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Encainide is a class Ic antiarrhythmic small molecule that acts as a voltage-gated sodium channel blocker. It was primarily used for the management of life-threatening ventricular arrhythmias, including ventricular tachycardia, atrial fibrillation, and atrial flutter. Encainide works by binding to and inhibiting voltage-gated sodium channels in cardiac tissue, which stabilizes the neuronal membrane and slows conduction velocity through the His-Purkinje system and myocardium. This results in decreased excitability, reduced automaticity, slowed conduction velocity, and increased refractory periods in cardiac tissues. The drug was developed by Bristol Myers Co but is no longer marketed due to its association with proarrhythmic adverse effects that led to increased mortality in certain patient populations[1][3][5]. Encainide undergoes hepatic metabolism to two active metabolites (ODE and MODE), which are more active than the parent compound[3][5]. The product was withdrawn from the US market in 1991.
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