Overview
- Sheets, P.L. et al. (2008) J. Pharmacol. Exp. Ther. 326, 89.
- Kuo, C.C. et al. (1997) Mol. Pharmacol. 51, 1077.
- Backonja, M.M. (2002) Neurology 59, S14.
Alomone Labs Carbamazepine inhibits NaV1.2 channels currents in Xenopus oocytes.A. Time course of NaV1.2 channel reversible inhibition by 100 µM and 1 mM Carbamazepine (#C-105). Currents were elicited by a voltage step to -20 mV (100 ms) every 10 seconds from a holding potential of -100 mV. B. Example traces of current response to voltage step application before and during 1 mM Carbamazepine application.
Voltage-gated sodium channels (VGSC, NaV) play a critical role in excitability of nociceptors (pain-sensing neurons). The peripheral-specific sodium channels NaV1.7, NaV1.8 and NaV1.9 are particularly important in the pathophysiology of different pain syndromes and hence, thought to be potential targets for pain therapeutics1,2.
Carbamazepine is a potent and state dependent inhibitor of neuronal NaV channels1. It is one of the most commonly prescribed antiepileptic drugs3 and has long been established as a treatment for neuropathic pain4. High doses of carbamazepine are effective in ameliorating symptoms of patients with Paroxysmal extreme pain disorder (PEPD) because this disorder involves changes in NaV inactivation, a process that is modulated by NaV blockers. In a recent investigation, patients with inherited erythromelalgia, characterized by a mutation in NaV1.7 (SCN9A) and a modified fast inactivation of Na+ current is present, reported an improvement of symptoms when treated with Carbamazepine5,6. In addition, clinical data also suggest that carbamazepine can reduce aura and migraine attacks7.
