CGRP may be a key mediator of inflammation in migraine. Several CGRP inhibitors are now being developed. Trials conducted to date show these to be of about equal effectiveness with triptans, but without the side effects that result from vasoconstriction by triptans.
Activation of NF-kB may lead to transcription and then release of CGRP.
Inhibiting NF-kB reduced CGRP levels.
An effective inhibitor of NF-kB might therefore perform as well, or better than, an inhibitor of CGRP.
Mechanism of interleukin-1 beta-induced calcitonin gene-related peptide production from dorsal root ganglion neurons of neonatal rats.
Summary of the abstract
Calcitonin gene-related peptide (CGRP) is synthesized in dorsal root ganglion (DRG) neurons and released from primary afferent neurons to mediate hemodynamic effects and neurogenic inflammation.
Inhibitors of NF-kB blocked IL-1beta-induced CGRP release.
These results indicate that IL-1beta may lead to activation of NF-kB which then induces alpha-CGRP gene expression and release from these sensory neurons.