Side effects of aimovig

Aimovig

The U.S. Food and Drug Administration (FDA) approved Aimovig (erenumab) on May 17, 2018, for the prevention of episodic and chronic migraine in adults. Jointly manufactured by Novartis and Amgen Pharmaceuticals, Aimovig was the first to be FDA-approved of a new class of drugs that work by blocking the activity of calcitonin gene-related peptide (CGRP). Whereas some of the migraine drugs in this class are monoclonal antibodies against the CGRP protein, Aimovig is a monoclonal antibody against the CGRP receptor.

Migraine, a type of debilitating headache, affects more than 36 million Americans, including 30 percent of women at some point in their lives. The World Health Organization puts migraine in the list of the Top 10 most disabling diseases on the planet.

Migraine involves an intense pulsing or throbbing pain in one area of the head. Other common migraine symptoms include:

  • Nausea
  • Vomiting
  • Sensitivity to light, sound, or smell

Typically lasting for 4 to 72 hours, migraine can last as long as several days.

CGRP plays an important role in migraines. Levels of CGRP go up during migraines, production of CGRP triggers migraine, and blocking CGRP relieves migraine.

Prior to its FDA approval, the effectiveness of Aimovig for the preventive treatment of migraine was evaluated in three significant clinical trials.

A large study published in November 2017 in the New England Journal of Medicine compared erenumab with placebo in 955 participants with a history of episodic migraine (4 to 14 migraine days per month). A placebo is a substance that has no known pharmacologically active ingredients but is used as a control in clinical trials testing new drugs. Over the course of six months, erenumab administered subcutaneously at a monthly dose of 70 milligrams (mg) or 140 mg significantly reduced migraine frequency, the effects of migraines on daily activities, and the use of acute migraine-specific medication.

Another clinical trial, published in September 2017 in the journal Neurology, included 472 people with a history of episodic migraine and compared Aimovig with placebo. Over the course of 12 weeks, Aimovig-treated participants experienced, on average, one fewer migraine day per month than those on placebo. The study also provided evidence that erenumab improves headache-related disability and migraine-specific quality of life.

A third study was published in June 2017 in the journal Lancet Neurology. This clinical trial evaluated 667 people with a history of chronic migraine (15 or more headache days per month with eight or more migraine days per month) and compared Aimovig with placebo. In that study, over the course of three months, participants treated with Aimovig experienced, on average, 2 ½ fewer monthly migraine days than those receiving placebo.

Prior to taking Aimovig, tell your doctor if you are pregnant or plan on getting pregnant. You will need to talk about the benefits and risks of using this drug while you are pregnant. Also, tell your doctor if you are breastfeeding. You will need to talk about any risks to your baby.

At Stake: The Possible Long-Term Side Effects of CGRP Antagonists

As AHS holds its annual meeting, very specific questions are arising about the use of CGRPs in migraine prevention. The author poses key considerations and sample cases for prescribing this new class of monoclonal antibodies.

A commentary for clinicians involved in the treatment of chronic headache and migraine

The novel class of monoclonal antibodies (mAbs) targeting calcitonin gene-related peptide (CGRP) are a valuable addition to our preventives for migraine. However, there are significant conceivable long-term adverse effects that need to be considered as these new products gain approval and enter the market. We will have a better feel for the true risk in 10 years. For each patient, we have to decide whether the benefits outweigh the possible risks. With luck, it may come to pass that the biologics targeting CGRP carry very few long-term risks. Certainly, these have been safe compounds for the short-term. Three-year safety data has recently been presented (see also “A New Frontier in Migraine Management: Inside CGRP Inhibitors & Migraine Prevention”). Herein, I discuss some of the possible long-term issues with these long-awaiting medications.

The following are presented as a series of questions related to core systems (eg, cardiovascular, central nervous, gastrointestinal, reproductive, and more) that need to be addressed before CGRP antagonists are used widely. Most of these questions do not have answers at this time. Much of the CGRP research to date has been conducted in animal models, which, as we know, does not always correlate with effects in humans. Hopefully, over time, the community will be able to determine which of our patients may be at increased risk for long-term adverse effects. (You can also see a Pro/Con debate on CGRP inhibitors which took place among Drs. Alan M. Rapoport and Robert B. Cowan at the 2019 AAPM meeting.)

Calcitonin

Cardiovascular and Pulmonary System

1. CGRP plays an important role in resisting the onset of hypertension (HTN); how relevant is this when prescribing to young patients, particularly those at higher risk for HTN? How much does vascular dilation redundancy matter (with other vasodilator mediators, such as PGs and NO, compensating for the loss of CGRP)?

2. With the onset of HTN, there is a compensatory release of CGRP: how relevant is this, and what effects do the antagonists have? In the face of HTN, CGRP release may become attenuated over time. There have been conflicting studies as to the amount of plasma CGRP present in those with HTN. To date, the antagonists have not appeared to affect blood pressure. Will CGRP antagonists be studied in those with HTN? Will these be evaluated in the face of poorly controlled HTN? Deletion of RAMP 1, for example, has been associated with cytokine production (proinflammatory) and HTN. Is this clinically relevant?

3. CGRP may delay or protect against the development of cardiovascular disease. For which patients is this relevant? CGRP is the most potent of all the vasodilators, so how might this influence prescribing for higher risk patients?

4. The effect of CGRP on the expression of endothelial nitric oxide synthase (eNOS): depleting CGRP may lead to enhanced loss of eNOS; what is the clinical relevance?

5. CGRP depletion may produce oxidative stress in the aorta; how clinically relevant is this?

6. If CGRP is knocked out, and the vasodilator effects are diminished, do other compounds (eg, nitrous oxide, substance P, prostaglandins) help to compensate (primarily at the resistance vessel level)? One study indicated that both substance P and CGRP had to be blocked for there to be a loss of vasodilatation.

7. There is polymorphism with the CALC 1 gene (this gene encodes CGRP and calcitonin, linked to essential HTN); is this clinically relevant in light of mAb use?

8. Evidence from KO mice indicates that reduction of CGRP on the cardiovasvular system may become pathologically relevant primarily in conjunction with compromised vasculature. Infusions of CGRP improve the circulation in the presence of heart disease. We need angiographic (and other) studies in patients with cardiovascular disease (CAD), ideally prior to and after treatment with the antagonist. Are further studies planned?

9. Could smaller cardiac or cerebral infarcts become more dangerous resulting from the protective effects of CGRP being blocked? CGRP protects against ischemia, cell death, and vascular inflammation in various organs (heart, brain, GI, kidney). When CGRP is seriously depleted, there is an increased susceptibility to injury via ischemia. How clinically relevant is blocking CGRP? This will need more research.

10. CGRP plays a role in heart failure. Infusion of CGRP improves circulation in the face of heart disease. Regarding microvascular growth, CGRP is an angiogenic facilitator. Should patients at high risk for failure, or with actual heart failure, not be prescribed these medications?

11. There is evidence that CGRP helps to protect the heart, and this effect is lessened in the presence of diabetes. For patients with both diabetes and CAD, should CGRP inhibitors be withheld?

12. CGRP levels decline with age (although there may be a bimodal effect) and CGRP helps to protect the myocardium; should CGRP inhibitors be withheld in older patients, particularly for those with heart disease?

13. Do the Amylin 1 receptors (or other calcitonin-group receptors) help to “cover” for the loss of beneficial effects, particularly vasodilatory, after the blocking of CGRP?

14. With regards to the cardiovascular system, is there a difference between antagonizing the ligand of CGRP, and blocking the receptor?

15. Regarding advanced CAD, how important is CGRP as a vasodilator? CGRP levels are increased during myocardial infarction. Could antagonizing CGRP lead to a more severe infarct? There was an erenumab-aooe (Aimovig, Amgen/Novartis – the first FDA approved CGRP mAb for migraine prevention) study of 90 patients with stable angina, who were given 140 mg IV as a one-time dose. There were no problems found in the 3 months post-infusion. Are further studies planned?

16. How clinically relevant is CGRP in the cerebral vasculature? CGRP is an inhibitor of platelet aggregation, through cAMP activity. Inhibiting CGRP could lead to embolic cardiac or cerebral events.

17. Is CGRP a vasodilator in both smaller and larger cerebral arteries?

18. CGRP and pulmonary HTN: CGRP is abundant in the lung; for high- risk individuals, would blocking CGRP increase the chance of developing pulmonary HTN? There is evidence that CGRP is beneficial in those with pulmonary HTN. Should patients with pulmonary HTN be excluded from receiving CGRP antagonists?

Central Nervous System (within the Blood-Brain Barrier)

1. There is slight penetration of these large-molecule mAbs into the CNS, from 0.1% to 1%; is this clinically relevant as to the mechanism of action of the mAbs? Probably not, but certainly it is possible.

2. Botox undergoes transcytosis (tracking along the axon from the trigeminal ganglion, into the brainstem): does this also occur with mAbs? Most likely it does not, but it may happen to a small degree. Radioisotope studies to identify elements of the mAb in the brainstem would be helpful.

3. How effectively do the peripheral (trigeminal ganglion) effects of the mAb dampen down central sensitization, and/or cortical spreading depression?

Central Nervous System (outside the Blood-Brain Barrier)

1. The anterior pituitary contains CGRP. Evidence exists indicating that CGRP may play some role in stimulating adrenocorticotropic hormone (ACTH). What are the possible effects on CGRP antagonism for the various hormones (GH, TSH, FSH, LH, ACTH, MSTH, and prolactin)? Should we be hesitant to prescribe for adolescents (off-label), due to possible effects on growth hormone? Should we measure hormone levels in those adolescents prescribed the mAbs? I am not aware of the various levels being drawn during the Phase 2 and 3 studies, but are there plans to evaluate these post-approval?

2. We do not know about the effect of this new mediation class on individuals with thyroid disease: should the mAbs be used with caution in diagnosed patients until more is known about the mAbs’ effect on thyroid-stimulating hormone, or TSH?

3. Should studies be done evaluating FSH, LH, and ACTH levels before and after these antagonists?

4. What is the effect on prolactin? Should those with pituitary microadenomas be restricted from use?

5. Might there be an effect on melatonin levels?

6. The choroid plexus: could CGRP knockout affect cerebrospinal fluid (CSF) production? Would the CSF inflammatory homeostasis, partially controlled by the choroid plexus, be affected? Can this be evaluated?

7. The median eminence: could CGRP knockout affect hypothalamic hormone release (of CRF, TRH, DA, GHRH, and GnRH)? Should these be tested?

8. Area postrema (part of the circumventricular organs): would regulation of nausea/vomiting be affected? Other circumventricular organs: would homeostasis of cardiovascular or immune functions, or fluid regulation, or thirst/feeding, be affected? How can this be evaluated?

Gastrointestinal System

1. (Beta) CGRP is primarily present in the GI system (versus alpha CGRP), and CGRP is important for mucosal protection. What is the effect of antagonizing CGRP on the GI mucosa?

2. CGRP is involved in the healing of GI ulcers. Should antagonists be restricted for those with ulcers? This most likely depends upon how recently the ulcer was present, and if the patient is at high risk for recurrence. Should these not be given to those with a recent past history of ulcers, or those at high risk?

3. For those with, or at high risk for Inflammatory Bowel Disease (IBD), should these antagonists be restricted? Caution is prudent in considering the mAbs for those with IBD, or at high risk.

4. CGRP acts in a biphasic manner on GI motility. Should the antagonists be used with caution for those with moderate or severe IBS? Particularly with IBS-C, the mAbs may exacerbate constipation. Less often, diarrhea may be worsened (in theory).

Skin, Wound Healing, Burns, and Bone Health

1. CGRP contributes to flushing and thermoregulation; what are the effects of blocking CGRP on these functions? In blushing syndromes (such as hot flushes), CGRP release is involved. Would blocking CGRP affect these syndromes? Is there an effect on Raynaud’s symptoms?

2. What clinical effect results from dampening the CGRP effects on local skin edema and itch? CGRP can inhibit allergic conditions, such as certain types of dermatitis (irritant dermatitis). What effects on dermatitis might be seen by inhibiting CGRP? Loss of alpha CGRP-containing nerves may be associated with cold hypersensitivity. CGRP may have a role in temperature regulation. Could inhibiting CGRP be clinically relevant with these issues?

3. CGRP facilitates tissue repair and wound healing. These effects are mediated via vasodilation, upregulating VEGF expression, and by limiting inflammatory processes. CGRP also promotes revascularization. What effect does blocking CGRP have on wound healing? Which receptor does CGRP engage with to facilitate wound healing? Should at-risk patients for wound healing be prescribed these antagonists with caution?

4. CGRP plays some role in regeneration of the skin, via promoting proliferation of keratinocytes. Will skin be able to regenerate as well after CGRP is diminished?

5. For those with burns, CGRP and SP facilitate acute edema formation. What is the clinical relevance of knocking out CGRP for those with more severe burns?

6. CGRP may regulate bone metabolism through stimulation of osteoblastic differentiation, as well as an effect on osteoclastic formation. Amylin and calcitonin are also vital for bone health. Might the CGRP antagonists inhibit normal bone growth and metabolism? Does diminishing CGRP play a role in the healing of bone?

Renal, Sepsis, Diabetes/Obesity

1. Renal effects: during dialysis, CGRP levels are raised, possibly as a defense mechanism. How does antagonizing CGRP affect the person undergoing dialysis? CGRP may protect against renal damage in certain pathological conditions. In light of kidney disease, should the CGRP antagonists be used sparingly?

2. CGRP levels are raised during sepsis. CGRP acts on macrophages and other cells partially via upregulating IL-10, and by decreasing inflammation. CGRP also may mediate hypotension during sepsis. What effect does blocking CGRP have on these effects? If a patient on an antagonist becomes septic, would the therapy change?

3. CGRP is active within the pancreas, and is involved with the regulation of insulin release; the effect may be to reduce insulin levels, which (in theory) may result in hyperglycemia. Would antagonizing CGRP theoretically help with diabetes? In the presence of diabetes, CGRP is lessened (through nerve growth factor, NGF) in sensory neurons; what is the relevance for peripheral neuropathy? In diabetics with cardiovascular disease, should extra precautions be taken regarding antagonizing CGRP?

4. CGRP knockout may affect metabolism, energy use, and body weight. Could the CGRP mAbs affect body weight? Could this be included in long-term post-approval studies?

Pregnancy, Arthritis and Other Pains, and Aging

1. Early in pregnancy, CGRP levels are minimal in the fetus: what are the risks if CGRP antagonists are given prior to pregnancy? Later in pregnancy, CGRP may play a role in mediating the adrenal glucocorticoid response to acute stress in the more mature fetus. Circulating CGRP levels (in the mother) are increased during pregnancy, peaking in the last trimester. CGRP levels are lower with pre-eclampsia. There was a prenatal and postnatal study in monkeys with Aimovig. The animals received 50 mg/kg of Aimovig every 2 weeks. No effects were apparent on the fetus or infant, with regards to growth and development. The follow-up was through 6 months after delivery. Towards the end of pregnancy, CGRP plays a role in cervical ripening, and is present in the placenta and fetus: how would lessening CGRP affect the latter stages of pregnancy? Could a CGRP mAb render it more difficult to become pregnant? Do the mAbs affect sperm in any fashion? There is a CGRP pregnancy registry that is being organized: is it coordinated among the various companies, and how does one access it?

2. Arthritis: could CGRP antagonism possibly help with rheumatoid or osteoarthritis? How about other pain syndromes, such as fibromyalgia, or peripheral neuropathy? What is the state of studies for these conditions? CGRP does show suppression of TNF alpha, through upregulation of other pathways. Is this clinically relevant? Arthritis patients have increased levels of CGRP in plasma and synovial fluid, and CGRP causes cytokine production in both rheumatoid arthritis and osteoarthritis. Could inhibiting CGRP help alleviate arthritis, or help in various pain syndromes?

3. CGRP levels may decline as one ages, although circulating levels may be increased in certain individuals. There may be a bimodal effect. Would the mAbs have more (or less) risk at age 70? At age 85 or 90? This population is at an increased risk for cardiovascular disease. Does this influence prescribing in the elderly? With declining stores of CGRP as one ages, the CGRP protective effect also (presumably) declines. Does this affect our prescribing after a certain age? Could eliminating some of the effects of CGRP actually help aging (there is some experimental evidence for this).

Amylin, Adrenomedullin, and CGRP Receptors

1. The AMY 1 receptor (and to a lesser degree the AMY 2 receptor), along with the ADM 1 and ADM 2 receptors, also have affinity for the CGRP ligand (although with lower specificity). Amylin, while mostly involved with glucose regulation, may be important in other functions (it is also located in the trigeminal ganglion and brainstem).

2. CGRP also functions at the amylin receptors; what is the result of blocking CGRP on the functioning of the amylin receptor. If one blocks the CGRP receptor, versus the ligand, is there a clinically relevant difference? By blocking the CGRP receptor, versus the ligand, CGRP may still attach to the amylin receptors.

3. Adrenomedullin (ADM) competes with CGRP at the receptor site, and under certain conditions, ADM may actually compete with and displace CGRP from the receptor. If the CGRP antagonists affect the actions of ADM, what clinical effects might we see, over the long-term?

4. The ADM 1 and 2 receptors also have affinity for the CGRP ligand. What effects may occur from lowering CGRP, with regards to these other receptors?

5. Intermedin (IMD) is a peptide with affinity for this family of receptors. What effect may occur from blocking some of the IMD effects?

6. What are the effects, after blocking CGRP, on these other ligands and receptors with regard to the vasodilator effects?

7. The CGRP receptors are complex. CGRP 1 is primarily CLR and RAMP1. The pharmacology is complex, as the other peptides in the calcitonin family may attach to the CGRP receptor. CGRP may also activate the amylin receptor. With this overlapping pharmacology, what should we know about the effects of 1) knocking out the CGRP receptor, and 2) knocking out CGRP ligand?

Theoretical “CGRP Risk Scale”

Serious adverse events from CGRP antagonists have not yet occurred. When patients who have been prescribed these antagonists do suffer from a GI ulcer, a myocardial infarction, hypertension, or any number of conditions, the “cause and effect” may be difficult to determine. Clinicians should consider developing a “CGRP Risk Scale” as a basis for assessing risk going forward. A numerical scale of risk could easily be developed.

However, we want to determine risk first, including those patients who might be identified as low, medium, or high risk for the antagonist. Some of this work is beginning and as our knowledge increases over time, clinical risk assessment will be more accurate.

Miscellaneous Issues

1. The receptor occupancy of Aimovig is approximately 89%. The blocking of the CGRP ligand (by the other three mAbs under regulatory review: eptinezumab, ALD403, Alder Pharmaceuticals; fremanezumab,TEV-48125, Teva Pharmaceuticals; and galcanezumab, LY2951742, Eli Lilly) is approximately 85%. Do these occupancy levels steadily decline over the weeks/months, or is there a precipitous fall off at some point? Is this clinically relevant?

2. NGF influences CGRP. What clinical relevance, if any, does NGF have regarding the mAbs? Also, TRPV1 agonists may help to regulate CGRP; what is the importance of this?

3. Differences between the ligand antagonists (the three compounds in development noted above) and the receptor antagonist (Aimovig, on the market): receptors (that CGRP may attach to) other than the CGRP receptor may compensate for loss of the CGRP receptor; on the other hand, antibodies directed at the ligand of CGRP would also block the effects at the other (particularly AMY 1) receptors. What is the clinical relevance of these differences between the ligand and the receptor antagonist?

4. With other meds (example: methysergide), we had patients take a “drug holiday” every 6 months. Does that make sense with these CGRP antagonists, at least until we are sure of long-term safety? Would doing this produce more antibodies, after re-introduction? There would also be the risk that, after re-introduction, the mAb would not be as effective.

5. Informed consent: should we obtain this from patients (ideally, yes), and if so, what should be included in the informed consent?

6. Monitoring of adverse events: we should encourage reporting to the company or to the FDA. As with a pooled pregnancy registry, are there any plans for a pooled “mAb” adverse event registry? This would be a good idea. In addition, evaluation of other beneficial effects should be encouraged (such as the effect on other pain syndromes).

7. There have been a number of patients who have experienced moderate or severe fatigue/asthenia after the Aimovig injection. The fatigue and asthenia usually is short-lived. In addition, some patients have had muscle and/or joint pains. The hypothalamic-pituitary-adrenal(HPA) axis may be the culprit. The HPA axis is not protected from the CGRP mAbs by the blood-brain barrier. In addition, the hypothalamic-pituitary-thyroid axis may be involved as well. With low cortisol levels, muscle or joint pains may also occur. It will be helpful to have studies investigating various hypothalamic and pituitary hormones, particularly cortisol, in these patients. Some patients have also experienced stroke-like symptoms as well. It would be helpful to investigate the etiology of these symptoms.

Sample Case Scenarios

In several years, we will have more information, regarding long-term safety and physiological effects of the CGRP antagonists. Short-term, these have been well tolerated. Until we know more, clinicians will have to decide which patients should not be given a CGRP antagonist using a combination of available evidence, clinical judgment, patient preference, and risk versus benefit. It is not fair to compare these new antagonists to “nothing:” patients are not on “nothing.” Other medications consumed by patients may have significant short and long-term adverse effects. Quality of life issues also play a role. Many migraineurs have significantly diminished quality of life due to poorly controlled headaches.

The following are sample scenarios where clinicians may or may not choose to prescribe the CGRP antagonists. The selections posed include the author’s opinion alone.

CASE #1: Heather is 18 years old, with mild chronic migraine (CM) for 1 year. Heather recently sustained a fracture to her arm. Topiramate and amitriptyline have not been helpful, but the triptans do work abortively. Heather has not tried Botox. In this situation, I would suggest trying several other preventives, particularly Botox, and ARBs or beta-blockers. Petadolex may be worth prescribing. Pregnancy is always a concern in younger women, but the other medications also carry risks with pregnancy. mAbs would certainly be a consideration, but not until several others have been utilized. Her recent fracture of a bone plays a role in our decision, as CGRP is involved in bone healing.

CASE #2: Eric is a 32-year-old man with severe chronic migraine, and a history of a gastric ulcer 4 years ago. He has IBS and a strong family history of inflammatory bowel disease (IBD). He is refractory to many preventives, including Botox. This is another difficult decision. The family history of IBD, and his (remote) history of an ulcer may increase (in theory) risk for the mAbs. While it may be better to first try other refractory approaches, this is in that “gray zone.”

CASE #3: Sally is a 63-year-old insulin-dependent diabetic with a history of angina. She has high cholesterol. Sally has failed 4 preventives, including Botox. This is a tough call; with DM and angina, the lowering of the CGRP vasodilatation (among other effects) may increase (in theory) the risk for mAbs. If her life is devastated by migraine attacks, and she is informed of possible risks, it may be reasonable to prescribe the antagonist. However, it would be better if we can avoid the mAbs, until more is known about cardiovascular effects in those with DM and coronary disease.

CASE #4: John is a 52-year-old with chronic migraine, and a history of mild DM Type 2. He has a mild peripheral neuropathy, and a cut on his big toe is very slow to heal. John has been on 3 preventives, which did not help. He has not tried Botox. There are some (theoretical) potential problems from the use of mAbs: possible increased risk for cardiac disease, and diminished wound healing. Utilizing a mAb would be reasonable, but if possible Botox may be a better choice in this situation.

CASE #5: Caitlin is a 39-year-old with hypothyroidism and an increased prolactin due to a small pituitary microadenoma. She has been refractory to many preventives, including Botox. Triptans work well for Caitlin. In view of the pituitary dysfunction, mAbs should be used with some caution (until we know more about the possible effects of diminishing CGRP on the pituitary hormones). If we do use a CGRP antagonist, I would suggest closely monitoring the hormonal levels. It is possible that we should evaluate hormone levels in most (or all) patients.

Conclusion

The CGRP antagonists for migraine prevention and certain chronic headache indications are potentially terrific options for patients with these conditions. Patients and the healthcare community at large desperately need improved treatments in this area. However, CGRP is involved in a multitude of physiological processes and we are only dealing with theoretical side effects at this time. It is the author’s opinion that it is prudent to screen patients, using the limited knowledge available, before prescribing this new class of medications. Over the next 5 to 10 years, we will be in a better place to determine who is at risk for these antagonists and who may see life-changing benefit.

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3. Edvinsson L. The trigeminovascular pathway: role of CGRP and CGRP receptors in migraine. Headache. 2017;57:47-55.

4. 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.

7. Brain SD, Grant AD. Vascular actions of calcitonin gene-related peptide and adrenomedullin. Physiol Rev. 2004;84(3):903-934.

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Last updated on: June 6, 2019 Continue Reading: Special Report: CGRP Monoclonal Antibodies for Chronic Migraine

Erenumab-aooe Injection

Erenumab-aooe injection comes as a solution (liquid) to be injected subcutaneously (under the skin). It is usually given once a month. Use erenumab-aooe injection at around the same day every month. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Use erenumab-aooe injection exactly as directed. Do not use more or less of it or use it more often than prescribed by your doctor.

You may be able to inject the medication yourself at home or have a friend or relative perform the injections. Ask your doctor to show you or the person who will be performing the injections how to inject the medication.

Erenumab-aooe injection comes as a prefilled syringe and as a prefilled autoinjector. Allow the syringe and autoinjector to warm to room temperature for 30 minutes away from direct sunlight before you inject the medication. Do not try to warm the medication by heating it in a microwave, placing it in hot water, or through any other method. Use each syringe or autoinjector only once and inject all the solution in the syringe. Dispose of used syringes and autoinjector in a puncture-resistant container. Talk to your doctor or pharmacist about how to dispose of the puncture-resistant container.

Inject erenumab-aooe injection into thigh or stomach area. If someone else will be injecting the medication for you, that person can also inject it into your upper arm. Do not inject into an area where the skin is tender, thick, bruised, red, scaly, hard, or has scars or stretch marks.

Always look at erenumab-aooe before you inject it. It should be clear and colorless. Do not use erenumab-aooe injection, if it is colored, cloudy, or contains flakes or solid particles. Do not shake it.

If your doctor tells you to inject two separate injections one after another, use a different autoinjector or syringe for each injection. If you use the same body site (upper arm, thigh, or stomach) for the two separate injections, make sure the second injection it is not at the exact same spot you used for the first injection.

Erenumab-aooe injection helps to prevent migraines but does not cure them. Continue to inject erenumab-aooe injection even if you feel well. Do not stop using erenumab-aooe injection without talking to your doctor.

Ask your pharmacist or doctor for a copy of the manufacturer’s information for the patient.

Aimovig (erenumab-aooe)

You may wonder how Aimovig compares to other medications that are prescribed for similar uses. Below are comparisons between Aimovig and several medications.

Aimovig vs. Ajovy

Aimovig contains the drug erenumab, which is a monoclonal antibody. Ajovy contains the drug fremanezumab, which is also a monoclonal antibody. Monoclonal antibodies are medications created in a lab. These drugs are developed from immune system cells. They work by blocking the activity of certain proteins in your body.

Aimovig and Ajovy both stop the activity of a protein called calcitonin gene-related peptide (CGRP). CGRP causes inflammation and vasodilation (widening of blood vessels) in the brain, which may result in migraine headaches. Blocking CGRP helps prevent migraine headaches.

Uses

Aimovig and Ajovy are both FDA-approved to prevent migraine headaches in adults.

Forms and administration

Aimovig and Ajovy both come in an injectable form that’s administered under your skin (subcutaneous). You can give the injection to yourself at home. Both drugs can be self-injected in certain areas, such as:

  • your belly
  • the front of your thighs
  • the back of your upper arms

Aimovig is supplied as a single-dose prefilled autoinjector. It’s usually given as a 70-mg injection once per month. However, some people are prescribed a higher dose of 140 mg each month.

Ajovy is supplied as a single-dose prefilled syringe. It can be given as a single injection of 225 mg once each month. Or it can be given as three injections of 225 mg once every three months.

Side effects and risks

Aimovig and Ajovy work in similar ways and cause some of the same side effects. The common and serious side effects of both drugs are below.

More common side effects

These lists contain examples of more common side effects that can occur with Aimovig, with Ajovy, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • constipation
    • muscle cramps or spasms
    • upper respiratory infection (such as the common cold or a sinus infection)
    • flu-like symptoms
    • back pain
  • Can occur with Ajovy:
    • no unique common side effects
  • Can occur with both Aimovig and Ajovy:
    • injection site reactions such as pain, itchiness, or redness

Serious side effects

The primary serious side effect for both Aimovig and Ajovy is a severe allergic reaction. Such a reaction isn’t common, but it is possible. (For more information, see “Allergic reaction” under “Aimovig side effects” above).

Immune reaction

In clinical trials done for both Aimovig and Ajovy, a small number of people had an immune reaction to the drugs. The reaction caused their bodies to develop antibodies against the medications.

Antibodies are proteins made by the immune system to fight off foreign substances in your body. Your body can develop antibodies to any foreign substance, including monoclonal antibodies. If your body makes antibodies to Aimovig or Ajovy, the drug may no longer work for you.

In clinical trials for Aimovig, more than 6 percent of people developed antibodies to the drug. In ongoing clinical studies, fewer than 2 percent of people developed antibodies to Ajovy.

Because Aimovig and Ajovy were approved in 2018, it’s still too early to know how common this effect might be and how it might affect how people use these drugs in the future.

Effectiveness

Aimovig and Ajovy are both effective at preventing migraine headaches, but they haven’t been directly compared in clinical trials.

However, migraine treatment guidelines recommend either drug as an option for certain people. These include people who:

  • can’t reduce their monthly migraine days enough with other medications
  • can’t tolerate other medications because of side effects or drug interactions

Episodic migraine

Separate studies of Aimovig and Ajovy showed effectiveness for preventing episodic migraine headaches.

  • In clinical studies of Aimovig, about 40 percent of people with episodic migraine who received 70 mg of the drug monthly cut their migraine days by at least half over six months. Up to 50 percent of people who received 140 mg had similar results.
  • In a clinical study of Ajovy, around 48 percent of people with episodic migraine who received monthly treatment with the drug cut their migraine days by at least half over three months. About 44 percent of people who received Ajovy every three months had similar results.

Chronic migraine

Separate studies of Aimovig and Ajovy also showed effectiveness for preventing chronic migraine headaches.

  • In a three-month clinical study of Aimovig, about 40 percent of people with chronic migraine who received either 70 mg or 140 mg of the drug monthly had half as many migraine days or fewer.
  • In a three-month clinical study of Ajovy, almost 41 percent of people with chronic migraine who received monthly Ajovy therapy had half as many migraine days after treatment or fewer. Of the people who received Ajovy every three months, around 37 percent had similar results.

Costs

Aimovig and Ajovy are both brand-name medications. There are no generic forms of either drug available. Brand-name medications generally cost more than generic forms.

Based on estimates from GoodRx.com, Aimovig and Ajovy cost roughly the same amount. The actual price you would pay for either drug would depend on your insurance plan, your location, and the pharmacy you use. Your price for Aimovig would also depend on your dose.

Aimovig vs. Botox

Aimovig contains a monoclonal antibody called erenumab. A monoclonal antibody is a type of drug developed in a lab. These drugs are made from immune system cells. Aimovig works to prevent migraine headaches by blocking the activity of a specific protein that can cause them.

Botox contains the drug onabotulinumtoxinA. This drug belongs to a class of medications called neurotoxins. Botox works by temporarily paralyzing the muscles that it’s injected into. This effect prevents pain signals in the muscles from being activated. It’s thought that this process helps prevent migraine headaches before they start.

Uses

Aimovig is approved by the FDA to prevent episodic or chronic migraine headaches in adults.

Botox is FDA-approved to prevent chronic migraine headaches in adults. Botox is also approved to treat several other conditions, such as:

  • cervical dystonia (painfully twisted neck)
  • eyelid spasms
  • overactive bladder
  • muscle spasticity
  • excessive sweating

Forms and administration

Aimovig comes as a single-dose prefilled autoinjector. It’s given as an injection under your skin (subcutaneous) that you can give yourself at home. It’s given at a dose of 70 mg or 140 mg per month.

Aimovig can be injected in certain areas of body. These are:

  • your belly
  • the front of your thighs
  • the back of your upper arms

Botox is only given in a doctor’s office. It’s injected with a syringe into a muscle (intramuscular), usually every 12 weeks. The usual sites for injection include:

  • your forehead
  • the back of your neck and shoulders
  • above and near your ears
  • near your hairline at the base of your neck

Your doctor will typically give you 31 small injections in these areas at each appointment.

Side effects and risks

Aimovig and Botox are both used to prevent migraine headaches, but they work in different ways. Therefore, they have some similar side effects and some different.

More common side effects

These lists contain examples of serious side effects that can occur with Aimovig, with Botox, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • constipation
    • muscle cramps
    • muscles spasms
    • back pain
    • upper respiratory infection (such as the common cold or a sinus infection)
  • Can occur with Botox:
    • headache or worsening migraine
    • eyelid droop
    • facial muscle paralysis
    • neck pain
    • muscle stiffness
    • muscle pain and weakness
  • Can occur with both Aimovig and Botox:
    • injection site reactions
    • flu-like symptoms

Serious side effects

These lists contain examples of serious side effects that can occur with Aimovig, with Botox, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • few unique serious side effects
  • Can occur with Botox:
    • spread of paralysis to nearby muscles*
    • trouble swallowing and breathing
    • serious infection
  • Can occur with both Aimovig and Botox:
    • serious allergic reactions

* Botox has a boxed warning from the FDA for spread of paralysis to nearby muscles following injection. A boxed warning is the strongest warning the FDA requires. It alerts doctors and patients about drug effects that may be dangerous.

Effectiveness

The only condition that both Aimovig and Botox are used to prevent is chronic migraine headaches.

Treatment guidelines recommend Aimovig as an option for people who can’t reduce their number of migraine days enough with alternative drugs. It’s also recommended for people who can’t take other medications because of side effects or drug interactions.

Botox is recommended by the American Academy of Neurology as an option for treatment in people with chronic migraine.

The effectiveness of these drugs hasn’t been directly compared in clinical studies. However, in separate studies, Aimovig and Botox both achieved effective results in preventing chronic migraine headaches.

  • In a clinical study of Aimovig, about 40 percent of people with chronic migraine who received either 70 mg or 140 mg had half as many migraine days or fewer after three months.
  • In clinical studies of people with chronic migraine, Botox reduced the number of headache days by up to 9.2 days on average per month, over 24 weeks. In another study, around 47 percent of people decreased their number of headache days by at least half.

Costs

Aimovig and Botox are both brand-name medications. There are currently no generic forms available of either drug.

According to estimates from GoodRx.com, Botox is typically less expensive than Aimovig. The actual price you would pay for either drug would depend on your dose, insurance plan, your location, and the pharmacy you use.

Aimovig vs. Emgality

Aimovig contains a monoclonal antibody called erenumab. Emgality contains a monoclonal antibody called galcanezumab. A monoclonal antibody is a type of drug developed in a lab. These drugs are made from immune system cells. They work by blocking the activity of specific proteins in your body.

Aimovig and Emgality both block the activity of a protein in your body called calcitonin gene-related peptide (CGRP). CGRP causes inflammation and vasodilation (widening of blood vessels) in the brain, which can result in migraine headaches. By blocking the activity of CGRP, these drugs help stop inflammation and vasodilation. This helps to prevent migraine headaches.

Uses

Aimovig and Emgality are both FDA-approved to prevent migraine headaches in adults.

Forms and administration

Aimovig is supplied in a single-dose prefilled autoinjector. Emgality is supplied in a single-dose prefilled syringe and a single-dose prefilled pen. Both drugs are given as a subcutaneous injection (an injection under the skin). You can give the injections to yourself at home once a month.

Both drugs can be injected under the skin at certain places on your body. These are:

  • your belly
  • the front of your thighs
  • the back of your upper arms

Emgality can also be injected under the skin of your buttocks.

Aimovig is prescribed as a 70-mg or 140-mg monthly injection. Emgality is prescribed as a 120-mg monthly injection.

Side effects and risks

Aimovig and Emgality are similar drugs that cause some of the same common and serious side effects. Below are examples of these side effects.

More common side effects

These lists contain examples of serious side effects that can occur with Aimovig, with Emgality, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • constipation
    • muscle cramps
    • muscles spasms
    • flu-like symptoms
  • Can occur with Emgality:
    • sore throat
  • Can occur with both Aimovig and Emgality:
    • injection site reactions
    • back pain
    • upper respiratory tract infection (such as the common cold or a sinus infection)

Serious side effects

Severe allergic reaction is a rare serious side effect for both Aimovig and Emgality. (For more information, see “Allergic reaction” under “Aimovig side effects” above).

Immune reaction

In clinical trials for each drug, a small number of people had an immune reaction to Aimovig and Emgality. With this kind of reaction, the body’s immune system developed antibodies against the drugs.

Antibodies are proteins in your immune system that fight off foreign substances in your body. Your body can make antibodies to any foreign substance, including monoclonal antibodies such as Aimovig and Emgality.

If your body develops antibodies to one of these drugs, it’s possible that the drug will no longer work to prevent migraine headaches for you.

In clinical studies of Aimovig, more than 6 percent of people taking the drug developed antibodies to it. And in clinical studies of Emgality, almost 5 percent of people developed antibodies to Emgality.

Because Aimovig and Emgality were approved in 2018, it’s too early to know how many people might have this kind of reaction. It’s also too early to know how it could affect how people use these drugs in the future.

Effectiveness

Aimovig and Emgality haven’t been compared in clinical studies, but both are effective for preventing migraine headaches.

Treatment guidelines recommend Aimovig and Emgality as options for people with episodic or chronic migraine who:

  • can’t take other medications because of side effects or drug interactions
  • can’t reduce their number of monthly migraine days enough with other medications

Episodic migraine

Separate studies of Aimovig and Emgality showed that both medications are effective for preventing episodic migraine headaches:

  • In clinical studies of Aimovig, up to 50 percent of people with episodic migraine who received 140 mg of the drug reduced their migraine days by at least half over six months. About 40 percent of people who received 70 mg saw similar results.
  • In Emgality’s clinical studies of people with episodic migraine, around 60 percent of people reduced their number of migraine days by at least half over six months of Emgality treatment. Up to 16 percent were migraine-free after six months of treatment.

Chronic migraine

Separate studies of Aimovig and Emgality showed that both medications are effective for preventing chronic migraine headaches:

  • In a three-month clinical study of people with chronic migraine, about 40 percent of people who took either 70 mg or 140 mg of Aimovig had half as many migraine days or fewer with treatment.
  • In a three-month clinical study of people with chronic migraine, almost 30 percent of people who took Emgality for three months had half as many migraine days or fewer with treatment.

Costs

Aimovig and Emgality are both brand-name medications. There are currently no generic forms available of either drug. Brand-name drugs usually cost more than generics.

According to estimates from GoodRx.com, Aimovig and Emgality cost nearly the same amount. The actual price you would pay for either drug would depend on your dose, insurance plan, your location, and the pharmacy you use.

Aimovig vs. Topamax

Aimovig contains a monoclonal antibody called erenumab. A monoclonal antibody is a type of drug developed from immune system cells. Drugs of this type are made in a lab. Aimovig helps to prevent migraine headaches by stopping the activity of specific proteins that cause them.

Topamax contains topiramate, a type of drug that’s also used to treat seizures. It’s not well understood how Topamax works to prevent migraine headaches. It’s thought that the drug decreases overactive nerve cells in the brain that might cause migraine headaches.

Uses

Both Aimovig and Topamax are FDA-approved to prevent migraine headaches. Aimovig is approved for use in adults, while Topamax is approved for use in adults and children aged 12 and older.

Topamax is also approved to treat epilepsy.

Forms and administration

Aimovig comes in a single-dose prefilled autoinjector. It’s given as an injection under your skin (subcutaneous) that you give yourself at home once per month. The typical dose is 70 mg, but some people may benefit from a 140-mg dose.

Topamax comes as an oral capsule or oral tablet. The usual dosage is 50 mg taken twice daily. Depending on your doctor’s recommendation, you may start on a lower dosage and increase it to the usual dosage over a couple of months.

Side effects and risks

Aimovig and Topamax work in different ways in the body and therefore have different side effects. Some of the common and serious side effects of both drugs are below. The list below does not include all possible side effects.

More common side effects

These lists contain examples of serious side effects that can occur with Aimovig, with Topamax, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • injection site reactions
    • back pain
    • constipation
    • muscle cramps
    • muscle spasms
    • flu-like symptoms
  • Can occur with Topamax:
    • sore throat
    • fatigue
    • paresthesia (feeling of “pins and needles”)
    • nausea
    • diarrhea
    • weight loss
    • loss of appetite
    • trouble concentrating
  • Can occur with both Aimovig and Topamax:
    • respiratory tract infection (such as the common cold or a sinus infection)

Serious side effects

These lists contain examples of serious side effects that can occur with Aimovig, with Topamax, or with both drugs (when taken individually).

  • Can occur with Aimovig:
    • few unique serious side effects
  • Can occur with Topamax:
    • vision problems, including glaucoma
    • decreased sweating (inability to regulate body temperature)
    • metabolic acidosis
    • suicidal thoughts and actions
    • thought problems such as confusion and memory issues
    • depression
    • encephalopathy (brain disease)
    • kidney stones
    • increased seizures when drug is stopped suddenly (when drug is used for seizure treatment)
  • Can occur with both Aimovig and Topamax:
    • serious allergic reactions

Effectiveness

The only purpose both Aimovig and Topamax are FDA-approved for is migraine prevention.

Treatment guidelines recommend Aimovig as an option for preventing episodic or chronic migraine headaches in people who:

  • can’t take other medications because of side effects or drug interactions
  • can’t reduce their number of monthly migraine headaches enough with other medications

Treatment guidelines recommend Topiramate as an option for preventing episodic migraine headaches.

Clinical studies have not directly compared the effectiveness of these two drugs in preventing migraine headaches. But the drugs have been studied separately.

Episodic migraine

Separate studies of Aimovig and Topamax showed that both drugs were effective in preventing episodic migraine headaches:

  • In Aimovig clinical studies, up to 50 percent of people with episodic migraine who received 140 mg cut their migraine days by at least half over six months of treatment. About 40 percent of people who received 70 mg saw similar results.
  • In clinical studies of people with episodic migraine who took Topamax, those aged 12 years and older had about two fewer migraine headaches each month. Children aged 12 through 17 with episodic migraine had three fewer migraine headaches each month.

Chronic migraine

Separate studies of the drugs showed that both Aimovig and Topamax were effective in preventing chronic migraine headaches:

  • In a three-month clinical study of Aimovig, about 40 percent of people with chronic migraine headaches who received either 70 mg or 140 mg had half as many migraine days or fewer after treatment.
  • In a study that looked at the results of several clinical trials found that in people with chronic migraine, Topamax reduced the number of migraine headaches or headaches by about five to nine each month.

Costs

Aimovig and Topamax are both brand-name medications. Brand-name medications usually cost more than generic medications. Aimovig is not available in a generic form, but Topamax comes as a generic called topiramate.

According to estimates from GoodRx.com, Topamax may cost more or less than Aimovig, depending on your dose. And topiramate, the generic form of Topamax, will cost less than either Topamax or Aimovig.

The actual price you would pay for any of these drugs would depend on your dose, your insurance plan, your location, and the pharmacy you use.

SIDE EFFECTS

Clinical Trials Experience

Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.

The safety of AIMOVIG has been evaluated in 2,537 patients with migraine who received at least one dose of AIMOVIG, representing 2,310 patient-years of exposure. Of these, 2,057 patients were exposed to 70 mg or 140 mg once monthly for at least 6 months, 1,198 patients were exposed for at least 12 months, and 287 patients were exposed for at least 18 months.

In placebo-controlled clinical studies (Studies 1, 2, and 3) of 2,184 patients, 787 patients received at least one dose of AIMOVIG 70 mg once monthly, 507 patients received at least one dose of AIMOVIG 140 mg once monthly, and 890 patients received placebo during 3 months or 6 months of double-blind treatment . Approximately 84% were female, 91% were white, and the mean age was 42 years at study entry.

The most common adverse reactions (incidence ≥ 3% and more often than placebo) in the migraine studies were injection site reactions and constipation. Table 1 summarizes the adverse reactions that occurred during the first 3 months in the migraine studies (Studies 1, 2, and 3).

Table 1: Adverse Reactions Occurring with an Incidence of at Least 2% for Either Dose of AIMOVIG and at Least 2% Greater than Placebo During the First 3 Months in Studies 1, 2, and 3

Adverse Reaction AIMOVIG 70 mg Once Monthly
N = 787 %
AIMOVIG 140 mg Once Monthly
N = 507 %
Placebo
N = 890 %
Injection site reactionsa 6 5 3
Constipation 1 3 1
Cramps, muscle spasms < 1 2 < 1
aInjection site reactions include multiple adverse reactions related terms, such as injection site pain and injection site erythema.

In Studies 1, 2, and 3, 1.3% of patients treated with AIMOVIG discontinued double-blind treatment because of adverse events. The most frequent injection site reactions were injection site pain, injection site erythema, and injection site pruritus.

Immunogenicity

As with all therapeutic proteins, there is potential for immunogenicity. The detection of antibody formation, including neutralizing antibodies, is highly dependent on the sensitivity and specificity of the assay. Additionally, the observed incidence of antibody (including neutralizing antibody) positivity in an assay may be influenced by several factors including assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies to erenumab-aooe in the studies described below with the incidence of antibodies in other studies or to other products may be misleading.

The immunogenicity of AIMOVIG has been evaluated using an immunoassay for the detection of binding anti-erenumab-aooe antibodies. For patients whose sera tested positive in the screening immunoassay, an in vitro biological assay was performed to detect neutralizing antibodies.

In controlled studies with AIMOVIG, the incidence of anti-erenumab-aooe antibody development was 6.2% (48/778) in patients receiving AIMOVIG 70 mg once monthly (2 of whom had in vitro neutralizing activity) and 2.6% (13/504) in patients receiving AIMOVIG 140 mg once monthly (none of whom had in vitro neutralizing activity). The neutralizing anti-erenumab-aooe antibody positive rate may be underestimated because of limitations of the assay. Although these data do not demonstrate an impact of anti-erenumab-aooe antibody development on the efficacy or safety of AIMOVIG in these patients, the available data are too limited to make definitive conclusions.

Read the entire FDA prescribing information for Aimovig (Erenumab-aooe Injection, for Subcutaneous Use)

Consumer medicine information

How to take AIMOVIG

Follow all directions given to you by your doctor or pharmacist carefully. They may differ from the information contained in this leaflet. If your doctor has prescribed AIMOVIG with another migraine medicine, follow your doctor’s instructions on how to use these medicines together.

If you do not understand the instructions on the box, ask your doctor or pharmacist for help.

How much to take

Each pen contains 70 mg or 140 mg AIMOVIG. The usual dose of Aimovig is 70 mg once every 4 weeks. Your doctor might also decide you need 140 mg once every 4 weeks. Take Aimovig exactly as instructed by your doctor.

70 mg/mL solution for injection
If your doctor prescribed the 70 mg dose you should have one injection once every 4 weeks in your abdomen, thigh or upper arm. If your doctor prescribed the 140 mg dose you should have two 70 mg injections once every 4 weeks. The second injection must be given immediately after the first.

140 mg/mL solution for injection
If your doctor prescribed the 140 mg dose, you will have one injection (subcutaneous) in your abdomen, thigh, or upper arm.

Make sure that you inject the entire contents of each pen.

How to take it

AIMOVIG is supplied in a pre-filled pen for single use. It is given as an injection under your skin (known as a subcutaneous injection). You or your caregiver can administer the injection into your abdomen, thigh or into the outer area of the upper arm (only if someone else is giving you the injection). Injection sites should be rotated and injections should not be given into areas where the skin is tender, bruised, red or hard.

Your doctor or nurse will give you or your caregiver training in the right way to prepare and inject AIMOVIG. Do not try to inject AIMOVIG until this training has been given.

Instructions for use of Aimovig pre-filled pen

Important: Needle is inside the pen

Single-Use Autoinjector/Pen 70 mg/mL

Single-Use Autoinjector/Pen 140 mg/mL

Step 1: Prepare

Your healthcare provider has prescribed a 70 mg or a 140 mg dose.

For a 70 mg dose, inject one autoinjector of 70 mg/mL.

For a 140 mg dose, inject either two autoinjectors of 70 mg/mL one after the other, or one autoinjector of 140 mg/mL if you were prescribed the 140 mg/mL formulation.

A) Carefully lift the pen(s) out of the carton

To avoid discomfort at the site of injection, leave the pen(s) at room temperature for at least 30 minutes before injecting.

Important:

  • Do not put the pen(s) back in the refrigerator once they have reached room temperature.
  • Do not try to warm the pen(s) by using a heat source such as hot water or microwave.
  • Do not leave the pen(s) in direct sunlight.
  • Do not shake the pen(s).
  • Do not remove the white cap from the pen(s) at this stage.

B) Inspect each pen

Make sure the solution you see in the window is clear and colourless to light yellow.

Important:

  • Do not use the pen if you notice that the solution contains easily visible particles, is cloudy or is distinctly yellow.
  • Do not use the pen if any part of it appears cracked or broken.
  • Do not use the pen if it has been dropped.
  • Do not use the pen if white or orange cap is missing or is not securely attached.
  • Do not use the pen after the expiry date stated on the label.

In all cases described above, use a new pen, and if you are unsure contact your doctor or pharmacist.

C) Gather all materials needed for the injection(s):

Wash your hands thoroughly with soap and water.

On a clean, well-lit work surface, place the:

  • One or two new pen(s)
  • Alcohol wipes
  • Cotton balls or gauze pads
  • Adhesive plasters
  • Sharps disposal container

D) Prepare and clean the injection site(s).

You can use any of the following injection sites:

  • Thigh
  • Stomach area (abdomen) (except for a 5 cm area around the navel)
  • Outer area of upper arm (only if someone else is giving you the injection)

Clean the injection site with an alcohol wipe and let the skin dry.

Choose a different site each time you give yourself an injection. If you need to use the same injection site, just make sure it is not the same spot on that site you used last time.

Important:

  • After you have cleaned the area, do not touch it again before injecting.
  • Do not choose an area where the skin is tender, bruised, red, or hard. Avoid injecting into a raised, thick, red or scaly skin patch or lesion, or areas with scars or stretch marks.

Step 2: Get ready

E) Pull the white or orange cap straight off, only when you are ready to inject. The injection must be administered within 5 minutes. It is normal to see a drop of liquid at the end of the needle or green or yellow safety guard.

Important:

  • Do not remove the white or orange cap from the pen until you are ready to inject.

  • Do not leave the white or orange cap off for more than 5 minutes. This can dry out the medicine.
  • Do not twist or bend the white orange cap.
  • Do not put the white or orange cap back onto the pen once it has been removed.

F) Stretch or pinch the injection site to create a firm surface.

Stretch method

Stretch skin firmly by moving your thumb and fingers in opposite directions, creating an area about five cm wide.

Or

Pinch method

Pinch skin firmly between your thumb and fingers, creating an area about five cm wide.

Important:

Keep skin stretched or pinched while injecting.

Step 3: Inject

G) Keep holding the stretch or pinch. With the white or orange cap off, place the pen on the skin at an angle of 90 degrees.

Important:

Do not touch the purple or grey start button yet.

H) Firmly push the pen down onto the skin until it stops moving.

Important: You must push all the way down but do not touch the purple or grey start button until you are ready to inject.

I) When you are ready to inject, press the purple or grey start button.

You will hear a click.

J) Keep pushing down on the skin. The injection could take about 15 seconds.

Important: Window turns yellow when injection is completed.

Note: After you remove the pen from the skin, the needle will automatically be covered by the green or yellow safety guard.

Important: When you remove the pen, if the window has not turned yellow, or if it looks like the medicine is still injecting, this means you have not received a full dose.

Contact your doctor immediately.

Step 4: Finish

K) Discard the used pen and the white or orange cap.

Put the used pen in a sharps disposal container immediately after use. Talk to your doctor or pharmacist about proper disposal. There may be local regulations for disposal.

Important:

  • Do not reuse the pen.
  • Do not recycle the pen or sharps disposal container, or throw them into household waste.

Always keep the sharps disposal container out of the sight and reach of children.

L) Examine the injection site.

If there is a small sign of blood, press a cotton ball or gauze pad onto the injection site. Do not rub the injection site. Apply an adhesive plaster if needed.

If you have been prescribed a 140 mg dose using two 70 mg/mL pens, a second injection is required. Repeat all steps with the second pen to inject the full 140 mg dose.

When to take it

The usual dose of Aimovig is 70 mg once every 4 weeks. Your doctor might also decide you need 140 mg once every 4 weeks. Take Aimovig exactly as instructed by your doctor. Each pen contains 70 mg or 140 mg AIMOVIG.

How long to take it

Continue taking your medicine for as long as your doctor tells you.

You should see your doctor after you have been using AIMOVIG for 8 to 12 weeks to discuss whether you should keep using AIMOVIG or whether your dose should be changed. You should continue to see your doctor every 3 to 6 months while taking AIMOVIG.

If you forget to take it

Take it as soon as you remember, and then contact your doctor, who will tell you when you should schedule your next dose. Follow the new schedule exactly as your doctor has told you.

Do not take a double dose to make up for the dose that you missed.

If you are not sure what to do, ask your doctor or pharmacist.

If you have trouble remembering to take your medicine, ask your pharmacist for some hints.

If you take too much (overdose)

Immediately telephone your doctor or the Poisons Information Centre (telephone 13 11 26) for advice if you think that you or anyone else may have taken too much AIMOVIG. Do this even if there are no signs of discomfort or poisoning.

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