It exerts its antiarrhythmic effect by induction of slow inward sodium current, which prolongs action potential and refractory period of myocardial cells.

[1] Ibutilide, like other class III antiarrhythmic drugs, blocks delayed rectified potassium current.

[3] Ibutilide's unique mechanism works by an activation of a specific inward sodium current, thus producing its therapeutic response in which a prolonged action potential increases myocytes’ cardiac refractoriness in case of atrial fibrillation and flutter.

[4] Ibutilide has a high systemic plasma clearance that closes to the hepatic blood flow (29mL/min/kg).

Its metabolic pathway is via liver's cytochrome P450 system by isoenzymes other than CYP3A4 and CYP2D6 by which the heptyl side chain of ibutilide is oxidized.

Consequently, the drug is contraindicated in patients that are likely to develop abnormal heart rhythms; this includes individuals who have previously experienced polymorphic ventricular tachycardia, have a prolonged QT interval, sick sinus syndrome, or have recently had a myocardial infarction, among other conditions.