Ivabradine is not an inhibitor or an inducer of CYP3A4.

Ivabradine is indicated for the treatment of coronary artery disease, for the symptomatic treatment of chronic stable angina pectoris in coronary artery disease adults with normal sinus rhythm and for the treatment of chronic heart failure. Common side effects are headache and dizziness.

Under physiological conditions ivabradine is highly water-soluble and is extensively metabolised by CYP3A4. The major active metabolite is N-desmethyl-ivabradine (S 18982) which is also metabolised by CYP3A4 (SPC). The half-life elimination of ivabradine is 2 hours in plasma and the effective half-life is 11 hours. Ivabradine has low affinity for CYP3A4 and are therefore a very weak inhibitor of CYP3A4 (SPC). Both in vitro and in vivo data have shown that it is unlikely to influence the pharmacokinetics and pharmacodynamics of other CYP3A4 substrates (Portolés 2006 and SPC). No drug-drug interactions with ivabradine as a perpetrator are observed (Interaksjoner and Interaktionsdatabasen), which indicate that ivabradine is not an inhibitor or inducer of CYP enzymes. The summary of product characteristics states that a specific drug-drug interaction study has shown that ivabradine does not have a clinical significant effect on the pharmacokinetics of simvastatin, a CYP3A4 substrate. This also indicates that ivabradine is not an inhibitor or an inducer of CYP3A4.

Uneventful use reported in 1 patient with acute porphyria.