Pregabalin is an antagonist of voltage gated Ca2+ channels and specifically binds to alpha-2-delta subunit to
produce antiepileptic and analgesic actions. It successfully alleviates the symptoms of various types of neuropathic pain
and presents itself as a first line therapeutic agent with remarkable safety and efficacy. Preclinical studies in various
animal models of neuropathic pain have shown its effectiveness in treating the symptoms like allodynia and hyperalgesia.
Clinical studies in different age groups and in different types of neuropathic pain (peripheral diabetic neuropathy,
fibromyalgia, post-herpetic neuralgia, cancer chemotherapy-induced neuropathic pain) have projected it as the most
effective agent either as monotherapy or in combined regimens in terms of cost effectiveness, tolerability and overall
improvement in neuropathic pain states. Preclinical studies employing pregabalin in different neuropathic pain models
have explored various molecular targets and the signaling systems including Ca2+ channel-mediated neurotransmitter
release, activation of excitatory amino acid transporters (EAATs), potassium channels and inhibition of pathways
involving inflammatory mediators. The present review summarizes the important aspects of pregabalin as analgesic in
preclinical and clinical studies as well as focuses on the possible mechanisms.