Anti-CGRP monoclonal antibodies for prevention of migraine …

Neuropharmacology & Neurotherapeutics

Updated 07.09.2025
Released 03.26.2018
Expires For CME 07.09.2028

Anti-CGRP monoclonal antibodies for prevention of migraine

Authors: Suraj Malhan DO MS, Stephen D Silberstein MD

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Editor: Stephen D Silberstein MD

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Anti-CGRP monoclonal antibodies for prevention of migraine

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Introduction

Overview

Monoclonal antibodies (mAbs) targeting calcitonin gene-related peptide (CGRP) or its receptor have emerged as an effective preventive treatment for migraine (30). These therapies offer targeted treatment with a favorable safety profile compared to traditional treatment options. Since the approval of the first CGRP mAb in 2018, real-world evidence has continued to support their efficacy and safety. In 2024, the American Headache Society (AHS) updated its position statement, recommending CGRP-targeting therapies as a first-line approach for migraine prevention without a requirement for prior failure of other classes of migraine preventive treatment (05).

Key points

	• Monoclonal antibodies (mAbs) for migraine prophylaxis target the calcitonin gene-related peptide (CGRP) pathway by binding to either the ligand or blocking its receptor.
	• The rationale for this approach is based on the role of CGRP in the pathogenesis of migraine.
	• Three of the four mAbs in development (eptinezumab, fremanezumab, and galcanezumab) target CGRP itself, whereas the fourth, erenumab, targets CGRP receptor.
	• Clinical trials have shown the efficacy and safety of anti-CGRP mAbs in reducing migraine attacks.
	• Erenumab (Aimovig) and galcanezumab (Emgality) were approved in 2018. Eptinezumab (Vyepti) and fremanezumab (Ajovy) were approved by the FDA in 2020 (32).

Historical note and terminology

Historically, most preventive treatments for migraine were nonspecific, and their efficacy and safety were often unsatisfactory. The development of mAbs that target CGRP or its receptor bring a shift toward migraine-specific treatments. CGRP is a neuropeptide found in both central and peripheral neurons and plays a role in modulating pain and vascular tone (10; 17).

CGRP targeted therapies are in two distinct forms: small molecule receptor antagonists (gepants) and monoclonal antibodies. Gepants were initially developed for acute migraine treatment, but early compounds (telcagepant) faced setbacks due to initial concerns of hepatotoxicity (40). Newer gepants have been approved for abortive and preventive treatment of migraine. However, gepants are outside the scope of this article and will not be discussed here.

This article focuses on four anti-GRCP mAbs, all of which have completed clinical trials and received regulatory approval.

	• Erenumab: The only agent that targets CGRP receptor and was approved by the U.S. Food and Drug Administration and the European Medicines Agency in 2018.
	• Eptinezumab: Administered intravenously and was approved in 2020
	• Fremanezumab: Targets CGRP ligand and was approved in 2018
	• Galcanezumab: Targets CGRP ligand and was approved in 2018

Pharmacology

Pharmacodynamics. The actions of CRGP antagonist mAbs are facilitated particularly by the location of CRGP in dorsal root and trigeminal ganglions, which makes its role in causing migraine plausible. CRGP is the main mediator of trigeminal pain signal and is involved in the cascade of molecular events leading to a painful crisis in migraine. Intravenous administration of CGRP to patients prone to migraine can induce migraine-like headache. CGRP, and not substance P, is elevated in the cranial circulation during acute migraine. This explains the failure of substance P/neurokinin-1 receptor antagonists and the success of blocking CGRP mechanisms for relieving the pain of acute migraine. CGRP promotes mast cell degranulation, which results in the release of several inflammatory and proinflammatory substances. By binding to its glial receptors, CGRP promotes the release of cytokines in the trigeminal ganglia and nerve, which, in turn, produces sensitization of sensory neurons. CGRP significantly increases the expression and activity of cyclooxygenase 2, as well as the expression of the inducible form of nitric oxide synthase and IL-1β, and these effects are reversed by a specific CGRP receptor antagonist (06). CGRP is also involved in other migraine-related phenomena, eg, photophobia and gastrointestinal symptoms, such as nausea.

Involvement of CGRP in the pathophysiological processes underlying migraine led to the development of CGRP antagonists: gepants and four monoclonal antibodies targeting CGRP receptor (erenumab) or targeting CGRP ligand (eptinezumab, fremanezumab, and galcanezumab). Anti-CGRP mAbs either remove excessive CGRP released at the perivascular trigeminal sensory nerve fibers or block the receptor from signaling. Thus, mAbs against both the CGRP ligand and receptor would inhibit CGRP-induced activation of sensitized trigeminal pathways to decrease headache frequency over time (04). Animal studies to date have confirmed the minimal central penetration (< 0.04%) of CGRP reinforcing the conclusion that the primary site of action is peripheral (20). Compared with small molecules, mAbs are highly specific for their target. Anti-CGRP pathway mAbs specifically target the CGRP receptor or ligand and are not associated with the off-target toxicity that can occur when targeting the immune system. Due to their large size, mAbs do not penetrate the blood-brain barrier. This is not a limiting factor because the primary site of action of anti-CGRP, the trigeminovascular system, is outside the blood-brain barrier (11). It has been concluded that the efficacy of anti-CGRP mAbs goes beyond the mere control of pain and prevents the activation of mechanisms involved in the complete manifestations of the migraine attack (38).

Pharmacokinetics. Most of the mAbs have nonlinear pharmacokinetics. Anti-CGRP mAbs have long terminal half-lives that allow for less frequent dosing, such as once monthly or greater, but, unlike small molecules, they must be injected. Subcutaneous bioavailability for most mAb therapeutics is 50% to 100%. They are not metabolized in the liver, and, therefore, hepatotoxicity is not expected. Most of these are administered subcutaneously, except eptinezumab, which has an intravenous formulation.

Erenumab. This is a fully human immunoglobulin-2 mAb that targets the CGRP receptor instead of the ligand, with high specificity and affinity of binding. In vitro studies have demonstrated its picomolar affinity for the human CGRP receptor, exceeding the binding affinity of endogenous CGRP by over a 1000-fold. Erenumab shows no cross reactivity or antagonist activity against related peptide receptors including adrenomedullin (ADM1, ADM2), calcitonin, and amylin (29). Its mechanism of action involves binding to the extracellular domain of CGRP receptor complex comprised of calcitonin receptor-like receptor and receptor activity-modifying protein 1.

In clinical practice, erenumab is administered as subcutaneous injection at either 70 or 140 mg a month. In healthy adults, peak serum concentration is achieved in 4 to 6 days with an absolute bioavailability of 54% and increases to 82% following repeated administration (39). The median time to peak serum concentration is 4 to 11 days (mean approximately 5.5 days). Elimination follows nonlinear pharmacokinetics with a dual elimination mechanism. At low concentrations elimination occurs via saturable binding to CGRP receptors, whereas at high concentrations clearance occurs through non-specific proteolytic catabolism. The overall elimination half-life is approximately 28 days with a terminal phase half-life of 21 to 23 days. Despite a noticeable difference in exposure between 70 and 140 mg, pharmacokinetic shows no consistent correlation between drug concentration and efficacy, consistent with the absence of a dose-response.

Fremanezumab. This is a humanized IgG2 monoclonal antibody that binds with affinity to both α- and β-CGRP isoform. After a single dose, the median time to peak plasma concentration is 5 to 7 days. It has dose-proportional pharmacokinetics, with plasma concentrations increasing with higher doses. Steady state concentration is typically achieved within 168 days. The mean elimination half-life is 31 days.

Galcanezumab. This is a humanized IgG4 mAb with high affinity for both α and β isoforms of CGRP ligand (21). Upon binding, it forms a new ligand-antibody complex that undergoes structural changes and prevents CGRP from binding onto the receptor. This interaction is reversible, but dissociation is slow (18). Following a monthly subcutaneous injection of 120 or 240 mg, peak plasma concentrations are reached within 5 to 7 days and increase proportionally with multiple doses. It is degraded via proteolytic catabolism with an elimination half-life of approximately 27 days.

Eptinezumab. This is a genetically engineered, desialylated, humanized IgG1κ monoclonal antibody that binds with high affinity to both α- and β-isoforms of the CGRP ligand. It is the first and the only intravenous anti-CGRP mAb approved for prevention of migraine (12). Its binding affinity allows it to inhibit CGRP with high specificity while sparing other neuropeptides in the CGRP family. In binding analyses, eptinezumab exhibits rapid binding to the CGRP ligand, with slower dissociation suggesting strong, sustained ligand engagement (35). Following infusion of 100 or 300 mg, it reaches maximal serum concentration with 100% bioavailability and has a half-life of approximately 27 days. Compared to other mABs, eptinezumab has a shorter time to maximal concentration and greater exposure, leading to rapid treatment effects (02).

Clinical trials

The status of anti-CGRP MAbs in development for migraine is shown in Table 1.

Table 1. Clinical Trials of Anti-CGRP Monoclonal Antibodies for Migraine Prevention

Drug	Results of clinical trials	Status
Erenumab (Aimovig or AMG 334)	STRIVE phase III trial showed significantly reduced migraine frequency, effects of migraine on daily activity, and use of acute migraine medication over 6 months in patients in episodic migraine (14). APPRAISE trial showed patients treated with erenumab were six times more likely to achieve ≥50% reduction in MMD compared to nonspecific oral preventives (26). APOLLON trial confirmed long-term safety and tolerability of erenumab over 128 weeks (15).	Approved in U.S. and Europe
Fremanezumab (Ajovy or TEV-48125)	The HALO EM phase III clinical trial showed fremanezumab significantly reduced number of monthly migraine days in patients with episodic migraine by 3.7 days compared to placebo (08). The HALO CM phase III trial showed fremanezumab significantly reduced number of monthly headache days by 4.6 in patients with chronic migraine compared to placebo (31). The phase IV UNITE trial showed fremanezumab reduced MMD and depressive symptoms in patients with comorbid major depressive disorder.	Approved in U.S. and Europe
Galcanezumab (Emgality or LY2951742)	The EVOLVE-1 trial showed galcanezumab significantly reduced MMD compared to by 4.7 (120 mg) and 4.6 days (240 mg) in patients with episodic migraine (34). The REGAIN phase III trial showed galcanezumab was superior to placebo and reduced MMD in chronic migraine patients by 4.8 days (120 mg) and 4.6 days (240 mg) (07).	Approved in U.S. and Europe
Eptinezumab (Vyepti or ALD403)	The PROMISE-1 trial showed eptinezumab significantly reduced MMD compared with placebo by 3.9 (100 mg) and 4.3 days (300 mg) in patients with episodic migraine (01). The PROMISE-2 trial showed eptinezumab significantly reduced MMD compared with placebo by 7.7 (100 mg) and 8.2 days (300 mg) in patients with chronic migraine (22).	Approved in U.S. and Europe
MMD=monthly migraine days

The clinical efficacy and safety of CGRP-antagonist mAbs fremanezumab, erenumab, galcanezumab, and eptinezumab have been demonstrated in multiple randomized, placebo-controlled trials. They showed an increase in migraine-free days versus baseline. These mAbs appear to be well-tolerated, with no significant adverse events across the studies and no emerging safety issues from earlier studies (41; 13).

For fremanezumab, the HALO EM trial showed a reduction in monthly migraine days (MMD) by 3.7 days in episodic migraine (09), whereas the HALO CM 12-week phase III trial showed a reduction in monthly headache days by 4.6 in chronic migraine (31). The phase IV UNITE trial showed fremanezumab’s benefit in reducing both monthly migraine days and depressive symptoms in patients with comorbid major depressive disorder.

For erenumab, the STRIVE phase III trial showed significantly reduced migraine frequency, effects of migraines on daily activities, and the use of acute migraine-specific medication (14). The APPRAISE trial found patients were six times more likely to achieve greater than or equal to 50% monthly migraine days reduction compared to oral preventives (26), whereas the APOLLON trial showed long-term safety over 128 weeks (15).

A metaanalysis was conducted to identify placebo and nocebo phenomena in the placebo-controlled randomized trials with the monoclonal antibodies targeting the calcitonin gene-related peptide pathway (19). Results showed that the stronger placebo and weaker nocebo phenomena in trials with anti-CGRP mAbs versus those with topiramate in the prophylaxis of episodic migraine may decisively determine the success of treatment with anti-CGRP mAbs. No differences were detected between the anti-CGRP mAbs and onabotulinumtoxinA (BoNT-A) in the treatment of chronic migraine.

References

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Suraj Malhan DO MS

Dr. Malhan has no relevant financial relationships to disclose.
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Stephen D Silberstein MD

Dr. Silberstein, Director of the Jefferson Headache Center at Thomas Jefferson University has no relevant financial relationships to disclose.
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Editor

Stephen D Silberstein MD

Dr. Silberstein, Director of the Jefferson Headache Center at Thomas Jefferson University has no relevant financial relationships to disclose.
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K K Jain MD†

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Anti-CGRP monoclonal antibodies for prevention of migraine

Other Pertinent Drugs

gepants
olcegepant
rimegepant
telcagepant
ubrogepant

Anti-CGRP monoclonal antibodies for prevention of migraine …

Anti-CGRP monoclonal antibodies for prevention of migraine

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Pharmacology

Clinical trials

Table 1. Clinical Trials of Anti-CGRP Monoclonal Antibodies for Migraine Prevention

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Authors

Editor

Former Authors

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Drug-induced myasthenic syndromes

Suzetrigine

Upadacitinib

Fenfluramine

Tovorafenib

Givinostat

Vorasidenib

Zilucoplan

Eptinezumab	Single intravenous dose of 100 or 300 mg given every 3 months
Erenumab	70 or 140 mg subcutaneously once a month by an autoinjector
Fremanezumab	225 mg monthly or 675 mg subcutaneously every 3 months
Galcanezumab	240 mg loading dose, followed by 120 mg subcutaneously once monthly

Anti-CGRP monoclonal antibodies for prevention of migraine

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Pharmacology

Clinical trials

Table 1. Clinical Trials of Anti-CGRP Monoclonal Antibodies for Migraine Prevention

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Authors

Editor

Former Authors

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Drug-induced myasthenic syndromes

Suzetrigine

Upadacitinib

Fenfluramine

Tovorafenib

Givinostat

Vorasidenib

Zilucoplan

This is an article preview.
Start a Free Account
to access the full version.