Mechanism of action Like other class III antiarrhythmics,<unk>  blocks atrial potassium channels, thereby prolonging repolarization. It differs from typical class III agents by blocking a certain type of potassium channel, the cardiac transient outward potassium current, with increased potency as the heart rate increases. This means that it is more effective at high heart rates, while other class III agents tend to lose effectiveness under these circumstances. It also slightly blocks the hERG potassium channel, leading to a prolonged QT interval. This may theoretically increase the risk of ventricular tachycardia, though this does not seem to be clinically relevant. The drug also blocks atrial sodium channels. Pharmacokinetics and pharmacogenomics After infusion, the substance is rapidly distributed in the body. In the blood serum, 53–56% are circulating freely and are not bound to plasma proteins. In people with normal CYP2D6 function, the main route of degradation is by O-demethylation via this enzyme. In 2D6 poor metabolizers,<unk>  is mainly inactivated by glucuronidation and excreted by the kidney. Elimination half-life is three hours in 2D6 extensive (normal) metabolizers and 5.5 hours in poor metabolizers. The differences between poor and extensive metabolizers regarding peak concentrations, AUC and half-life are not clinically relevant.<unk>  does not inhibit the enzymes CYP3A4, CYP1A2, CYP2C9, CYP2C19, CYP2E1, nor the transporter protein P-gp.
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