| Bioactivity | Licarbazepine (BIA 2-005; GP 47779) is a voltage-gated sodium channel blocker with anticonvulsant and mood-stabilizing effects[1]. | ||||||||||||
| Target | Sodium Channel | ||||||||||||
| In Vivo | Eslicarbazepine acetate (ESL) is an oral pro-drug that is rapidly and extensively metabolized by the liver via a hydrolytic first-pass metabolism into S-Licarbazepine, the biologically active drug. The plasma level of the prodrug remains below quantification[1]. ESL is a potent antiepileptic agent with a spectrum of action essentially limited to partial-onset and generalized tonic-clonic seizures. Its main mechanism of action is by blocking the voltage-gated sodium channel. ESL works by blocking the voltage-gated sodium channel, which play an essential role in the generation and propagation of the epileptic discharge. ESL is well absorbed after oral administration with a bio-availability about 16% higher than that observed after an equivalent dose of Oxcarbazepine (OXC)[1]. | ||||||||||||
| Name | Licarbazepine | ||||||||||||
| CAS | 29331-92-8 | ||||||||||||
| Formula | C15H14N2O2 | ||||||||||||
| Molar Mass | 254.28 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Rajinder P Singh, et al. A review of eslicarbazepine acetate for the adjunctive treatment of partial-onset epilepsy. J Cent Nerv Syst Dis. 2011 Jul 20;3:179-87. |