Gabapentin for the prevention of cinv

Abstract

Gabapentin is a gamma-aminobutyric acid (GABA) analogue initially approved by the Food and Drug Administration (FDA) in 1993 for the treatment of seizures. Gabapentin was soon found to be highly effective for treating neuropathic pain [1] and then restless legs syndrome [2] and presently is FDA approved for all three indications. Despite its chemical structure, gabapentin has no effect on GABA receptors or GABA breakdown by GABA transaminase but does increase brain GABA synthesis in rats and humans [3, 4]. Gabapentin’s mechanism of action for treating neuropathic pain, which is its main clinical use, is dependent upon its binding to the alpha-2/delta subunit of neuronal voltage-gated calcium channels [5] and likely involves the mitigation of neuronal calcium currents [6, 7].