy Assay [3] Cell Line: AW8507 and SCC029B cells Concentration: 400 nM Incubation Time: 24 hours Result: Induced autophagy in OSCC cells. Cell Cycle Analysis [1] Cell Line: HCT116 and HT-29 cells Concentration: 50, 100, 200 nM Incubation Time: 24 hours Result: Provoked a dose-dependent increase in the G1-phase cell populations. Western Blot Analysis [1] Cell Line: HCT116, HT-29 and LoVo cells Concentration: 50, 100, 200 nM Incubation Time: 24 hours Result: Indicated a marked drop in cyclin D1 levels as low as 50 nM. |