Rasagiline is not an inhibitor or inducer of CYP1A2 and CYP3A4 in vivo. In vitro data indicates that it is not an inhibitor of CYP2C9.

N-propynyl indanamine. The terminal acetylenic function may be associated with mechanism-based CYP-inhibition.

Rasagiline is indicated for the treatment of Parkinsons disease. It is an irreversible MAO-B inhibitor which slows down the degradation of dopamine and inhibits reuptake of dopamine at the presynaptic dopamine receptor. Common side effects are influenza and musculoskeletal pain. A less common side effect is reduced appetite.

Rasagiline is metabolised via N-dealkylation and hydroxylation to 1-Aminoindan, 3-hydroxy-N-propargyl-1 aminoindan and 3-hydroxy-1-aminoindan (SPC). In vitro data indicates that CYP450 enzymes are involved in the metabolism and that CYP1A2 is the most important isoenzyme (SPC). Co-administration of rasagiline and ciprofloxacin, a CYP1A2 inhibitor, increased the AUC of rasagiline by 83% (Chen 2005, 2006 and SPC). This confirms that rasagiline is a CYP1A2 substrate. An in vitro study showed that rasagiline does not inhibit CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4 and CYP4A (Chen 2005, 2006 and SPC). Co-administration of rasagiline and theophylline, a substrate of CYP1A2 and CYP3A4, showed that rasagiline did not influence the pharmacokinetics of theophylline (Chen 2005, 2006 and SPC). This indicates that rasagiline is not an inhibitor or inducer of CYP1A2 and CYP3A4.

Uneventful use reported in 1 patient with acute porphyria.