Key result
Intravenous administration of AP-792 effectively suppressed ventricular arrhythmias in canine models, demonstrating a slow-onset and long-lasting antiarrhythmic action.
AP-792 demonstrates potential as a unique, long-acting antiarrhythmic drug in canine models of ventricular arrhythmia.
Supports further preclinical development of AP-792; leaves open translation to human ventricular arrhythmia therapy.
The antiarrhythmic effects of a novel antiarrhythmic drug AP-792, 4-(5H-dibenzo[a,d]cyclohepten-5-ylidene)-1-[4-cyclohexylbutyl]piperidine hydrochloride, were analyzed using the epinephrine-, digitalis- and two-stage coronary ligation-induced canine ventricular arrhythmia models. Intravenous administration of AP-792 (0.3 or 1.0 mg/kg) effectively suppressed each of the ventricular arrhythmias, an action that resembles that of a typical cardioselective Ca2+ channel blocker, AH-1058. The antiarrhythmic action of AP-792 was slow in onset and longer-lasting than those in our previous studies using more than 50 antiarrhythmic drugs, including Na+ and Ca2+ channel blockers. These results suggest that AP-792 can become a unique long-acting antiarrhythmic drug.
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Takahara et al. (2001) studied Ventricular arrhythmia. AP-792 was evaluated on Suppression of ventricular arrhythmias. Intravenous administration of AP-792 effectively suppressed ventricular arrhythmias in canine models, demonstrating a slow-onset and long-lasting antiarrhythmic action.
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