Migraine is a highly prevalent neurovascular disorder that can be provoked by 
infusion of calcitonin gene-related peptide (CGRP). CGRP, a neuropeptide 
released from activated trigeminal sensory nerves, dilates intracranial and 
extracranial blood vessels and centrally modulates vascular nociception. On this 
basis, it has been proposed that: (i) CGRP may play an important role in the 
pathophysiology of migraine; and (ii) blockade of CGRP receptors may abort 
migraine. With the advent of potent and selective CGRP receptor antagonists, the 
importance of CGRP in the pathophysiology of migraine and the therapeutic 
principle of CGRP receptor antagonism were clearly established. Indeed, both 
olcegepant (BIBN4096BS, given intravenously) and telcagepant (MK-0974, given 
orally) have been shown to be safe, well tolerated and effective acute 
antimigraine agents in phase I, phase II, and for telcagepant phase III, 
studies. However, recent data reported elevated liver transaminases when 
telcagepant was dosed twice daily for three months for the prevention of 
migraine rather than acutely. The potential for a specific acute antimigraine 
drug, without producing vasoconstriction or vascular side effects and with an 
efficacy comparable to triptans, is enormous. The present review will discuss 
the role of CGRP in the pathophysiology of migraine and the various treatment 
modalities that are currently available to target this neuropeptide.