BACKGROUND: Migraine is associated with activation of the trigeminovascular 
system, release of calcitonin gene-related peptide (CGRP) and dilation of dural 
arteries. Novel treatments target calcitonin gene-related peptide or its 
receptor, which are present in all vascular beds, raising cardiovascular 
concerns. Erenumab is a human CGRP-receptor antibody approved for the 
prophylactic treatment of migraine.
METHODS: We characterised the relaxant responses to CGRP in the absence and 
presence of erenumab (1 μM) in isolated human middle meningeal, internal mammary 
and (proximal and distal) coronary arteries. Furthermore, in human internal 
mammary arteries from cardiovascularly-compromised patients, we assessed the 
pharmacological specificity of erenumab by investigating whether the 
vasodilatory responses to acetylcholine, sodium nitroprusside, pituitary 
adenylate cyclase activating polypeptide-38 (PACAP), vasoactive intestinal 
peptide and nicardipine, along with the vasoconstrictor responses to 
dihydroergotamine, were modified by erenumab.
RESULTS: Calcitonin gene-related peptide induced concentration-dependent 
vasodilatory responses in all vessels studied that were significantly 
antagonised by erenumab. In human internal mammary arteries from 
cardiovascularly-compromised patients, the responses to acetylcholine, sodium 
nitroprusside, PACAP, vasoactive intestinal peptide, nicardipine and 
dihydroergotamine were unaffected by erenumab.
CONCLUSION: Erenumab inhibits calcitonin gene-related peptide-induced 
vasodilatory responses in human middle meningeal arteries, human internal 
mammary arteries and human coronary arteries. Moreover, erenumab shows 
functional specificity as no interaction was observed with the relaxant 
responses to several vasodilators, nor the dihydroergotamine-dependent 
vasoconstrictor responses.