CGRP plays a key role in central chronic pain by mediating “neurogenic inflammation”. In this process, sensory nerves which usually carry electrical signal from the body instead broadcast inflammatory signals into it. CGRP is the most important of the inflammatory signals. Treating CGRP can be helpful for chronic migraine & pain.
Small sensory nerves throughout the body gather information & interact with the body directly. This nerve-body interface underlies many diseases.
In chronic pain, these nerves release signal molecules to trigger “neurogenic inflammation” by activating blood vessels & immune cells. This can cause redness, swelling, & inflammation in the tissue, without a frank source such as an infection or an injury.
This process is complex and is a topic of intense scientific research. What is currently known is that CGRP is a key signal molecule. CGRP binds to 2 receptors, CGRP receptor and AMY1 receptor.
Traditional treatments that affect CGRP
- Triptan medications reduce neuron synthesis of CGRP as well as release of CGRP.
- Botox™ reduces the ability of cells to release signal molecules. When applied to head & neck nerves, these nerves release less CGRP.
Antibody therapies in general require injections to get into the body. The 3 anti-CGRP antibody therapies are all injected by the patient at home, typically on a monthly schedule:
- Aimovig™ (erenumab) is an antibody that targets the CGRP receptor. It does not target the AMY1 receptor. It is packaged in an auto-injector.
- Emgality™ (galcanezumab) is an antibody that targets the CGRP molecule itself. It is packaged in an auto-injector.
- Ajovi™ (fremanezumab) is an antibody that targets the CGRP molecule itself. It is packaged as a vial which the patients will draw from and inject.
Pain physician & PhD computational biologist @StanfordPain • Advanced pain interventions with CIPS & FIPP • Opinions mine & not medical advice