Hair Loss and CGRP Migraine Drugs: What the Evidence Shows

The Question Patients Ask

Hair loss did not show up as a side effect in the pre-approval trials of erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), eptinezumab (Vyepti), or any of the gepants. It started showing up afterward, in adverse event reports, in headache clinic case series, and in patient forums. By now it is one of the most common safety questions people ask about these drugs, and it has been hard to answer because the evidence is scattered across pharmacovigilance databases and single-patient reports.

A review published in Frontiers in Neurology in September 2026 by a neurology and dermatology team at Vilnius University collected everything published through August 2026 on hair loss with CGRP-targeting therapy, summarized the pattern, laid out the biological reasons it might be real, and proposed a practical approach for clinicians. It is a narrative review built on low-level evidence, and the authors say so repeatedly. It is still the most complete summary of this question to date.

What the Review Covered

The authors searched PubMed through August 17, 2026 for any publication linking CGRP-targeting drugs to alopecia, hair loss, telogen effluvium, or alopecia areata. The search returned 31 records. After screening, 11 publications directly addressed hair loss with these drugs and formed the evidence base.

Most of the weight comes from analyses of the FDA Adverse Event Reporting System (FAERS), a database where anyone, including patients, can file a report. Several of the included analyses used overlapping FAERS data from overlapping years, so their report counts cannot be added together. Two prospective real-world registries, one French (144 patients on erenumab, Aimovig) and one Greek (204 patients on fremanezumab, Ajovy), recorded hair loss as an adverse event in 0.7% and 1.0% of patients respectively. Those are the only figures in the review with a real denominator, and they are small studies that were not designed to look for hair loss.

Because the evidence was almost entirely spontaneous reports and case descriptions, the authors did no formal quality assessment and synthesized it narratively.

What the Hair Loss Looks Like

Across the reports, the picture is fairly consistent.

Telogen effluvium is the kind of hair loss that follows a physical shock to the body: an illness, surgery, childbirth, a crash diet, a new medication. A larger than usual share of hair follicles shift into the resting phase at once, and two to three months later those hairs shed together. It is diffuse rather than patchy, it does not scar, and it reverses once the trigger is removed. That matches what most of the CGRP reports describe.

The female predominance in the reports, above 90% for every antibody in one FAERS analysis, is what you would expect given who takes these drugs. Migraine affects women roughly three times as often as men, and women make up the large majority of people on CGRP therapy. The review is explicit that this does not show women are more susceptible.

Which Drugs Are Involved

All of them, as far as the reporting goes. Hair loss has been reported with erenumab (Aimovig), galcanezumab (Emgality), fremanezumab (Ajovy), eptinezumab (Vyepti), atogepant (Qulipta), rimegepant (Nurtec ODT), and ubrogepant (Ubrelvy).

Raw report counts from the pharmacovigilance studies the review summarized. These reflect how long each drug has been on the market and how many people take it, not how risky it is.

Erenumab's (Aimovig's) lead in raw counts is almost certainly an artifact of time on market. It was approved first and has the most patient-years behind it. The review considered whether erenumab's distinct mechanism (it blocks the receptor rather than the CGRP molecule itself) could matter for hair, since the two approaches may differ in how completely and how long they shut down CGRP signaling in peripheral tissue. There is no direct evidence either way, and the authors warn against reading the reporting differences as evidence of a mechanistic difference in risk.

The gepant signal is worth watching. Rimegepant in particular showed a relatively higher proportion of alopecia among its reports in some analyses, but prescribing patterns, how often people take it, and how aware prescribers are of the issue all shape those numbers.

Why CGRP Blockade Might Affect Hair

CGRP is not only a migraine molecule. It is released by sensory nerves throughout the skin, where it has at least three jobs that matter for hair follicles. The review lays out three overlapping mechanisms. All of them are plausible and none has been shown to operate in a patient.

The authors point out that these pathways would be expected to interact, and that a functional disruption of follicle activity, rather than structural destruction, would explain why the hair loss is usually reversible.

Other Explanations

A new drug followed by hair loss is suggestive, not proof. The population taking CGRP therapy has several features that cause hair loss on their own.

• Disease burden and stress. Most people on these drugs have chronic migraine or frequent episodic migraine. Chronic physical and psychological stress is a classic trigger for telogen effluvium and can worsen alopecia areata.
• Sleep disruption. Common in migraine and independently associated with hair shedding.
• Other medications. Many patients have been on or are still on preventives that cause hair loss themselves, including some antidepressants, beta-blockers, and anticonvulsants such as valproate (Depakote) and topiramate (Topamax).
• Background rates. Telogen effluvium affects up to 30% of adults at some point. Alopecia areata has a lifetime risk near 2%. Some hair loss in a large treated population would occur with no drug involved.
• Reporting behavior. Once a side effect becomes known, it gets reported more. FAERS signals can grow because awareness grows, not because risk does.

None of these can be adjusted for in spontaneous report data. That is why the review's central claim is deliberately modest: the signal is consistent and biologically plausible, and causation and incidence remain unestablished.

What to Do If It Happens

The review proposes a stepwise approach, and it is the most practically useful part of the paper.

Supportive treatment follows the usual approach to non-scarring hair loss. Topical minoxidil is first line (5% twice daily for men, once daily for women, typically before bed). Low-dose oral minoxidil is an off-label alternative that has gained ground. Minoxidil causes an initial shedding in the first weeks as resting hairs are pushed out, visible improvement takes 3 to 6 months, and the full effect takes 6 to 12 months. It has to be continued to keep working. Oral minoxidil should be avoided in people with unstable angina, a recent heart attack, or heart failure, and minoxidil in any form is contraindicated in pregnancy and breastfeeding. Iron and vitamin D should be corrected if low.

Key Takeaways

The practical message for patients is that hair loss on a CGRP drug is a recognized, reportable, and usually reversible event, not a sign that something is permanently wrong, and not a reason to stop a working preventive without talking it through. The message for clinicians is to ask about it, document it, rule out the ordinary causes, and report it, because the one thing that would move this from signal to answer is a prospective study with a denominator.