Neurodegenerative disorders are increasingly identified as one of the major causes of epilepsy. The relationship
of epileptic activity to Alzheimer’s disease (AD) is of clinical importance. Voltage-gated sodium channel (VSC) is one of
the best targets in the treatment of epilepsy while β-secretase (BACE) has long been observed as a curative target for AD.
To explore a possible link between the treatment of AD and epilepsy, the molecular interactions of recently Food and
Drug Administration approved antiepileptic drug Aptiom (Eslicarbazepine acetate) with BACE and VSC were studied.
Docking study was performed using ‘Autodock4.2’. Hydrophobic and pi-pi interactions play critical role in the correct
positioning of Eslicarbazepine acetate within the catalytic site of VSC and BACE enzyme to permit docking. Free energy
of binding (ΔG) of ‘Eslicarbazepine acetate-VSC’ interaction and ‘Eslicarbazepine acetate-CAS domain of BACE’
interaction was found to be -5.97 and -7.19 kcal/mol, respectively. Hence, Eslicarbazepine acetate might act as a potent
dual inhibitor of BACE and VSC. However, scope still remains in the determination of the three-dimensional structure of
BACE- Eslicarbazepine acetate and VSC-Eslicarbazepine acetate complexes by X-ray crystallography to validate the
described data. Further, Aptiom (Eslicarbazepine acetate) could be expected to form the basis of future dual therapy
against epilepsy associated neurological disorders.
Keywords: Alzheimer's disease, β-secretase, epilepsy, eslicarbazepine acetate, voltage-gated sodium channel.
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