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Clinical response and tolerability of eslicarbazepine in treatment of partial onset seizures: impact of a novel metabolic pathway

Authors Serrano E, Harden C

Published 20 April 2011 Volume 2011:4 Pages 23—28

DOI https://doi.org/10.2147/JRLCR.S16729

Review by Single-blind

Peer reviewer comments 2


Enrique Serrano1, Cynthia L Harden2
1Comprehensive Epilepsy Center, Department of Neurology, University of Miami, Miami, FL, USA; 2Comprehensive Epilepsy Care Institute, Long Island Jewish School of Medicine, Hofstra North Shore, New Hyde Park, NY, USA

Abstract: Epilepsy is a common chronic neurological condition affecting 50 million people worldwide. Because at least 30% of patients with partial seizures do not achieve seizure control with the current antiepileptic drugs, there remains an urgent need for novel antiepileptic drugs with more favorable safety profiles. Eslicarbazepine acetate (formerly known as BIA 2-093) is a novel voltage-gated sodium channel blocker used as adjunctive therapy in the treatment of refractory partial-onset seizures. Eslicarbazepine acetate is a dibenzazepine that is chemically related to carbamazepine and oxcarbazepine, designed to avoid production of active metabolites, as occurs with both carbamazepine and oxcarbazepine. Carbamazepine is metabolized by the liver to the active metabolite, carbamazepine-10, 11-epoxide, which contributes to clinical toxicity. Eslicarbazepine acetate is reduced by esterases in the liver to the active metabolite eslicarbazepine, the S (+) enantiomer of licarbazepine,27 without production of the 10,11-epoxide, resulting in a lower drug interaction potential and fewer adverse neurological effects. Further, while oxcarbazepine is a prodrug that is metabolized into both the S- and R- enantiomers of licarbazepine, eslicarbazepine acetate is metabolized to solely the S- enantiomer of licarbazepine. Eslicarbazepine acetate stabilizes the inactivated state of the voltage-gated sodium channels, preventing their return to an activated state and sustaining repetitive neuronal firing. Eslicarbazepine acetate also has a higher affinity for the inactivated state of the sodium channel compared with the resting state, suggesting enhanced selective inhibition of rapidly firing neurons associated with epileptic discharges. Consequently, eslicarbazepine acetate is less likely to bind to normally active neurons, and, therefore, less likely to cause adverse neurological effects. In clinical trials, eslicarbazepine acetate shows significant efficacy in reducing seizure frequency, and a favorable adverse effect profile at once per day doses of 800 mg or 1200 mg. This novel antiepileptic drug is a promising addition to the treatments for people with partial epilepsy.

Keywords: antiepileptic drugs, neurotransmission, seizures

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