Moclombeide is most probably not a mechanism-based inhibitor or an inducer of any major CYP enzymes. Risk for gastrointestinal adverse events in the form of nausea and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Moclobemide is a reversible monoamine oxidase (MAO) A inhibitor. Common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are nausea and diarrhoea. Other common side effects are sleeping disorders, dizziness and headache.

Moclobemide is completely metabolised by the liver (Bonnet 2006 and Mayersohn 1995). The metabolism of moclobemide is primarily morpholine N-oxidation, aromatic hydroxylation, morpholine C-oxidation and deamination (Jauch 1990). It is metabolised by CYP2C19 (Fleishaker 2001 and Gram 1995) and the half-life elimination is 1-2 hours (Bonnet 2002). Two metabolites have been detected in plasma, Ro 12-5637 and Ro 12-8095 (Bonnet 2006). Ro 12-8095 is inactive while Ro 12-5637 have some activity, but it is only present in trace amounts (Bonnet 2002). Moclobemide is listed as a moderate CYP2C19 inhibitor in vivo (FDA & Isoherranen 2009). In vitro data indicate minor time-dependent inhibition of CYP2D6 and CYP1A2 by moclobemide (Polasek 2006). An in vivo study has shown that moclobemide increased the AUC of almotriptan by 37% when co-administrated (Fleishaker 2001). Monoamine oxidase is responsible for the almotriptan metabolism in man with minor contributions by CYP3A4 and CYP2D6 (Fleishaker 2001 and SPC), this indicates that the increase in AUC of almotriptan is because of inhibition of monoamine oxidase by moclobemide, rather than inhibition of CYP3A4. No clinically relevant interaction has been observed between moclobemide and oral contraceptives. The pharmacokinetics parameters were however, not measured. A conclusion on the effect on CYP enzymes by moclobemide can therefore not be made (Amrein 1992 and Zimmer 1990).