Dequalinium Chloride

Dequalinium Chloride (DECA)是蛋白激酶C(PKC)的抑制剂（IC50值7-18 μM），也是apamin-敏感性K+通道的一个选择性阻断剂（IC50值1.1 μM）[1，3]。

PKC是一个单体的Ca2+和磷脂-依赖性丝氨酸/苏氨酸蛋白激酶，它在生长因子激活信号和恶性转变过程中发挥至关重要的作用[1]。

DECA是一个抗肿瘤剂。可选择性地积累和保留在癌细胞的线粒体内，阻止线粒体酶干扰细胞能量产生，最终导致细胞死亡[2]。Dequalinium是肝细胞的apamin-敏感性K+通道和骨骼肌的烟碱酸反应中的有效的抑制剂。Dequalinium抑制angiotensin II-evoked K+ loss的IC50值为1.5 μM，抑制125I - monoiodoapamin binding的Ki值为1.1 μM[3]。

DECA，作为一种线粒体毒药，可增强肿瘤坏死因子（TNF）抗卵巢癌细胞系效应。DECA可延长移植PA-1卵巢癌动物的存活率。单独DECA处理提高了37%的动物存活率，而人类TNF增加了12%的动物（注射TNF三天后）存活率。DECA/TNF组合增加了45%的动物存活率[4]。

参考文献：
[1]. Rotenberg SA, Sun XG. Photoinduced inactivation of protein kinase C by dequalinium identifies the RACK-1-binding domain as a recognition site. J Biol Chem, 1998, 273(4): 2390-2395.
[2]. Manetta A, Emma D, Gamboa G, et al. Failure to enhance the in vivo killing of human ovarian carcinoma by sequential treatment with dequalinium chloride and tumor necrosis factor. Gynecol Oncol, 1993, 50(1): 38-44.
[3]. Castle NA, Haylett DG, Morgan JM, et al. Dequalinium: a potent inhibitor of apamin-sensitive K+ channels in hepatocytes and of nicotinic responses in skeletal muscle. Eur J Pharmacol, 1993, 236(2): 201-207.
[4]. Manetta A, Emma D, Fuchtner C, et al. Effect of recombinant human tumor-necrosis-factor-alpha and dequalinium chloride on human ovarian-cancer cell-lines in-vitro. Int J Oncol, 1993, 3(1): 127-33.