FDA Approved Biologics for Migraine: A Reference Guide

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Introduction to FDA Approved Biologics for Migraine

Migraine is a complex neurological disorder affecting approximately 15% of the global population, characterized by recurrent moderate-to-severe headaches often accompanied by nausea, photophobia, and phonophobia. For decades, preventive therapy relied on repurposed medications—beta-blockers, anticonvulsants, antidepressants, and calcium channel blockers—none of which were developed specifically for migraine. The approval of four biologic agents targeting the calcitonin gene-related peptide (CGRP) pathway between 2018 and 2020 fundamentally changed the preventive treatment landscape.

What Are Migraine Biologics?

Biologics are therapeutic agents produced by living organisms through recombinant DNA technology, as opposed to chemically synthesized small molecules. The migraine biologics are all fully humanized or human monoclonal antibodies (mAbs) that interfere with CGRP signaling. These agents represent the first class of preventive medications designed specifically for migraine, offering target specificity that oral preventives lack. Unlike small-molecule CGRP receptor antagonists (gepants) that require daily oral dosing and have drug-drug interaction liabilities, the monoclonal antibodies have long half-lives, are administered monthly or quarterly, and are not metabolized by cytochrome P450 enzymes.

The four FDA approved biologics for migraine—erenumab, galcanezumab, fremanezumab, and eptinezumab—share a common therapeutic goal: reducing CGRP-mediated vasodilation and neurogenic inflammation implicated in migraine pathogenesis. Their development followed the Biologics License Application FDA pathway, requiring demonstration of safety, purity, and potency through extensive preclinical and clinical testing.

The CGRP Pathway as a Therapeutic Target

CGRP is a 37-amino acid neuropeptide belonging to the calcitonin family, which also includes calcitonin, amylin, and adrenomedullin. It exists in two isoforms: α-CGRP, encoded by the CALCA gene on chromosome 11, and β-CGRP, encoded by CALCB on the same chromosome. α-CGRP is the predominant isoform in the trigeminal ganglion and central nervous system.

During a migraine attack, trigeminal sensory neurons release CGRP from their peripheral and central terminals. Peripheral release causes vasodilation of intracranial and extracranial blood vessels, mast cell degranulation, and plasma protein extravasation—collectively termed neurogenic inflammation. Central release facilitates nociceptive transmission to second-order neurons in the trigeminal nucleus caudalis. Elevated CGRP levels have been measured in the jugular venous blood during spontaneous migraine attacks, and intravenous CGRP infusion reliably triggers migraine-like headaches in susceptible individuals.

The CGRP receptor is a heterodimer composed of the calcitonin receptor-like receptor (CALCRL) and receptor activity-modifying protein 1 (RAMP1). CALCRL requires RAMP1 for ligand binding specificity and cell surface expression. The receptor couples to Gαs, activating adenylyl cyclase and increasing intracellular cyclic AMP (cAMP) in target cells including vascular smooth muscle and neurons. This signaling cascade underlies CGRP's vasodilatory and pronociceptive effects.

The therapeutic rationale is straightforward: neutralize CGRP ligand or block the receptor to interrupt this signaling cascade. The four approved biologics accomplish this through two distinct mechanisms—three target the ligand itself, and one targets the receptor.

Mechanism of Action of Migraine Biologics

CGRP Ligand Inhibition

Galcanezumab, fremanezumab, and eptinezumab are high-affinity monoclonal antibodies that bind soluble CGRP and prevent its interaction with the CGRP receptor. By sequestering the ligand, these antibodies effectively reduce the free CGRP concentration available to activate CALCRL/RAMP1 complexes on vascular smooth muscle, trigeminal neurons, and other target cells.

Galcanezumab is a humanized IgG4 monoclonal antibody that binds both α- and β-CGRP isoforms with high affinity (dissociation constant [Kd] approximately 31 pM). The IgG4 backbone was selected to minimize effector function—antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity—thereby reducing the risk of CGRP-bound cell lysis. Fremanezumab is also a humanized IgG2 antibody with comparable affinity for both CGRP isoforms (Kd approximately 31 pM for α-CGRP). The IgG2 isotype similarly exhibits minimal effector function. Eptinezumab is a humanized IgG1 antibody with a Kd of approximately 21 pM for α-CGRP. Unlike the other two ligand-binding antibodies, eptinezumab retains the IgG1 backbone, which has greater effector function potential, though no clinically significant consequences of this isotype difference have been demonstrated.

The pharmacokinetic-pharmacodynamic relationship for ligand-binding antibodies is governed by target-mediated drug disposition. Because CGRP is present at low picomolar concentrations in plasma, the antibody:ligand molar ratio is overwhelmingly in favor of the antibody at therapeutic doses. This ensures sustained neutralization of CGRP throughout the dosing interval.

CGRP Receptor Antagonism

Erenumab is the sole FDA approved biologic targeting the CGRP receptor rather than the ligand. It is a fully human IgG2 monoclonal antibody that binds the extracellular domain of CALCRL with high specificity (Kd approximately 34 pM). Importantly, erenumab does not bind the closely related calcitonin receptor or amylin receptors, which share CALCRL as a subunit but pair with different RAMPs. This selectivity is clinically relevant because amylin receptors mediate metabolic effects, and off-target blockade could theoretically impair glucose homeostasis.

By occupying the ligand-binding site on CALCRL, erenumab prevents CGRP from initiating intracellular signaling. Receptor antagonism offers a theoretical advantage over ligand neutralization: it blocks signaling regardless of local CGRP concentration, including situations where CGRP levels may transiently exceed antibody binding capacity. However, both approaches have demonstrated comparable clinical efficacy in pivotal trials.

Overview of FDA Approved Agents

Erenumab (Aimovig)

Erenumab was the first FDA approved biologic for migraine prevention. It is administered subcutaneously at doses of 70 mg or 140 mg once monthly. The 140 mg dose provides approximately 2-fold higher steady-state trough concentrations and has shown modestly greater efficacy in some analyses, though the 70 mg dose remains the standard starting dose. Erenumab is approved for both episodic migraine (fewer than 15 headache days per month) and chronic migraine (15 or more headache days per month).

Galcanezumab (Emgality)

Galcanezumab is approved for episodic and chronic migraine prevention at a fixed dose of 240 mg loading dose followed by 120 mg monthly. The loading dose achieves steady-state concentrations more rapidly, which is clinically relevant given the expectation of benefit within the first month of treatment. Galcanezumab is also approved for cluster headache prevention, a distinct indication not shared by other CGRP biologics.

Fremanezumab (Ajovy)

Fremanezumab offers flexible dosing: 225 mg monthly or 675 mg quarterly (every 3 months). The quarterly regimen provides a higher single dose (675 mg) that maintains therapeutic concentrations throughout the 3-month interval. This flexibility is valuable for patients who prefer fewer injections or who travel frequently. Fremanezumab is approved for both episodic and chronic migraine.

Eptinezumab (Vyepti)

Eptinezumab is the only intravenously administered CGRP biologic. It is given as a 100 mg or 300 mg infusion over approximately 30 minutes every 12 weeks. The intravenous route achieves peak concentrations within hours, enabling rapid onset of effect—clinical trials demonstrated efficacy as early as day 1 post-infusion. This distinguishes eptinezumab from the subcutaneous agents, which require several days to reach therapeutic concentrations.

Clinical Efficacy Evidence

Phase 3 Trial Outcomes

The pivotal trials for each biologic enrolled patients with episodic or chronic migraine who had inadequate response to 2 to 4 prior preventive medications. The primary efficacy endpoint across all programs was the change from baseline in mean monthly migraine days (MMD) during the treatment period compared with placebo.

For erenumab, the Phase 3 STRIVE trial in episodic migraine demonstrated a mean reduction of 3.2 MMD from a baseline of 8.3 days with the 70 mg dose, compared with 1.8 days with placebo at month 3. The 140 mg dose produced a 3.7-day reduction. In the chronic migraine population (CM trial), erenumab 70 mg and 140 mg reduced MMD by 6.6 and 6.6 days, respectively, from a baseline of approximately 18 days, versus 4.2 days with placebo.

Galcanezumab's EVOLVE-1 and EVOLVE-2 trials in episodic migraine showed mean reductions of 4.7 and 4.3 MMD, respectively, with the 120 mg dose, compared with 2.8 and 2.3 days with placebo. The REGAIN trial in chronic migraine demonstrated a 4.8-day reduction with galcanezumab versus 2.7 days with placebo.

Fremanezumab's HALO trials evaluated both monthly and quarterly dosing. In episodic migraine, monthly dosing reduced MMD by 3.7 days versus 2.2 days with placebo; quarterly dosing reduced MMD by 3.4 days. In chronic migraine, monthly dosing produced a 4.6-day reduction and quarterly dosing a 4.3-day reduction, versus 2.5 days with placebo.

Eptinezumab's PROMISE-1 (episodic) and PROMISE-2 (chronic) trials demonstrated reductions of 4.0 and 4.3 MMD with the 100 mg dose, and 3.9 and 4.3 MMD with the 300 mg dose, respectively. Notably, PROMISE-2 showed that 28% of chronic migraine patients achieved at least a 75% reduction in MMD at week 12, compared with 15% on placebo.

A consistent finding across trials is the 50% responder rate—the proportion of patients achieving at least a 50% reduction in MMD. This metric ranged from 39% to 50% for active treatment versus 16% to 24% for placebo, representing a clinically meaningful number needed to treat of approximately 4 to 5.

Head-to-Head Comparisons

No adequately powered head-to-head trials directly comparing the four CGRP biologics have been published. Indirect comparisons from meta-analyses suggest broadly similar efficacy, with erenumab 140 mg and eptinezumab 300 mg showing marginally larger mean reductions in MMD. However, these differences are small relative to inter-individual variability and are unlikely to guide drug selection in clinical practice.

The choice among agents is therefore driven primarily by administration preferences, dosing frequency, and payer considerations rather than efficacy differences. Patients who prefer quarterly dosing may choose fremanezumab or eptinezumab; those who prefer at-home self-administration may select erenumab, galcanezumab, or fremanezumab; and those who desire rapid onset may benefit from eptinezumab's intravenous route.

Safety and Tolerability Profile

Common Adverse Events

The CGRP biologics are generally well tolerated, with adverse event profiles comparable to placebo in clinical trials. The most commonly reported adverse events are injection-site reactions, occurring in approximately 4% to 10% of patients receiving subcutaneous agents. These reactions—erythema, pruritus, swelling, or pain at the injection site—are typically mild and self-limiting, rarely leading to treatment discontinuation.

Eptinezumab's intravenous administration is associated with infusion-related reactions in approximately 9% of patients, including headache, fatigue, and nausea. These reactions are generally mild and manageable with premedication or slowing the infusion rate. Anaphylaxis has been reported rarely with eptinezumab, and the prescribing information includes a warning to monitor patients during and after infusion.

Constipation is a notable adverse event for erenumab, occurring in approximately 3% of patients in clinical trials. This reflects CGRP's role in gastrointestinal motility—CGRP receptor blockade can slow colonic transit. Serious cases of constipation, including cases requiring hospitalization, have been reported in postmarketing surveillance. Patients with pre-existing gastrointestinal motility disorders should be monitored closely.

Hypertension has been reported with erenumab, particularly in patients with pre-existing hypertension. The mechanism is thought to involve reduced CGRP-mediated vasodilation, though the effect is modest and typically manageable. Blood pressure monitoring is recommended during the first months of treatment.

Immunogenicity and Anti-Drug Antibodies

All therapeutic monoclonal antibodies carry immunogenic potential. The incidence of anti-drug antibodies (ADAs) varies among the four agents:

• Erenumab: approximately 6% of patients develop ADAs; neutralizing antibodies are detected in approximately 1%.
• Galcanezumab: approximately 12% develop ADAs; neutralizing antibodies in approximately 1%.
• Fremanezumab: approximately 3% develop ADAs; neutralizing antibodies in less than 1%.
• Eptinezumab: approximately 18% develop ADAs; neutralizing antibodies in approximately 2%.

The clinical significance of ADAs is generally low. No consistent association between ADA status and reduced efficacy or increased adverse events has been demonstrated for any of the agents. However, the presence of neutralizing antibodies could theoretically reduce drug exposure and efficacy over time. The higher immunogenicity rates for eptinezumab and galcanezumab may reflect assay sensitivity differences rather than true biological differences, and no clinical consequences have been established.

Long-term safety data from open-label extension studies extending to 3 to 5 years have not revealed new safety signals. Cardiovascular events, a theoretical concern given CGRP's role in vasodilation, have not been observed at increased rates compared with placebo or expected population rates. This is reassuring but warrants continued pharmacovigilance, particularly in patients with cardiovascular risk factors.

Pharmacokinetics and Dosing Considerations

Subcutaneous vs. Intravenous Administration

The pharmacokinetic profiles of the subcutaneous agents are characterized by slow absorption from the injection site, with peak concentrations (Cmax) achieved at 5 to 7 days post-dose. Bioavailability ranges from 60% to 80% for subcutaneous administration. The intravenous route used for eptinezumab achieves Cmax immediately at the end of the 30-minute infusion, with 100% bioavailability.

All four agents have long elimination half-lives consistent with IgG monoclonal antibodies:

• Erenumab: 28 days
• Galcanezumab: 27 days
• Fremanezumab: 30 days
• Eptinezumab: 27 days

These half-lives are governed by FcRn-mediated recycling, which protects IgG antibodies from lysosomal degradation and extends their circulating half-life. The target-mediated clearance component—binding to CGRP or the CGRP receptor—contributes minimally to overall clearance at therapeutic doses.

Dosing Regimens

The dosing regimens are designed to maintain trough concentrations above the minimum effective concentration throughout the dosing interval:

For galcanezumab, the 240 mg loading dose is administered as two 120 mg injections on the same day. This achieves steady-state concentrations approximately 2 weeks earlier than without a loading dose. The quarterly fremanezumab regimen (675 mg) is administered as three 225 mg injections on the same day. Eptinezumab 300 mg is administered as two consecutive 30-minute infusions of 150 mg each.

No dose adjustment is required for renal or hepatic impairment, as monoclonal antibodies are not cleared by renal or hepatic pathways. The agents have not been studied in pregnant women; animal studies have not shown teratogenic effects, but the agents should be used during pregnancy only if clearly needed. The long half-lives mean that drug exposure persists for approximately 5 months after the last dose, which should be considered when planning pregnancy.

Patient Selection and Clinical Use

Indications and Contraindications

All four biologics are indicated for the preventive treatment of migraine in adults. Erenumab, galcanezumab, and fremanezumab are approved for both episodic and chronic migraine. Eptinezumab is approved for both, with the 100 mg dose indicated for episodic migraine and the 300 mg dose for chronic migraine. Galcanezumab additionally carries an indication for episodic cluster headache.

The typical candidate has failed at least one oral preventive medication due to inadequate efficacy or intolerable side effects. Clinical guidelines generally recommend trying 2 to 3 oral preventives before initiating a biologic, though patients with severe, disabling migraine may be considered earlier. Biologics are appropriate for patients with:

• Four or more migraine days per month
• Significant disability despite acute treatment optimization
• Contraindications or intolerance to oral preventives
• Medication overuse headache, provided acute medication overuse is addressed

Contraindications are limited to a history of hypersensitivity to the agent or any of its excipients. Erenumab should be used with caution in patients with a history of constipation or gastrointestinal motility disorders. Eptinezumab should be used with caution in patients with a history of hypersensitivity reactions to other monoclonal antibodies.

Switching Between Biologics

Data guiding switching between CGRP biologics are limited, but clinical experience suggests that patients who fail one biologic may respond to another. The rationale for switching is based on the different targets (ligand versus receptor) and the possibility that individual patients may respond better to one mechanism.

A practical approach is to evaluate response after 3 months of treatment—the time point at which pivotal trials demonstrated maximal benefit. Non-responders, defined as those with less than 30% reduction in MMD, may be considered for a switch. A washout period is not strictly required, as the long half-lives mean that the previous agent will be largely cleared over 3 to 4 months. However, overlapping exposure may occur if the new agent is started immediately, and the clinical significance of this is unknown.

Switching from a subcutaneous agent to eptinezumab may be advantageous for patients who cannot tolerate self-injection or who require rapid onset of effect. Conversely, switching from eptinezumab to a subcutaneous agent may be appropriate for patients who prefer at-home administration or who experience infusion-related reactions.

Regulatory and Reimbursement Landscape

FDA Approval Timeline

The four biologics were approved through the standard FDA Approval Process for Biologics, which requires demonstration of substantial evidence of efficacy from adequate and well-controlled trials, plus evidence of safety. All four received priority review designation, reflecting the unmet medical need in migraine prevention.

The approval of erenumab in May 2018 marked the first new class of migraine preventive medications in over two decades. The subsequent approvals of galcanezumab and fremanezumab within months of each other created a competitive market that has influenced pricing and access. The FDA Approved Biologics by Year resource provides context on the broader landscape of biologic approvals during this period.

Post-approval, the manufacturers have obligations under the FDA Post Approval Changes Guidance Biologics to report manufacturing changes and conduct postmarketing studies. These include long-term safety registries and pregnancy exposure registries to monitor for rare adverse events.

Reimbursement and Prior Authorization

Despite FDA approval, access to CGRP biologics is often limited by payer policies. Most commercial insurers require prior authorization, which typically mandates documentation of:

1. A diagnosis of episodic or chronic migraine confirmed by a neurologist
2. Failure of at least 2 oral preventive medications from different classes
3. No contraindications to the requested agent
4. Documentation of migraine frequency and disability (e.g., MIDAS or HIT-6 scores)

Step therapy requirements may mandate trials of specific oral preventives before biologic approval. Some payers prefer one biologic over others based on negotiated rebates, creating formulary tiers that influence prescribing. Patients who fail one biologic may face additional authorization hurdles for a second agent.

Medicare Part D covers CGRP biologics for patients with migraine, though cost-sharing can be substantial. Manufacturer copay assistance programs can reduce out-of-pocket costs for commercially insured patients, but these programs are not available to Medicare beneficiaries. The Biologics Regulatory Affairs Course provides additional context on the regulatory and access landscape for biologic therapies.

Common Pitfalls and Practical Considerations

Misunderstanding Mechanism

A common error is assuming that CGRP biologics are acute treatments—medications to be taken at the onset of a migraine attack. These agents are exclusively preventive; they reduce the frequency, severity, and duration of migraine attacks over time but do not abort an ongoing attack. Patients must be counseled to continue using their acute medications (triptans, NSAIDs, gepants) for breakthrough attacks.

Another misconception is that all CGRP biologics are interchangeable. While they share a common pathway, their targets differ (ligand versus receptor), and individual patients may respond differently. A patient who fails one agent may respond to another, and switching is a reasonable clinical strategy.

Overlooking Drug Interactions

Because monoclonal antibodies are not metabolized by cytochrome P450 enzymes and are not substrates for drug transporters, clinically significant pharmacokinetic drug-drug interactions are unlikely. However, pharmacodynamic interactions are possible. Combining a CGRP biologic with a small-molecule CGRP receptor antagonist (gepant) such as ubrogepant or rimegepant for acute treatment is theoretically redundant but not contraindicated. The clinical significance of combined CGRP pathway blockade is unknown, and patients should be monitored for additive effects such as constipation or hypotension.

Concomitant use of CGRP biologics with other preventive medications is common and generally well tolerated. Beta-blockers, anticonvulsants, and antidepressants do not interact pharmacokinetically with monoclonal antibodies. However, the additive efficacy of combining a biologic with an oral preventive has not been rigorously studied, and polypharmacy should be justified by inadequate response to monotherapy.

Expecting Immediate Relief

The onset of preventive efficacy is gradual. Clinical trials measured outcomes at 4 to 12 weeks, with maximal benefit typically observed by month 3. Patients who do not experience improvement after the first dose should be counseled that 2 to 3 months of treatment may be required to assess response. Premature discontinuation—before 3 months—is a common reason for perceived treatment failure.

Conversely, some patients experience benefit within the first week, particularly with eptinezumab given its intravenous route and rapid attainment of therapeutic concentrations. This early response is a positive prognostic indicator but should not be used to justify early discontinuation of other preventive measures.

Ignoring Injection Technique

Subcutaneous administration requires proper technique to minimize injection-site reactions and ensure consistent drug delivery. Patients should be instructed to:

1. Remove the prefilled syringe or autoinjector from refrigeration 30 minutes before injection to reduce injection-site discomfort
2. Rotate injection sites (abdomen, thigh, upper arm) to avoid lipohypertrophy
3. Pinch a fold of skin and inject at a 45- to 90-degree angle depending on the device
4. Avoid injecting into areas of skin that are tender, bruised, or scarred

Failing to Address Medication Overuse

Medication overuse headache (MOH) is a common comorbidity in patients with frequent migraine. Patients using acute medications (triptans, opioids, combination analgesics) on 10 or more days per month may have refractory headache that responds poorly to preventive therapy. Before initiating a CGRP biologic, patients should be counseled to limit acute medication use. Biologics can be effective in patients with MOH, but outcomes are improved when acute medication overuse is addressed concurrently.

Neglecting Cardiovascular Monitoring

While clinical trials did not demonstrate increased cardiovascular events with CGRP biologics, the theoretical risk of reduced CGRP-mediated vasodilation warrants caution in patients with cardiovascular disease. Patients with a history of myocardial infarction, stroke, or peripheral vascular disease should be monitored for new or worsening cardiovascular symptoms. Erenumab, in particular, has been associated with hypertension in postmarketing reports, and blood pressure should be checked at baseline and periodically during treatment.

Frequently Asked Questions

What are FDA approved biologics for migraine?

FDA approved biologics for migraine are monoclonal antibodies that target the calcitonin gene-related peptide (CGRP) pathway. Four agents are approved: erenumab (Aimovig), galcanezumab (Emgality), fremanezumab (Ajovy), and eptinezumab (Vyepti). They are used for the preventive treatment of episodic and chronic migraine in adults.

How do migraine biologics work?

Migraine biologics interfere with CGRP signaling, which is elevated during migraine attacks and contributes to vasodilation and neurogenic inflammation. Erenumab blocks the CGRP receptor (CALCRL), while galcanezumab, fremanezumab, and eptinezumab bind and neutralize the CGRP ligand itself. By interrupting this pathway, they reduce the frequency and severity of migraine attacks.

Which biologics are FDA approved for migraine?

The four FDA approved biologics for migraine are erenumab (Aimovig, May 2018), galcanezumab (Emgality, September 2018), fremanezumab (Ajovy, September 2018), and eptinezumab (Vyepti, February 2020). All are approved for episodic and chronic migraine; galcanezumab is also approved for episodic cluster headache.

Are migraine biologics effective for chronic migraine?

Yes. All four biologics have demonstrated efficacy in chronic migraine (15 or more headache days per month) in pivotal Phase 3 trials. Mean reductions in monthly migraine days range from approximately 4.3 to 6.6 days, compared with 2.5 to 4.2 days with placebo. Approximately 25% to 35% of chronic migraine patients achieve at least a 50% reduction in migraine days.

What are the common side effects of migraine biologics?

The most common side effects are injection-site reactions (pain, erythema, swelling) for the subcutaneous agents and infusion-related reactions (headache, fatigue, nausea) for eptinezumab. Erenumab is associated with constipation and hypertension in some patients. Overall, the agents are well tolerated, with adverse event rates similar to placebo in clinical trials.

How often are migraine biologics administered?

Erenumab, galcanezumab, and fremanezumab are administered subcutaneously once monthly. Fremanezumab also offers a quarterly (every 3 months) regimen of 675 mg. Eptinezumab is administered intravenously every 12 weeks. Galcanezumab requires a 240 mg loading dose at initiation.

Can migraine biologics be used with other preventive medications?

Yes. CGRP biologics can be combined with oral preventive medications such as beta-blockers, anticonvulsants, and antidepressants. No pharmacokinetic drug-drug interactions are expected because monoclonal antibodies are not metabolized by cytochrome P450 enzymes. However, the additive efficacy of combination therapy has not been rigorously studied, and patients should be monitored for additive adverse effects.

Key Takeaways

• Four FDA approved biologics—erenumab, galcanezumab, fremanezumab, and eptinezumab—target the CGRP pathway for migraine prevention, representing the first class of preventive medications developed specifically for migraine.
• Three agents neutralize CGRP ligand (galcanezumab, fremanezumab, eptinezumab), while one blocks the CGRP receptor (erenumab); all demonstrate comparable efficacy in pivotal trials.
• Clinical trials show mean reductions of 3 to 6 monthly migraine days versus placebo, with 50% responder rates of approximately 40% to 50% across agents.
• The biologics are well tolerated, with injection-site reactions, constipation (erenumab), and infusion-related reactions (eptinezumab) being the most notable adverse events; immunogenicity is low and rarely clinically significant.
• Dosing varies from monthly subcutaneous injections to quarterly intravenous infusions, allowing treatment to be tailored to patient preference and clinical need.
• Patients are typically candidates after failing 2 to 3 oral preventives; response should be assessed after 3 months of treatment before considering a switch.
• Reimbursement requires prior authorization in most settings, with documentation of migraine frequency, disability, and failure of oral preventives.

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