In vitro activity: Dequalinium chloride (DECA) is a cationic, lipophilic compound with structure similar to the dye rhodamine 123. DECA is selectively accumulated and retained within the mitochondria of carcinoma cells where it acts as a mitochondrial poison by blocking mitochondrial enzymes which can then disrupt cellular energy production, eventually resulting in cell death. Dequalinium Chloride is a blocker of ganglionic transmission (EC50 = 2 μM). Dequalinium is a potent inhibitor of apamin-sensitive K+ channels in hepatocytes and of nicotinic responses in skeletal muscle. Dequalinium blocks angiotensin II-evoked K+ loss with an IC50 of 1.5 μM and also inhibited125I - monoiodoapamin binding with Ki of 1.1 μM. Dequalinium produces a rapid and reversible inhibition of the slow apamin-sensitive component of the afterhyperpolarization (AHP) which follows a single action potential in cultured rat sympathetic neurons. Dequalinium Chloride (DECA) is a dicationic lipophilic PKC inhibitor. When exposed to UV light, DECA covalently binds to and irreversibly inhibits PKCα and PKCβ.

Cell Assay: DECA, as a mitochondrial poison, is an agent with capable of potentiating the effects of tumor necrosis factor against ovarian cancer cell lines.

Gynecol Oncol. 1993 Jul;50(1):38-44; Eur J Pharmacol. 1993 May 19;236(2):201-7; Proc Natl Acad Sci U S A. 1987 Aug;84(15):5444-8.