Calcitonin gene-related peptide (CGRP) is a 37-amino-acid neuropeptide produced by alternative splicing of the calcitonin gene transcript and is the most potent endogenous vasodilator of cranial vessels yet characterized. Its discovery as a trigeminal sensory neuropeptide and its demonstration of elevated levels during acute migraine attacks were the foundational observations that established CGRP as the primary pharmacological target for migraine therapy, a translation from bench to clinic that produced the first drug class designed specifically for migraine pathophysiology rather than adapted from cardiovascular or neurological indications.1
Two isoforms of CGRP are encoded by distinct genes: alpha-CGRP (CALCA gene, chromosome 11), which predominates in the peripheral and central nervous system including the trigeminal ganglion, and beta-CGRP (CALCB gene), which is expressed primarily in the enteric nervous system. In migraine pharmacology, alpha-CGRP is the relevant isoform. The mature 37-amino-acid peptide is characterized by an N-terminal disulfide bridge between cysteines at positions 2 and 7, which forms a ring structure essential for receptor binding, and a C-terminal amide group required for full biological activity. Both the gepant small-molecule antagonists and the monoclonal antibodies exploit the structural features of CGRP and its receptor to achieve therapeutic blockade.1
CGRP is synthesized in the small- to medium-diameter pseudounipolar neurons of the trigeminal ganglion (TGG), which are unmyelinated or thinly myelinated C- and A-delta fibers. These neurons send peripheral projections to the meningeal dura mater, large cerebral arteries, and extracranial vessels, and central projections to the trigeminal nucleus caudalis (TNC) in the brainstem. CGRP is stored in dense-core vesicles and released from both peripheral and central trigeminal terminals upon depolarization. The seminal clinical demonstration of its role in migraine came from Goadsby, Edvinsson, and Ekman, who showed elevated CGRP in the external jugular venous blood ipsilateral to the headache side during spontaneous migraine attacks, with normalization following successful sumatriptan treatment.2 This observation established the trigeminovascular hypothesis of migraine and provided the rationale for anti-CGRP pharmacotherapy.
The triggers of CGRP release from trigeminal afferents are multiple and partially understood. Cortical spreading depression (CSD), the neurophysiological correlate of the migraine aura, propagates across the cortex at 3 to 5 mm per minute and activates trigeminal pain fibers at the meningeal level, driving CGRP release peripherally and centrally. Additional stimuli include inflammatory mediators such as bradykinin, prostaglandins, and histamine acting on transient receptor potential (TRP) ion channels on trigeminal terminals, particularly TRPV1 and TRPA1, which are co-expressed with CGRP in nociceptive neurons. The resulting peripheral sensitization of meningeal nociceptors, mediated in part by CGRP itself through its potent vasodilatory and plasma extravasation-promoting effects, is thought to contribute to the throbbing, pulsatile quality of migraine pain and the allodynia that characterizes the sensitized migraine state.3
The CGRP receptor is pharmacologically unusual in that it is not encoded by a single gene but is instead a heterodimeric complex assembled from two distinct proteins: calcitonin receptor-like receptor (CLR), a seven-transmembrane Gs-coupled receptor that cannot reach the plasma membrane alone, and receptor activity-modifying protein 1 (RAMP1), a single-transmembrane chaperone protein that escorts CLR to the cell surface and determines its ligand specificity. The CLR/RAMP1 complex constitutes the canonical CGRP receptor; CLR paired with RAMP2 or RAMP3 instead forms the adrenomedullin receptor, demonstrating how RAMP identity controls receptor pharmacology.4
Upon CGRP binding to the CLR/RAMP1 heterodimer, the receptor activates Gs, stimulating adenylyl cyclase to generate cyclic AMP. PKA (protein kinase A) activated by cAMP phosphorylates multiple downstream targets in vascular smooth muscle cells, including myosin light chain kinase and ATP-sensitive potassium (KATP) channels, leading to smooth muscle relaxation and vasodilation. In cranial vessels, where CGRP receptor density is high, this pathway mediates the sustained vasodilation that accompanies trigeminal activation during migraine. CGRP also signals in trigeminal ganglion neurons and central neurons, where it modulates nociceptive transmission through mechanisms that include sensitization of TRPV1 channels and potentiation of glutamate signaling at the TNC; these non-vascular central mechanisms are now considered as important as the peripheral vasodilatory effects in the overall pharmacology of CGRP in migraine.4
The RAMP1 component of the receptor is particularly important for understanding therapeutic targeting. Erenumab, the monoclonal antibody targeting the CGRP receptor rather than the CGRP peptide itself, binds to an extracellular domain formed by the CLR/RAMP1 interface rather than to CLR or RAMP1 alone, meaning its epitope is unique to the assembled heterodimer. This binding site overlaps with the CGRP peptide binding domain, explaining its competitive antagonism. The gepant small molecules occupy the same receptor binding pocket and achieve functional antagonism without activating the receptor, acting as pure competitive antagonists with rapid reversibility. The distinction between receptor-targeted (erenumab, gepants) and ligand-targeted (fremanezumab, galcanezumab, eptinezumab) strategies has practical implications for patients who fail one class, since the mechanisms of escape from each differ.45
CGRP receptors are expressed on multiple cell types relevant to migraine: vascular smooth muscle cells of the dura mater and cerebral arteries (peripheral vasodilatory targets), trigeminal ganglion satellite glial cells, neurons of the trigeminal nucleus caudalis (central sensitization targets), and cells of the sphenopalatine ganglion. The blood-brain barrier is largely impermeable to both the monoclonal antibodies (too large, ~150 kDa) and the older gepants, meaning their primary sites of action are peripheral: the meningeal vasculature, trigeminal ganglion (which lies outside the blood-brain barrier), and perivascular nerve terminals. Newer, more lipophilic gepants such as rimegepant and ubrogepant may penetrate to central sites to some extent, though this remains under active investigation. The clinical implication is that peripheral CGRP blockade is sufficient for therapeutic efficacy, and the concern that central CGRP signaling might serve protective functions that would be disrupted by systemic blockade has not been borne out in clinical trial safety data to date.5
| Receptor Component | Gene | Role | Signaling | Therapeutic Relevance |
|---|---|---|---|---|
| CLR (calcitonin receptor-like receptor) | CALCRL | Seven-transmembrane Gs-coupled receptor; cannot reach plasma membrane without RAMP | Gs → cAMP → PKA → vasodilation; KATP channel opening | Binding site for gepants; shared epitope with erenumab at CLR/RAMP1 interface |
| RAMP1 (receptor activity-modifying protein 1) | RAMP1 | Single-transmembrane chaperone; escorts CLR to membrane; determines CGRP vs. adrenomedullin specificity | Structural modifier; no independent signaling | RAMP1 identity (not RAMP2/3) confers CGRP selectivity; erenumab epitope spans CLR/RAMP1 interface |
The gepants are a class of small-molecule, competitive, reversible antagonists at the CLR/RAMP1 CGRP receptor. Their defining pharmacological characteristic, relative to the triptans they are increasingly positioned alongside, is the complete absence of vasoconstrictive activity: gepants block CGRP-mediated vasodilation without agonizing 5-HT1B receptors on coronary or cerebral vessels. This profile makes them usable in patients with cardiovascular disease or vascular risk factors who are contraindicated from triptans, and extends the pharmacological toolkit for migraine to a previously underserved population.6
The first-generation gepant candidate, telcagepant, demonstrated clinical proof of concept for CGRP receptor antagonism in acute migraine but was discontinued due to hepatotoxicity signals at the doses required for preventive use. The current approved gepants have addressed this liability through structural optimization: ubrogepant (Ubrelvy), rimegepant (Nurtec ODT), atogepant (Qulipta), and zavegepant (Zavzpret, intranasal) are all approved in the United States, with rimegepant and atogepant carrying both acute and preventive indications. The hepatotoxicity observed with telcagepant was attributed to high plasma exposures from the dosing required for prevention and has not been reproduced with the current agents at approved doses, though liver function monitoring is recommended for patients taking gepants with concomitant hepatotoxic drugs.6
Ubrogepant (Ubrelvy) is approved for acute treatment of migraine with or without aura in adults, dosed at 50 or 100 mg orally, with a second dose permitted at 2 hours if needed (maximum 200 mg per day). Its oral bioavailability is approximately 7 percent due to extensive first-pass metabolism by CYP3A4; consequently, strong CYP3A4 inhibitors (such as clarithromycin or ketoconazole) dramatically increase ubrogepant exposure and are contraindicated, while strong CYP3A4 inducers (such as rifampin) reduce efficacy. Clinical trials demonstrated statistically significant freedom from pain at 2 hours versus placebo and non-inferiority to sumatriptan on key endpoints, with the important distinction of no vasoconstrictor liability and efficacy in patients who had previously used triptans.6
Rimegepant (Nurtec ODT) is uniquely approved for both acute migraine treatment (75 mg orally disintegrating tablet, single dose) and preventive treatment (75 mg every other day). Its dual indication is supported by the observation that regular use reduces monthly migraine days in a manner consistent with ongoing receptor blockade reducing central sensitization. Like ubrogepant, rimegepant is a CYP3A4 substrate; co-administration with strong CYP3A4 inhibitors approximately doubles exposure and is not recommended. The orally disintegrating formulation offers practical advantages in patients who experience nausea or vomiting with migraine attacks, as it absorbs through the oral mucosa without requiring water.7
Atogepant (Qulipta) is approved exclusively for migraine prevention, dosed at 10, 30, or 60 mg once daily depending on concomitant medications. Its oral bioavailability is approximately 44 percent, substantially higher than ubrogepant, reflecting reduced first-pass extraction. Atogepant undergoes CYP3A4 metabolism, and dose adjustments are required with strong CYP3A4 inhibitors (reduce to 10 mg daily) or inducers (avoid combination or use 60 mg daily). Pivotal phase 3 trials (ADVANCE and PROGRESS) demonstrated statistically significant reductions in mean monthly migraine days versus placebo across episodic and chronic migraine populations, establishing atogepant as a purely preventive oral CGRP antagonist with a once-daily dosing schedule that contrasts with the every-other-day preventive regimen of rimegepant.8
Zavegepant (Zavzpret) is the first intranasal gepant, approved for acute migraine treatment at a single 10 mg intranasal dose. The intranasal route bypasses gastrointestinal absorption and hepatic first-pass metabolism, achieving peak plasma concentrations within approximately 30 minutes, which is faster than oral gepants and comparable to subcutaneous triptans in onset profile. This makes zavegepant particularly useful for patients whose migraines begin with rapid escalation or who experience significant early nausea limiting oral medication utility. Its metabolism involves CYP3A4 to a lesser degree than the oral gepants, and it is not yet recommended for patients with severe hepatic impairment due to limited data in this population.
| Agent | Route | Indication | Dose | Bioavailability | Key CYP | Distinguishing Feature |
|---|---|---|---|---|---|---|
| Ubrogepant (Ubrelvy) | Oral | Acute only | 50 or 100 mg; repeat at 2 h PRN; max 200 mg/day | ~7% | CYP3A4 substrate; strong inhibitors CI | First oral gepant approved; widely studied alongside triptans |
| Rimegepant (Nurtec ODT) | Oral (ODT) | Acute + Preventive | Acute: 75 mg single dose; Preventive: 75 mg every other day | ~64% | CYP3A4 and P-gp substrate | Only gepant with dual acute/preventive approval; ODT useful with nausea |
| Atogepant (Qulipta) | Oral | Preventive only | 10, 30, or 60 mg once daily | ~44% | CYP3A4 substrate; dose adjust with inhibitors/inducers | Only once-daily oral preventive gepant; approved for both episodic and chronic migraine |
| Zavegepant (Zavzpret) | Intranasal | Acute only | 10 mg single intranasal dose | Bypasses first-pass; rapid onset ~30 min | Minimal CYP3A4 | First intranasal gepant; fastest onset; useful with early nausea |
Four monoclonal antibodies targeting the CGRP pathway are approved for migraine prevention, representing the first biologics specifically designed for this indication. They divide mechanistically into receptor-targeted (erenumab) and ligand-targeted (fremanezumab, galcanezumab, eptinezumab) agents. All are administered parenterally, have half-lives of weeks to over a month allowing monthly or quarterly dosing, and have demonstrated statistically significant reductions in monthly migraine days in phase 3 trials across episodic and chronic migraine populations. Their long half-lives and predictable pharmacokinetics represent a major practical advantage over daily oral preventive medications that require patient adherence to complex dosing schedules.9
Erenumab (Aimovig) is the only monoclonal antibody targeting the CGRP receptor (CLR/RAMP1 heterodimer) rather than the CGRP peptide. It is a fully human IgG2 antibody administered as a 70 or 140 mg subcutaneous injection once monthly. The IgG2 subclass has reduced Fc receptor engagement compared to IgG1, minimizing complement activation and antibody-dependent cellular cytotoxicity, which is pharmacologically appropriate for a long-term monthly preventive. Its target engagement is confined to peripheral CLR/RAMP1 complexes because, at approximately 150 kDa, it does not cross the blood-brain barrier under normal conditions. Phase 3 trials (ARISE and STRIVE for episodic migraine; LIBERTY for difficult-to-treat episodic migraine) demonstrated 3.2 to 6.6 mean monthly migraine day reductions versus placebo.9
Fremanezumab (Ajovy) targets the CGRP peptide itself (anti-ligand strategy), binding to both alpha- and beta-CGRP with high affinity. It is a humanized IgG2a antibody administered subcutaneously as either 225 mg monthly or 675 mg quarterly, the latter option offering reduced injection frequency for adherence-challenged patients. The monthly versus quarterly schedule produces equivalent annualized prevention, and the choice between them is clinically driven by patient preference. Phase 3 trials (HALO-EM for episodic migraine; HALO-CM for chronic migraine) demonstrated 3.4 to 4.6 monthly migraine day reductions versus placebo in the monthly dosing arm.10
Galcanezumab (Emgality) also targets the CGRP ligand and is a humanized IgG4 antibody. It is administered as a 240 mg loading dose (two 120 mg injections) followed by 120 mg subcutaneously monthly. The IgG4 subclass undergoes Fab-arm exchange in vivo, producing bispecific antibodies with reduced effector function, which is clinically acceptable for a purely blocking antibody. A distinct indication for galcanezumab is episodic cluster headache prevention, where it is dosed at 300 mg subcutaneously monthly during the cluster period. Phase 3 trials in migraine (EVOLVE-1 and EVOLVE-2 for episodic; REGAIN for chronic) demonstrated monthly migraine day reductions of 4.3 to 6.3 days versus placebo. The availability of a cluster headache indication distinguishes galcanezumab from the other anti-CGRP antibodies in terms of licensed use.10
Eptinezumab (Vyepti) is the only anti-CGRP antibody administered intravenously, given as a 100 or 300 mg quarterly IV (intravenous) infusion over 30 minutes. The IV route achieves immediate maximal plasma concentrations at the time of infusion, which has been proposed as an advantage for patients experiencing a migraine attack at the time of their quarterly preventive dose, since the antibody can be expected to produce rapid peripheral CGRP blockade from the moment of infusion. Like fremanezumab and galcanezumab, it targets the CGRP ligand. Pivotal trials (PROMISE-1 for episodic; PROMISE-2 for chronic migraine) demonstrated statistically significant monthly migraine day reductions beginning as early as day 1 post-infusion, consistent with the immediate peak pharmacokinetics of IV administration. The quarterly IV schedule may favor patients who have difficulty with or prefer to avoid self-injection.10
| Agent | Target | IgG Subclass | Route & Frequency | Approved Indications | Key Trials |
|---|---|---|---|---|---|
| Erenumab (Aimovig) | CGRP receptor (CLR/RAMP1) | IgG2 (fully human) | 70 or 140 mg SC monthly | Episodic + chronic migraine prevention | ARISE, STRIVE, LIBERTY |
| Fremanezumab (Ajovy) | CGRP ligand (α and β) | IgG2a (humanized) | 225 mg SC monthly OR 675 mg SC quarterly | Episodic + chronic migraine prevention | HALO-EM, HALO-CM |
| Galcanezumab (Emgality) | CGRP ligand | IgG4 (humanized) | 240 mg loading; 120 mg SC monthly | Episodic + chronic migraine; episodic cluster headache | EVOLVE-1/2, REGAIN |
| Eptinezumab (Vyepti) | CGRP ligand | IgG1 (humanized) | 100 or 300 mg IV quarterly | Episodic + chronic migraine prevention | PROMISE-1, PROMISE-2 |
The pharmacokinetics of the anti-CGRP monoclonal antibodies follow the general rules governing therapeutic IgG antibodies. Subcutaneous bioavailability ranges from 50 to 80 percent across the class, with a typical time to peak plasma concentration of 3 to 7 days after subcutaneous injection. Volume of distribution is low (approximately 3 to 6 liters), reflecting the predominantly intravascular and extracellular distribution typical of large antibody molecules that do not penetrate cell membranes or, as noted, the blood-brain barrier to any clinically meaningful degree. Elimination is primarily via target-mediated drug disposition (TMDD) at low antibody concentrations and by FcRn-mediated recycling and non-specific proteolytic catabolism at higher concentrations, the same mechanisms governing all therapeutic IgG molecules. Terminal half-lives range from 27 days (erenumab) to approximately 31 days (fremanezumab, galcanezumab), which supports monthly dosing, and approximately 27 days for eptinezumab despite its IV administration. The anti-CGRP antibodies do not undergo hepatic CYP450 metabolism, meaning they have no pharmacokinetic interactions with the CYP3A4 pathway that must be managed with gepants, and no dose adjustments are required for hepatic impairment in standard clinical practice. They are also not renally eliminated and do not require dose adjustment for renal impairment, which is a practical advantage in the elderly migraine population.910
The most clinically consequential pharmacological question surrounding CGRP-targeted therapy is the cardiovascular safety of sustained CGRP blockade. CGRP is not merely a trigeminal neuropeptide; it is expressed throughout the cardiovascular system, where it is a potent endogenous coronary vasodilator and cardioprotective peptide released during ischemic preconditioning and cardiac stress. This dual role as both a migraine mediator and a cardiovascular protective signal raised legitimate concern during drug development that chronic CGRP blockade might worsen ischemic heart disease or impair recovery from myocardial infarction, concerns that have substantially — though not entirely — been addressed by clinical trial safety data.510
The cardiovascular safety concern is mechanistically grounded. CGRP is released from perivascular trigeminal and cardiac sensory nerve terminals in response to ischemia, where it causes coronary vasodilation, reduces heart rate through peripheral baroreceptor sensitization, and exerts direct cardioprotective effects on cardiomyocytes through cAMP (cyclic AMP)-mediated anti-apoptotic signaling. Animal studies of myocardial infarction showed that CGRP receptor antagonism with gepants worsened infarct size and impaired ischemic preconditioning. These preclinical signals led to the exclusion of patients with recent myocardial infarction, unstable angina, stroke within 6 months, or uncontrolled hypertension from the pivotal CGRP antibody trials, meaning the safety database in high-risk cardiovascular patients is deliberately limited and cannot be considered definitive.5
The accumulated clinical trial safety data, now spanning several years of post-marketing surveillance, have been reassuring in the populations studied. Cardiovascular adverse events in phase 3 trials were not significantly elevated over placebo for any of the four approved monoclonal antibodies or for the approved gepants. Blood pressure elevation has been noted with erenumab at the 140 mg dose in a subset of trials, possibly related to CGRP's known vasodilatory role in maintaining resting vascular tone; this effect is mild and has not driven any class-wide blood pressure monitoring requirement, but monitoring is prudent in patients with pre-existing hypertension on erenumab. Current American Headache Society guidance recommends avoiding anti-CGRP therapies in patients with recent (within 3 to 6 months) major cardiovascular events, including myocardial infarction, stroke, and unstable angina, and exercise of clinical judgment in patients with stable cardiovascular disease.10
The pharmacokinetic contrast between gepants and monoclonal antibodies is substantial and drives the clinical positioning of each class. Gepants are small molecules (molecular weight approximately 500 to 600 Da) with oral or intranasal bioavailability, rapid absorption and onset (1 to 2 hours for oral gepants; 30 minutes for zavegepant), short half-lives of approximately 6 to 11 hours requiring dosing on a per-attack or daily/every-other-day basis, hepatic CYP3A4 metabolism with attendant drug interaction potential, and the capacity for dose adjustment. Monoclonal antibodies are large proteins (approximately 147 to 150 kDa) requiring subcutaneous or intravenous administration, with onset of maximal steady-state prevention taking 1 to 3 months, half-lives of approximately 27 to 31 days enabling monthly or quarterly dosing, proteolytic catabolism rather than CYP metabolism meaning no CYP drug interactions, and no standard dose adjustment for organ impairment. These pharmacokinetic profiles make gepants the preferred class for on-demand acute treatment and optional every-other-day prevention, while monoclonal antibodies are the preferred class for continuous prevention in patients with frequent episodic or chronic migraine who cannot sustain daily oral preventive medication adherence.89
The choice between gepants and monoclonal antibodies for migraine prevention depends on several factors: migraine frequency and burden, prior preventive failure history, patient preference for route and frequency of administration, cardiovascular comorbidities, concomitant medications with CYP3A4 interaction potential, and payer access. For acute treatment, gepants are preferred over triptans specifically in patients with cardiovascular contraindications to triptans, triptan failures, or medication overuse headache risk with triptans; in patients without cardiovascular contraindications, triptans remain first-line for cost and evidence reasons. For prevention, anti-CGRP monoclonal antibodies are preferred in patients who have failed 2 or more oral preventives (beta-blockers, topiramate, amitriptyline, valproate) due to efficacy or tolerability, given their favorable adverse effect profiles compared to the older agents. Gepants (rimegepant, atogepant) are reasonable preventive choices for patients who prefer oral therapy, have concerns about injections, or who need both acute and preventive coverage from a single agent class.10
| Parameter | Gepants | Anti-CGRP mAbs |
|---|---|---|
| Molecular weight | ~500–600 Da (small molecule) | ~147–150 kDa (protein) |
| Administration | Oral or intranasal (self-administered) | SC (self-administered autoinjector) or IV (intravenous, clinic-administered) |
| Onset | 1–2 h oral; ~30 min intranasal | Prevention onset 4–12 weeks to maximal effect |
| Half-life | ~6–11 hours | ~27–31 days |
| Dosing frequency | Per attack (acute); daily or every other day (preventive) | Monthly or quarterly |
| Metabolism | CYP3A4 (hepatic); drug interactions significant | Proteolytic catabolism; no CYP interactions |
| Blood-brain barrier | Limited (may vary by lipophilicity) | Does not cross (too large) |
| MOH risk | Substantially lower than triptans; not established as cause | Not applicable (preventive only) |
| Cardiovascular risk | No vasoconstriction; avoid in recent major CV events (preclinical concern) | No vasoconstriction; same preclinical concern; monitor BP (blood pressure) with erenumab |
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Goadsby PJ, Edvinsson L, Ekman R. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann Neurol. 1990;28(2):183–187. doi:10.1002/ana.410280213
Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine: a disorder of sensory processing. Physiol Rev. 2017;97(2):553–622. doi:10.1152/physrev.00034.2015
Hay DL, Garelja ML, Poyner DR, Walker CS. Update on the pharmacology of calcitonin/CGRP family of peptides: IUPHAR review 25. Br J Pharmacol. 2018;175(1):3–17. doi:10.1111/bph.14075
Deen M, Correnti E, Kamm K, et al. Blocking CGRP in migraine patients — a review of pros and cons. J Headache Pain. 2017;18(1):96. doi:10.1186/s10194-017-0807-1
Lipton RB, Dodick DW, Ailani J, et al. Effect of ubrogepant vs placebo on pain and the most bothersome associated symptom in the acute treatment of migraine: the ACHIEVE II randomized clinical trial. JAMA. 2019;322(19):1887–1898. doi:10.1001/jama.2019.16711
Croop R, Lipton RB, Kudrow D, et al. Oral rimegepant for preventive treatment of migraine: a phase 2/3, randomised, double-blind, placebo-controlled trial. Lancet. 2021;397(10268):51–60. doi:10.1016/S0140-6736(20)32544-7
Ailani J, Lipton RB, Goadsby PJ, et al. Atogepant for the preventive treatment of migraine. N Engl J Med. 2021;385(8):695–706. doi:10.1056/NEJMoa2035908
Ashina M, Goadsby PJ, Reuter U, et al. Long-term efficacy and safety of erenumab in migraine prevention: results from a 5-year, open-label treatment phase of a randomized clinical trial. Eur J Neurol. 2021;28(5):1716–1725. doi:10.1111/ene.14715
Ailani J, Burch RC, Robbins MS; Board of Directors of the American Headache Society. The American Headache Society Consensus Statement: update on integrating new migraine treatments into clinical practice. Headache. 2021;61(7):1021–1039. doi:10.1111/head.14153