Cinepazide Maleate (CM) is a vasodilator. Among various concentrations, 10 μM CM exhibited most significant protection on PC12 cells against OGD (oxygen-glucose deprivation) injury. CM was found to suppress OGD-induced oxidative stress, as supported by its capability of reducing intracellular reactive oxygen species and malondialdehyde production and enhancing superoxide dismutase activity. CM can protect neuronal cells against OGD injury by preserving mitochondrial functions[2]. T2D (type 2 diabetes) exacerbated CCH-induced (chronic cerebral hypoperfusion) brain damage and cognitive impairment, and CM (cinepazide maleate) ameliorated these effects[1]. Cinepazide (3 - 30 mg/kg, i.v.) produced a dose-related and transient increase in vertebral, carotid, renal and femoral arterial flow as well as cardiac output and a decrease in total peripheral resistance in anesthetized dogs. Cinepazide resembled cinnarizine and papaverine in that the drug antagonized rabbit aortic contraction induced by KCl, norepinephrine or CaCl2[3]. Cinepazide in concentrations ranging from 10(-6) to 10(-5) M augmented the relaxing responses to ATP, adenosine and cAMP. Cinepazide slightly reduced the 3H-efflux evoked by electrical stimulation. However, the relaxing response was mostly augmented by the treatment with cinepazide[4]. Cinepazide maleate combined with edaravone can effectively increase the survival rate of brain cells and promote the volatilization of neurological function in the treatment of hemorrhage in the subretinal space of the omentum[5].
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