Selegiline is not an inhibitor or inducer of CYP3A4 or CYP1A2 in vivo. Risk for gastrointestinal adverse events in the form of nausea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Selegiline is indicated for the treatment of Parkinsons disease. It is a selective MAO-B inhibitor which slows down the degradation of dopamine and inhibits reuptake of dopamine at the presynaptic dopamine receptor. A common side effect that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack is nausea.

Selegiline is metabolised to active metabolites, desmetylselegilin and l-metamfetamin, which is further metabolised to l-amfetamin (de la Torre 2004 and SPC). 84% is excreted in urine, mainly as metabolites and 40-60% as 1-metamfetamin (SPC). The half-life elimination is 1.5-3 hours. One in vitro study showed that CYP2B6 is the main enzyme involved in the metabolism of selegine with possible contribution of CYP3A4 and CYP2A6 (Benetton 2007). Another study, however, indicates that CYP1A2 and CYP3A4 are the two enzymes involved in the metabolism of selegine and that selegiline is a competitive inhibitor of CYP1A2 in vitro (Taavitsainen 2000) Selegiline transdermal system (STS) avoids extensive first-pass metabolism and the systemic bioavailability of selegiline is increased. A study showed that co-administration of STS and alprazolam, a CYP3A4 substrate (Norsk legemiddelhåndbok), did not affect the AUC of alprazolam (Azzaro 2007). Co-administration of STS and olanzapine, a CYP1A2 substrate (Norsk legemiddelhåndbok), also showed that selegiline did not have any effect on the AUC of olanzapine (Azzaro 2007). These data indicate that selegiline is not an inducer of an inhibitor of CYP3A4 or CYP1A2 in vivo. Metamfetamine is metabolised by CYP2D6 (Cruickshank 2009).