Ibutilide is a potent IKr blocker with EC 50 value of 20 nM at +20 mV in atrial tumor myocytes (AT-1) cells [1]. Ibutilide blocks I Kr in cells expressing HERG+MDR11 to the same extent as cells expressing HERG alone (IC 50 : 22.5±0.9 vs 27.4±2.5 nM). However, cells expressing MDR17 show a marked resistance to Ibutilide (IC 50 : 105.3±1.42 nM vs 27.4±2.5 nM) [2].

Ibutilide prolongs cardiac repolarization in vitro and in vivo [1]. Ibutilide infusions (administered cumulatively in three doses, 0.01, 0.02 and 0.05 mg/kg i.v., each as a 10-min infusion) results in both polymorphic and monomorphic non-sustained ventricular tachycardia [3]. Animal Model: Fifteen adult mongrel dogs of either sex [1] Dosage: 0.01, 0.02 and 0.05 mg/kg Administration: Infusion Result: The action potential duration at 90% (APD 90 ) prolongation with Ibutilide (0.01 mg/kg) was significantly greater in congestive heart failure (CHF) vs. controls. An increased dispersion of left–right ventricular APD90 was observed in CHF at 0.01 mg/kg, but not in controls.