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Clofilium tosylate
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
Clofilium tosylate图片
CAS NO:92953-10-1
包装与价格：
包装价格(元)
10mM (in 1mL DMSO)电议
10mg电议
50mg电议

产品介绍
Clofiliumtosylate是一种钾通道(potassiumchannel)阻滞剂，作用于人早幼粒细胞白血病(HL-60)细胞，激活caspase-3而诱导凋亡。具有抗心律失常作用。
Cas No.92953-10-1
别名氯非铵甲苯磺酸盐
Canonical SMILESCCCCCCC[N+](CC)(CCCCC1=CC=C(Cl)C=C1)CC.O=S(C2=CC=C(C)C=C2)([O-])=O
分子式C28H44ClNO3S
分子量510.17
溶解度DMSO : 125 mg/mL (245.02 mM)
储存条件4°C, protect from light
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

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.