Licorice has been traditionally prescribed for palpitation, whereas its overdose may cause torsade de pointes. Licorice contains ≥2% (w/w) glycyrrhizic acid, being hydrolyzed to glycyrrhetinic acid (GRA) in the intestine. Since the electropharmacological properties of licorice is not fully understood, we assessed them using in vitro and in vivo models. GRA at 0.1, 1 and 10 μg/mL was applied to the hiPSC-CMs sheets (n=6). GRA elevated spontaneous activation rate, shortened repolarization period, and decreased maximum contraction velocity, indicating Ca channel blockade. It prolonged effective refractory period and post repolarization refractoriness with a steep frequency-dependency, whereas it delayed conduction with a modest use-dependency, mimicking Na channel blocking property of lidocaine. Next, Kanzoto, a decoction of licorice alone of 2 or 6 g/body/day, was orally administered to the conscious chronic atrioventricular block dogs for 3 days (n=4). Licorice prolonged QT interval with increasing its temporal dispersion, suggesting K channel suppression, and slightly decreased the plasma K⁺ concentration without inducing torsade de pointes. Moreover, it suppressed atrial and idioventricular rates, leading to sinus arrest along with cardiac arrest in one animal, suggesting Na channel blocking property. Thus, electropharmacological profile of licorice can be largely explained by Na channel blockade along with K and Ca channel suppression. Torsade de pointes was not induced in vivo because of its multichannel blocking action.