Clofilium tosylate, a potassium channel blocker, induces apoptosis of human promyelocytic leukemia (HL-60) cells via Bcl-2-insensitive activation of caspase-3. Antiarrhythmic agent[1].
HL-60 cells treated with Clofilium (0-20 μM; 24, 48, and 72 hours) lead to suppression of viability and proliferation in both time and concentration-dependent manners. Cell viability decreases significantly in HL-60 cells treated with 2.5 μM to 10 μM of Clofilium[1].Clofilium (10 μM, 12 hours) induces the proteolytic cleavage of inactive procaspase-3, p34 into its active form, p17 and subsequent cleavage of its substrate PARP at 2 h after exposure to 10 mM Clofilium. However, there is no significant change in expression of Bcl-2 and Bax proteins[1].|| Cell Viability Assay[1]||Cell Line:|HL-60 cells |Concentration:|0-20 μM|Incubation Time:|24, 48, and 72 hours|Result:|Inhibited HL-60 cells with IC50s of 6.3 μM for 24 hours, 3.4 μM for 48 hours, 2.4 μM for 72 hours, respectively.|| Western Blot Analysis[1]||Cell Line:|HL-60 cells|Concentration:|10 μM |Incubation Time:|12 hours|Result:|Induced proteolytic cleavage of caspase-3 and subsequent cleavage of its substrate, PARP, while Bcl-2 and Bax proteins were unaltered.
[1]. Choi BY, et al. Clofilium, a potassium channel blocker, induces apoptosis of human promyelocytic leukemia (HL-60) cells via Bcl-2-insensitive activation of caspase-3. Cancer Lett. 1999 Dec 1;147(1-2):85-93.