Insignificant hepatocellular exposure makes pharmacokinetics CYP-interactions unlikely. Rotigotine is not an inducer or inhibitor of CYP3A4 in vivo. Rotigotine does not inhibit or induce CYP isoforms in vitro. There are no pharmacodynamics effects of relevance in acute porphyria. Risk for gastrointestinal adverse events in the form of nausea, vomiting, obstipation, dyspepsia and weight loss motivates vigilance against insufficient intake of food, especially of carbohydrate.

Rotigotine is a dopamine agonist. Rotigotine is monotherapy indicated for the symptomatic treatment of moderate to severe idiopathic Restless Legs Syndrome in adults. It is also used in early MB-Parkinson as monotherapy, or as adjunct to L-dopa in late resistant stages of the disease. Very 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 vomiting. Common side effects are obstipation, dyspepsia and weight loss. Administration: administered as dermal patch releasing 1-(2) mg/24 h.

Low-dose transdermal administration, with reduction of the systemic concentration of the drug in cerebral target cells prior to reaching the liver, will make hepatocellular exposure insignificant.

Rotigotine is metabolised via N-dealkylation (SPC) by CYP3A4, CYP2C19, CYP1A and CYP2D6 (Braun 2009 and Chen 2009). Insignificant (<< 1 µM) hepatic exposure makes PXR/CAR effected (pharmacokinetics) CYP-interactions unlikely. Transdermal rotigotine had no effect on the pharmacokinetics of oral contraceptives, ethinyl estradiol and levonorgestrel (CYP3A4 substrates), when co-administered (Braun 2009 and SPC). This indicates that rotigotine is not an inducer or inhibitor of CYP3A4 in vivo. Rotigotine does not inhibit or induce CYP isoforms in vitro (Cada 2007 and Chen 2009). Pharmacodynamic mechanisms: Nucleous caudatus D1-D5 receptor agonist. No side effects pointing to activation of the mesolimbic receptors, which mediate dopamine-effects on the hypothalamic-pituitary HP axis (i.e. activation of the HP-adrenal axis and HP-growth hormone axis, and damping of HP-gonadotropin axis and HP-thyroid axis).