Peptide Profile
CGRP
Calcitonin Gene-Related Peptide · alpha-CGRP · beta-CGRP
CGRP (calcitonin gene-related peptide) is a 37-amino-acid endogenous neuropeptide produced by alternative splicing of the calcitonin gene, expressed predominantly in sensory neurons of the trigeminal system and peripheral…
- Half-life
- ~3.6 min / ~13.6 min (biphasic; sheep)
- Routes
- subcutaneous, intravenous
Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.
Educational research tools — not medical advice.
What CGRP is
About CGRP
Binds CLR/RAMP1 receptor complex. Causes vasodilation via cAMP/PKA/nitric oxide pathway. Modulates nociceptive signaling in the trigeminal system. Promotes bone healing and has anti-inflammatory effects in peripheral tissues.
CGRP (calcitonin gene-related peptide) is a 37-amino-acid endogenous neuropeptide produced by alternative splicing of the calcitonin gene, expressed predominantly in sensory neurons of the trigeminal system and peripheral vasculature, where it functions as a potent vasodilator and pain neuromodulator central to migraine pathophysiology. CGRP activates its receptor complex (CLR/RAMP1) to mediate vasodilation and nociceptive signal amplification; during migraine attacks, trigeminal activation releases CGRP at elevated plasma concentrations, and blockade of this pathway has been established as the primary validated pharmacological target for modern preventive migraine therapy. Phase 3 randomized controlled trials published in the New England Journal of Medicine and the Lancet — including the STRIVE trial (Goadsby et al. 2017) and a Phase 3b study in treatment-refractory patients — demonstrated that anti-CGRP monoclonal antibodies significantly reduced monthly migraine days versus placebo, validating the pathway and supporting FDA approval of erenumab, fremanezumab, and galcanezumab. CGRP itself is an endogenous neuropeptide and is not a therapeutic agent that is compounded or administered by providers; the FDA-approved interventions are monoclonal antibody and small-molecule receptor antagonists available by prescription, and exogenous CGRP peptide is exclusively a research tool compound used in vasodilatory and pain signaling pharmacology studies.
CGRP Benefits & Research Areas
What the evidence says about CGRP
Research Evidence
based on 10 studies · 2 RCTs · most recent 2026
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Not Evaluated
Native CGRP is not an FDA-approved drug substance; an openFDA ingredient search for "calcitonin gene-related" returns no approved product. The CGRP pathway is a validated migraine target, but via receptor ANTAGONISTS — erenumab (Aimovig, BLA 761077, approved 2018-05-17) and the gepants — not via CGRP itself. The 2018-05-17 date previously carried on this record was erenumab's approval date and has been removed.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
10 sources cited · 2 strong · 1 moderate · 7 weak
2 RCTs · 1 Cohort · 7 Animals
Efficacy and tolerability of erenumab in patients with episodic migraine in whom two-to-four previous preventive treatments were unsuccessful: a randomised, double-blind, placebo-controlled, phase 3b study
Lancet · 2018
The LIBERTY phase 3b trial found that monthly erenumab 140 mg achieved 50% or greater migraine day reduction in 30% of patients with episodic migraine who had failed 2 to 4 prior preventive treatments, compared with 14% for placebo, demonstrating CGRP receptor blockade efficacy even in difficult-to-treat migraine populations.
A Controlled Trial of Erenumab for Episodic Migraine
New England Journal of Medicine · 2017
The STRIVE phase 3 trial found that monthly subcutaneous erenumab (a CGRP receptor monoclonal antibody) at 70 mg and 140 mg reduced mean monthly migraine days by 3.2 and 3.7 compared with 1.8 for placebo over months 4 to 6, with 43 to 50% of participants achieving at least 50% migraine day reduction, establishing CGRP receptor blockade as an effective preventive approach.
Three-year real-world effectiveness, treatment persistence, and planned discontinuation of anti-calcitonin gene-related peptide monoclonal antibodies for migraine prevention: a single-center cohort from Japan.
Front Neurol · 2026
# Summary Research found that anti-CGRP monoclonal antibodies sustained their effectiveness for migraine prevention over three years, with 56% of patients continuing treatment and showing durable reductions in migraine days and disability measures. This study demonstrated that treatment discontinuation often reflected intentional completion after patients achieved their treatment goals, with no adverse events causing treatment withdrawal, supporting a personalized approach to therapy management.
Show 7 more sources ↓
Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.
J Physiol · 2026
# Summary Research found that Nav1.8 sodium channels carry the majority of sodium current during action potentials in mouse CGRP-lineage nociceptors and are the dominant driver of repetitive firing in these neurons. This study demonstrated that while Nav1.7 channels activate more rapidly with smaller depolarizations, Nav1.8 channels are equally critical for setting action potential threshold and controlling the upstroke phase due to their larger size.
CGRP-targeted migraine treatment and early pathophysiology in experimental subarachnoid hemorrhage.
J Headache Pain · 2026
# Summary Research found that CGRP blockade administered before experimental subarachnoid hemorrhage was associated with improved early cerebral blood flow and motor performance in rats. This study demonstrated that early subarachnoid hemorrhage alters trigeminovascular CGRP signaling, specifically reducing CGRP release from the dura mater while leaving trigeminal ganglion release unchanged.
A Self-Powered, Cold-Responsive Pyroelectric Biointerface Restores Implant Osseoperception and Osseointegration.
Adv Healthc Mater · 2026
# Summary Research found that a pyroelectric titanium coating on dental implants can convert cold thermal stimuli into electrical signals that activate neural pathways and increase calcitonin gene-related peptide (CGRP) secretion, which in turn promotes bone cell differentiation and integration. This study demonstrated that in a rat model, exposure to cold water triggered this self-powered biointerface to restore both sensory feedback and bone integration around dental implants without requiring external power sources or invasive wiring.
CXCL10 knockdown attenuates vestibular migraine in rats by inhibiting PI3K-mediated neuroinflammation and central sensitization.
J Headache Pain · 2026
# Research Summary Research found that CXCL10, a signaling molecule involved in immune responses, contributes to vestibular migraine development by activating inflammatory pathways and increasing pain sensitivity in brain regions associated with headache and balance control. This study demonstrated that reducing CXCL10 expression ameliorated migraine-related pain and vestibular dysfunction in an animal model, with effects mediated through the PI3K/AKT signaling pathway.
Luteolin reduces sciatic nerve damage and modulates TRPV1 and TRPM2 expression in diabetic rats.
Neurol Res · 2026
A Hydrogen Sulfide-Releasing Dynamic Hydrogel Modulates Coordinated Neurovascular, Immune, and Angiogenic Responses for Scar-Suppressed Diabetic Wound Repair.
Adv Sci (Weinh) · 2026
Pharmacokinetics and organ-specific metabolism of calcitonin gene-related peptide in sheep
J Endocrinol · 1988
CGRP Side Effects & Safety Considerations
Research-use compound with limited human data. Evidence strength varies — see the Evidence section.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician.
Common monitoring markers in research protocols
Under clinical review
Being verified by our medical team before we display monitoring guidance for this peptide.
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
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Frequently Asked Questions — CGRP
CGRP (calcitonin gene-related peptide) is a 37-amino-acid endogenous neuropeptide produced by alternative splicing of the calcitonin gene, expressed predominantly in sensory neurons of the trigeminal system and peripheral vasculature, where it functions as a potent vasodilator and pain neuromodulator central to migraine pathophysiology. CGRP activates its receptor complex (CLR/RAMP1) to mediate vasodilation and nociceptive signal amplification; during migraine attacks, trigeminal activation releases CGRP at elevated plasma concentrations, and blockade of this pathway has been established as the primary validated pharmacological target for modern preventive migraine therapy.
vasodilation, pain modulation, wound healing, bone repair.
Research on CGRP primarily documents effects related to vasodilation and pain modulation and wound healing and bone repair. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
For CGRP, its FDA status is not evaluated by the FDA, and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
2 providers in the directory currently offer CGRP.
The LIBERTY phase 3b trial found that monthly erenumab 140 mg achieved 50% or greater migraine day reduction in 30% of patients with episodic migraine who had failed 2 to 4 prior preventive treatments, compared with 14% for placebo, demonstrating CGRP receptor blockade efficacy even in difficult-to-treat migraine populations.
How to get CGRP
Where to buy CGRP
2 providersQuestions to ask your provider
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Tools & Guides
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Key factors that determine dosing in clinical practice.
Peptide Storage Guide
How to store lyophilized and reconstituted peptides.