ROLE OF CALCITONIN GENE RELATED PEPTIDE IN DEVELOPMENT OF mAB IN MIGRAINE: A REVIEW

Abstract

Migraine which was once believed to be caused by change in vascular activity in early twentieth century resulting from transient vasoconstriction in migraine aura and headache from rebound vasodilation is replaced with neurovascular phenomenon, predominantly neurovascular which is evoked by release of calcitonin gene-related peptide (CGRP), a vasoactive neuropeptide reported to be present in cranial nuclei from trigeminal sensory nerves. An elevated level of calcitonin gene-related peptide (CGRP) dilates the intracranial and extracranial blood vessels and regulates vascular nociception is a likely mechanism in migraine pathology. It is advocated that calcitonin gene-related peptide (CGRP) plays a profound role in pathophysiology of migraine. Monoclonal antibodies with promising safety and efficacy are advocated as prophylactic treatment for episodic and chronic migraine which targets against CGRP or CGRP receptor based on results obtained from phase II and III clinical trials.