📚 Wiki Cognitive & Mood CGRP

CGRP

✓ Approved (via antibody antagonists)
Calcitonin Gene-Related Peptide
Also known as: CGRP, alpha-CGRP, beta-CGRP, CGRP-I, CGRP-II
Page last reviewed

Quick Summary

Calcitonin gene-related peptide (CGRP) is a 37-amino acid neuropeptide produced by alternative splicing of the calcitonin gene in neurons. It is the most abundant neuropeptide in the sensory nervous system, expressed in trigeminal ganglion neurons and released from perivascular nerve terminals.

Neuropeptide FDA Approved (Anti-CGRP antibodies)
Calcitonin gene-related peptide (CGRP) is a 37-amino acid neuropeptide produced by alternative splicing of the calcitonin gene in neurons. It is the most abundant neuropeptide in the sensory nervous system, expressed in trigeminal ganglion neurons and released from perivascular nerve terminals. CGRP is a potent vasodilator and the principal mediator of neurogenic inflammation in migraine pathophysiology. Four FDA-approved monoclonal antibodies targeting CGRP or its receptor have transformed migraine prevention therapy, validating CGRP as one of the most important pharmacological targets in neurology.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

CLR/RAMP1 Receptor Complex

cgrp/" class="wiki-internal-link">CGRP acts via a heterodimeric receptor complex: calcitonin receptor-like receptor (CLR) paired with receptor activity-modifying protein 1 (RAMP1). This CLR/RAMP1 complex is Gs-coupled and highly expressed in vascular smooth muscle, trigeminal ganglion neurons, and dural blood vessels. CGRP binding activates adenylyl cyclase, increasing cAMP and causing potent, prolonged vasodilation. Adrenomedullin uses related receptor complexes, explaining some cross-pharmacology.

Migraine Pathophysiology

Trigeminal nerve activation in migraine releases CGRP from perivascular terminals in the dura mater, causing meningeal vasodilation, plasma protein extravasation (neurogenic inflammation), and activation of trigeminal pain pathways. CSF and plasma CGRP levels are elevated during migraine attacks and normalize with triptan treatment. Exogenous CGRP infusion provokes migraine in susceptible individuals, establishing causality.


Research Summary

Migraine Prevention (Anti-CGRP Antibodies)

FDA Approved

Four anti-CGRP pathway monoclonal antibodies are FDA-approved for migraine prevention: erenumab (targets CGRP receptor), fremanezumab, galcanezumab, and eptinezumab (target CGRP ligand). Phase III trials show 40-50% reduction in monthly migraine days vs placebo in episodic and chronic migraine. These antibodies represent the first migraine-specific preventive medications and have transformed the field.

Gepants (Small Molecule CGRP Antagonists)

FDA Approved

Small molecule CGRP receptor antagonists (gepants) including rimegepant (Nurtec) and ubrogepant (Ubrelvy) are FDA-approved for acute migraine treatment. Atogepant (Qulipta) is approved for prevention. Gepants offer an oral alternative to triptans with a different mechanism and potentially better tolerability in patients with cardiovascular contraindications to triptans.

Cardiovascular and Pulmonary Roles

Preclinical/Research

CGRP is cardioprotective during ischemia, promoting vasodilation and reducing infarct size in animal models. It is elevated in pulmonary arterial hypertension and heart failure as a compensatory vasodilator. Therapeutic CGRP supplementation for cardiovascular protection has been proposed but not clinically developed.


Calculate your CGRP dose Vial strength, BAC water, exact syringe draw in IU. Free, no signup. Open Calc →

Research Protocols

GoalDoseFrequencyRoute
Migraine prevention (erenumab)70-140 mg SC monthlyOnce monthlySubcutaneous
Acute migraine (rimegepant)75 mg orallyAs needed (max 1 per 24h)Oral
CGRP-induced migraine provocation (research)1.5 ug/min IV infusion x 20 minSingle infusionIntravenous

Native CGRP is not administered therapeutically. The clinical benefit is achieved via antibody or small molecule CGRP pathway blockade. Anti-CGRP antibody use requires physician oversight and is indicated only for migraine prevention.


Interactions

complementary
Triptans (sumatriptan, rizatriptan)
Triptans act on 5-HT1B/1D receptors to inhibit CGRP release and cause vasoconstriction; gepants block the downstream CGRP receptor instead
receptor overlap
Adrenomedullin
Both use CLR-based receptor complexes; adrenomedullin uses CLR/RAMP2 or RAMP3; partial pharmacological cross-reactivity
co-released
Both are trigeminal neuropeptides co-released during neurogenic inflammation; CGRP is dominant in migraine pathophysiology

Safety Profile

Anti-CGRP antibodies have excellent safety profiles in clinical trials: injection site reactions, constipation (erenumab), and mild nasopharyngitis. No hepatotoxicity (a concern that limited gepant development initially). Long-term safety data up to 5 years shows consistent tolerability. Cardiovascular safety monitoring is ongoing given CGRP's vasodilatory cardioprotective role. Gepants may cause constipation and somnolence. CGRP blockade during pregnancy is not recommended due to vasodilatory roles in placental circulation.


References

  • [1]Amara SG, et al. Alternative RNA processing in calcitonin gene expression generates mRNAs encoding different polypeptide products. Nature. 1982;298(5871):240-244.
  • [2]Goadsby PJ, et al. A controlled trial of erenumab for episodic migraine. N Engl J Med. 2017;377(22):2123-2132.
  • [3]Durham PL. CGRP-receptor antagonists, a fresh approach to migraine therapy. N Engl J Med. 2004;350(11):1073-1075.
Ready to dose CGRP?
Get the exact syringe draw
You have read the research. Now run the math. Pick your vial size and BAC water volume, get IU draw in seconds.
Open the Calculator →
Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

Suggest a Change

CGRP · wiki page