Retigabine is not metabolized by CYP enzymes and it is unlikely that it will be involved in drug-drug interactions. Risk for gastrointestinal adverse events in the form of nausea motivates vigilance against insufficient intake of food, especially of carbohydrate.

ethyl N-(2-amino-4-(4-fluorobenzylamino)phenyl) carbamate hydrochloride Retigabine is also known as ezogabine.

Retigabine is indicated as adjunctive treatment of partial onset seizures with or without secondary generalisation in adults aged 18 years and above with epilepsy. Common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and which also can be confused with an acute porphyria attack are fatigue, nausea and obstipation. Other common side effects are urinary hesitation, paraesthesia, disorientation, psychotic behaviour, hallucinations.

Retigabine is metabolized to an N-acetyl active metabolite (NAMR) and other inactive metabolites. Retigabine and NAMR are not metabolized by CYP450 enzymes (Bialer 2010, Luszczki 2009, SPC). The UGT isoforms are involved in the metabolism of retigabine (Borlak 2006).The half-life elimination is 6-10 hours. In vitro studies have shown that retigabine has little or no potential to inhibit CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4 and CYP3A5. The data also showed that it does not induce CYP1A2, CYP3A4 or CYP3A5. It is therefore unlikely that retigabine will be involved in drug-drug interactions (SPC). Retigabine is also listed with low potential to interact with other therapeutic agents (Pressman 2013). An in vivo study showed that there is a lack of pharmacokinetic interaction between retigabine and phenobarbital. Phenobarbital is a known nonspecific inducer of CYP enzymes and the data therefore confirms that retigabine is not a substrate of CYP enzymes (Ferron 2003).