Key result
AN-132 significantly inhibited chloroform-induced cardiac arrhythmias in a dose-related fashion and, unlike quinidine, did not significantly enhance plasma digoxin concentrations in rats.
May support AN-132 development avoiding digoxin interaction in models; hypothesis-generating and should not yet change practice.
The effects of AN-132, 3-(diisopropylaminoethyl-amino)-2',6'-dimethylpropionanilide.2H 3PO4, on chloroform-induced arrhythmias and plasma digoxin concentrations have been compared with those of quinidine in rats. AN-132 (0.01-3 mg kg-1) administered orally significantly inhibited the incidence of cardiac arrhythmias in a dose-related fashion. A single dose of digoxin (1 mg kg-1) given orally for 7 consecutive days was followed, on day 8, orally by digoxin alone, or together with AN-132 (50, 100 and 200 mg kg-1) or quinidine (25 and 50 mg kg-1). The AUC0-24 and Cmax of plasma digoxin were enhanced significantly by co-administration of quinidine, but not by AN-132.
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Sakai et al. (1988) studied Chloroform-induced arrhythmias and digoxin pharmacokinetics. AN-132 vs. Quinidine (25 and 50 mg kg-1) or digoxin alone was evaluated on Incidence of cardiac arrhythmias and plasma digoxin concentrations (AUC0-24 and Cmax). AN-132 significantly inhibited chloroform-induced cardiac arrhythmias in a dose-related fashion and, unlike quinidine, did not significantly enhance plasma digoxin concentrations in rats.
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