Mechanism of action<unk>  acts as a neuronal KCNQ/Kv7 potassium channel opener, a mechanism of action markedly different from that of any current anticonvulsants. This mechanism of action is similar to that of the chemically-similar flupirtine, which is used mainly for its analgesic properties. The term "channel opener" refers to a shift in the voltage dependence for channel opening towards more negative potentials. This means that KCNQ/Kv7 channels open at more negative potentials in the presence of<unk> . Recently, it has also been shown that<unk>  stabilizes the open Kv7.2/7.3 channel, making deactivation slower with little change in voltage dependence. This effect of<unk>  is observed at concentrations below 10 micromolar. A similar effect is observed on the homomeric Kv7.2 channel. Pharmacokinetics<unk>  is quickly absorbed, and reaches maximum plasma concentrations between half an hour and 2 hours after a single oral dose. It has a moderately high oral bioavailability (50–60%), a high volume of distribution (6.2 L/kg), and a terminal half-life of 8 to 11 hours.<unk>  requires thrice-daily dosing due to its short half-life.<unk>  is metabolized in the liver, by N-glucuronidation and acetylation. The cytochrome P450 system is not involved.<unk>  and its metabolites are excreted almost completely (84%) by the kidneys.
Retigabine
Tiagabine
Pivagabine
Ethosuximide
Mesuximide
Brivaracetam
Lamotrigine
Tetrabenazine