Anti-CGRP antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CGRP or Calcitonin Gene-Related Peptide is a 37-amino acid neuropeptide with a molecular mass of approximately 3.8 kDa. This peptide exists mainly in two forms alpha-CGRP and beta-CGRP differing slightly in amino acid sequence. CGRP expresses in peripheral and central nervous systems with high levels in the dorsal root ganglia and thyroid gland. It also has a significant presence in the enteric nervous system and some segments of the cardiovascular system. Scientists note that CGRP acts as a potent vasodilator and plays a significant role in transducing pain signals.

Biological function summary

CGRP contributes to numerous physiological processes including blood flow regulation body temperature control pain transmission and neurogenic inflammation. It acts independently and does not substantially form part of larger protein complexes in its primary activities. Through binding to the CGRP receptor a complex made up of the calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein 1 (RAMP1) CGRP initiates downstream signaling that results in its various biological effects.

Pathways

Studies place CGRP within the neuropeptide signaling pathway and the vasodilation pathway. It significantly influences the cyclic AMP (cAMP) signaling pathway where it works collaboratively with other neuropeptides like substance P. The interaction with CLR and RAMP1 triggers the production of cAMP which enhances vasodilation and pain transmission processes in the body.

Associated diseases and disorders

CGRP holds a notable connection to migraines and cardiovascular diseases. Elevated CGRP levels are observed in migraine sufferers and targeted treatments utilizing anti-CGRP antibodies have demonstrated efficacy in reducing migraine frequency. Additionally research links CGRP to blood pressure regulation abnormalities implicating its involvement in hypertension. Both conditions involve complex interactions with other proteins such as substance P and endothelial nitric oxide synthase (eNOS) which modulate vascular tone and inflammation.