Retigabine exhibits antiseizure effects in an array of in vivo seizure/epilepsy models. It is active in several models in which seizures do not respond to other antiepileptic drugs (AEDs). Early investigations showed that retigabine activated a voltage-sensitive, neuronal-specific outward potassium current that was later identified as the M-current that is mediated by KCNQ (Kv7) channels. Retigabine is cleared partly by renal excretion in unchanged form and partly by metabolic elimination. Population pharmacokinetic analysis of data from healthy volunteers and patients with epilepsy identified body surface area, age and creatinine clearance as co-variates having meaningful effects on retigabine pharmacokinetics. There is insufficient information on the value of monitoring serum retigabine levels, and there is no indication that monitoring serum retigabine concentrations may help in individualizing therapy, except for compliance assessment. Clinical studies have documented the efficacy of retigabine as adjunctive therapy in adults with refractory focal seizures.