Oxcarbazepine and its active metabolite (10,11-dihydro-10-hydroxy-carbazepine, MHD) have been effective in animal models of epilepsy that generally predict efficacy in generalized tonic-clonic seizures and partial seizures in humans. The pharmacokinetic profile of oxcarbazepine is less complicated than that of carbamazepine, with less metabolism by the cytochrome P450 system, no production of an epoxide metabolite, and lower plasma protein binding. The clinical efficacy and tolerability of oxcarbazepine have been demonstrated in trials in adults, children, and the elderly. The pharmacological activity of oxcarbazepine is primarily exerted through the 10-monohydroxy metabolite (MHD) of oxcarbazepine. The precise mechanism by which oxcarbazepine and MHD exert their antiseizure effect is unknown; however, in vitro electrophysiological studies indicate that they produce blockade of voltage-sensitive sodium channels, resulting in stabilization of hyperexcited neural membranes, inhibition of repetitive neuronal firing, and diminution of propagation of synaptic impulses. These actions are thought to be important in the prevention of seizure spread in the intact brain. In addition, increased potassium conductance and modulation of high-voltage activated calcium channels may contribute to the anticonvulsant effects of the drug.

Licarbazepine, (R)- is a hydroxy derivative of R-licarbazepine acetate. Eslicarbazepine acetate (ESL), or S-licarbazepine acetate (ESL), Licarbazepine, (R)- acetate and their racemic mixture, as well as other related compounds, were orally assessed in rats for anticonvulsant activity and compared with carbamazepine (CBZ) and oxcarbazepine (OXC). Metabolism of OXC and its derivatives varies considerably between species. Rats metabolize ESL to OXC with minimal (S)-licarbazepine or Licarbazepine, (R)- metabolites. Licarbazepine, (R)- undergoes a further oxidation to the trans-diol metabolite, demonstrating an increased predisposition to earlier inactivation. Administration of ESL and of eslicarbazepine significantly protected mice against Maximal electroshocks-induced seizures, whereas that of Licarbazepine, (R)- failed to provide protection. This finding raises doubts on the contribution of Licarbazepine, (R)- as an active anticonvulsant.