U.S. Full Prescribing Information, including Boxed WARNING

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Consider the Full Impact of Symptom Burden for Patients With Obstructive HCM When Choosing Treatment

Obstructive HCM can affect more than the heart—symptoms can take a toll on day-to-day activities1

Patients with symptomatic oHCM may present with chest pain, fatigue, exertional dyspnea, palpitations, dizziness, and syncope.2 Symptom progression can be gradual — patients may be doing worse than they realize by adapting their daily routine to manage their condition.2-5 These adaptations can result in patients living according to their limitations and also make recognition of symptoms more difficult.1,4 Ultimately, their decreased physical activity and anxiety over the condition can have a negative influence on a patient’s quality of life.1

Because HCM is estimated to be underdiagnosed* there may be more people with the condition than suspected.6 Currently, the estimated prevalence of HCM ranges between 1 in 200† to 1 in 500‡ people in the general population.7,8 The majority of HCM cases are obstructive and among these patients, 66% are symptomatic.9 When patients are diagnosed it may be as late as young adulthood, or in mid-life, (median age at diagnosis, 45.8 years, SHaRe Registry) when the disease has progressed.10

This can result in serious complications such as NYHA Class III/IV heart failure (~43%), atrial fibrillation (18-28%), stroke or other thromboembolism (~6%), and rarely, sudden cardiac death (<1%/year).11-13 Obstructive HCM can even progress while patients are on treatment which can also contribute to these complications.14

HCM=hypertrophic cardiomyopathy; oHCM=obstructive HCM.

  • *Estimated undiagnosed range is calculated using the prevalence range of 1:200 to 1:500, the estimated US population (334,668,850 in April 2023), and the estimated diagnosed population (~100,000) based on 2013 ICD-9 claims data.6
  • †The 2015 Semsarian publication identified that the prevalence of HCM gene carriers could be as high as 1:200.7
  • ‡The CARDIA study (published in 1995) was a multicenter, US-population-based echocardiography study of 4111 subjects (aged 23-35) that identified the prevalence of HCM as 1:500 people in the general population.6

When Dani was diagnosed with symptomatic obstructive HCM, she was first prescribed an oral medication. When her symptoms and obstruction didn’t improve she eventually needed open-heart surgery, a myectomy.

Her symptoms did improve initially but within a matter of months, Dani was symptomatic again, and her obstruction had returned. How would you counsel a patient like Dani?

Dani was compensated for
her time.

CAMZYOS (mavacamten) Patient Dani
HCP Monitoring Patient Icon

Without your help, patients may overlook the impact that obstructive HCM has had on their lives5

HCP Monitoring Patient Icon

Because some people adapt their lifestyle to symptomatic obstructive HCM, ask patients or their care partners about their limitations of activity to get a complete picture of disease severity4,5

  • How is symptomatic obstructive HCM limiting them?
  • What activities are they cutting back on or stopping?
  • How often do you experience palpitations, dizziness, or chest pain?
  • What do they want and expect out of treatment?

AHA/ACC guidelines on HCM recommend shared decision-making between
the healthcare provider and patient to manage their condition2

ACC=American College of Cardiology; AHA=American Heart Association.

You can provide patients the possibility of symptom reduction and improved function, regardless of where they are in their journey with obstructive HCM2,15

Recommendation from AHA/ACC/Multisociety Guideline for the Management of Hypertrophic Cardiomyopathy2

Recommended treatments for symptomatic obstructive HCM

Pills Icon

Conventional2

The role of 1L treatment options recommended in the AHA/ACC/MS Guideline is that of symptom management. Due to limited evidence from randomized controlled trials, management is often based on nonrandomized or limited data.

Target Icon

CAMZYOS2,15,16

Uniquely targets the source of obstructive HCM.§ The first and only FDA-approved cardiac myosin inhibitor to have a Class 1 recommendation when symptoms persist on 1L therapy. Studied with and without background therapy in 2 phase 3 trials and their ongoing long-term extensions.

Scalpel Icon

Invasive2

Guideline-recommended septal reduction therapy for patients whose symptoms are not relieved by 1L pharmacological therapy.

  • §CAMZYOS is an allosteric and reversible inhibitor selective for cardiac myosin that helps to modulate the number of myosin heads in the off state. This reduces the number of myosin-actin cross-bridges that form.15
  • Symptoms include effort-related dyspnea or chest pain and occasionally other exertional symptoms (eg, syncope, near syncope) that are attributed to LVOTO and interfere with everyday activity or quality of life despite beta blocker or nondihydropyridine calcium channel blocker.2

LTE=long-term extension.

Consider the next step—complement conventional therapy with CAMZYOS15

See how CAMZYOS works >

3500-US-2400470  12/24

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Important Safety
Information
WARNING: RISK OF HEART FAILURE

CAMZYOSTM (mavacamten) reduces left ventricular ejection fraction (LVEF) and can cause heart failure due to systolic dysfunction.

Echocardiogram assessments of LVEF are required prior to and during treatment with CAMZYOS. Initiation of CAMZYOS in patients with LVEF <55% is not recommended. Interrupt CAMZYOS if LVEF is <50% at any visit or if the patient experiences heart failure symptoms or worsening clinical status.

Concomitant use of CAMZYOS with certain cytochrome P450 inhibitors or discontinuation of certain cytochrome P450 inducers may increase the risk of heart failure due to systolic dysfunction; therefore, the use of CAMZYOS is contraindicated with the following:

  • Moderate to strong CYP2C19 inhibitors or strong CYP3A4 inhibitors
  • Moderate to strong CYP2C19 inducers or moderate to strong CYP3A4 inducers

Because of the risk of heart failure due to systolic dysfunction, CAMZYOS is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the CAMZYOS REMS PROGRAM.

CONTRAINDICATIONS

CAMZYOS is contraindicated with concomitant use of:

  • Moderate to strong CYP2C19 inhibitors or strong CYP3A4 inhibitors
  • Moderate to strong CYP2C19 inducers or moderate to strong CYP3A4 inducers
WARNINGS AND PRECAUTIONS

Heart Failure

CAMZYOS reduces systolic contraction and can cause heart failure or totally block ventricular function. Patients who experience a serious intercurrent illness (e.g., serious infection) or arrhythmia (e.g., atrial fibrillation or other uncontrolled tachyarrhythmia) are at greater risk of developing systolic dysfunction and heart failure.

Assess the patient’s clinical status and LVEF prior to and regularly during treatment and adjust the CAMZYOS dose accordingly. New or worsening arrhythmia, dyspnea, chest pain, fatigue, palpitations, leg edema, or elevations in N-terminal pro-B-type natriuretic peptide (NT-proBNP) may be signs and symptoms of heart failure and should also prompt an evaluation of cardiac function.

Asymptomatic LVEF reduction, intercurrent illnesses, and arrhythmias require additional dosing considerations.

Initiation of CAMZYOS in patients with LVEF <55% is not recommended. Avoid concomitant use of CAMZYOS in patients on disopyramide, ranolazine, verapamil with a beta blocker, or diltiazem with a beta blocker as these medications and combinations increase the risk of left ventricular systolic dysfunction and heart failure symptoms and clinical experience is limited.

CYP 450 Drug Interactions Leading to Heart Failure or Loss of Effectiveness

CAMZYOS is primarily metabolized by CYP2C19 and CYP3A4 enzymes. Concomitant use of CAMZYOS and drugs that interact with these enzymes may lead to life-threatening drug interactions such as heart failure or loss of effectiveness.

Advise patients of the potential for drug interactions, including with over-the-counter medications (such as omeprazole, esomeprazole, or cimetidine). Advise patients to inform their healthcare provider of all concomitant products prior to and during CAMZYOS treatment.

CAMZYOS Risk Evaluation and Mitigation Strategy (REMS) Program

CAMZYOS is only available through a restricted program called the CAMZYOS REMS Program because of the risk of heart failure due to systolic dysfunction. Notable requirements of the CAMZYOS REMS Program include the following:

  • Prescribers must be certified by enrolling in the REMS Program.
  • Patients must enroll in the REMS Program and comply with ongoing monitoring requirements.
  • Pharmacies must be certified by enrolling in the REMS Program and must only dispense to patients who are authorized to receive CAMZYOS.
  • Wholesalers and distributors must only distribute to certified pharmacies.

Further information is available at www.CAMZYOSREMS.com or by telephone at 1-833-628-7367.

Embryo-Fetal Toxicity

CAMZYOS may cause fetal toxicity when administered to a pregnant female, based on animal studies. Confirm absence of pregnancy in females of reproductive potential prior to treatment and advise patients to use effective contraception during treatment with CAMZYOS and for 4 months after the last dose. CHCs containing a combination of ethinyl estradiol and norethindrone may be used with CAMZYOS. However, CAMZYOS may reduce the effectiveness of certain other combined hormonal contraceptives (CHC). If these CHCs are used, advise patients to add nonhormonal contraception (such as condoms) during concomitant use and for 4 months after the last dose of CAMZYOS.

ADVERSE REACTIONS

In the EXPLORER-HCM trial, adverse reactions occurring in >5% of patients and more commonly in the CAMZYOS group than in the placebo group were dizziness (27% vs 18%) and syncope (6% vs 2%). There were no new adverse reactions identified in VALOR-HCM.

Effects on Systolic Function

In the EXPLORER-HCM trial, mean (SD) resting LVEF was 74% (6) at baseline in both treatment groups. Mean (SD) absolute change from baseline in LVEF was -4% (8) in the CAMZYOS group and 0% (7) in the placebo group over the 30-week treatment period. At Week 38, following an 8-week interruption of trial drug, mean LVEF was similar to baseline for both treatment groups. In the EXPLORER-HCM trial, 7 (6%) patients in the CAMZYOS group and 2 (2%) patients in the placebo group experienced reversible reductions in LVEF <50% (median 48%: range 35-49%) while on treatment. In all 7 patients treated with CAMZYOS, LVEF recovered following interruption of CAMZYOS.

DRUG INTERACTIONS

Potential for Other Drugs to Affect Plasma Concentrations of CAMZYOS

CAMZYOS is primarily metabolized by CYP2C19 and to a lesser extent by CYP3A4 and CYP2C9. Inducers and inhibitors of CYP2C19 and moderate to strong inhibitors or inducers of CYP3A4 may affect the exposures of CAMZYOS.

Impact of Other Drugs on CAMZYOS:

  • Moderate to Strong CYP2C19 Inhibitors or Strong CYP3A4 Inhibitors: Concomitant use increases CAMZYOS exposure, which may increase the risk of heart failure due to systolic dysfunction. Concomitant use is contraindicated.
  • Moderate to Strong CYP2C19 Inducers or Moderate to Strong CYP3A4 Inducers: Concomitant use decreases CAMZYOS exposure, which may reduce CAMZYOS’ efficacy. The risk of heart failure due to systolic dysfunction may increase with discontinuation of these inducers as the levels of induced enzyme normalizes. Concomitant use is contraindicated.
  • Weak CYP2C19 Inhibitors or Moderate CYP3A4 Inhibitors: Concomitant use with a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor increases CAMZYOS exposure, which may increase the risk of adverse drug reactions. Initiate CAMZYOS at the recommended starting dose of 5 mg orally once daily in patients who are on stable therapy with a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor. Reduce dose of CAMZYOS by one level (i.e., 15 to 10 mg, 10 to 5 mg, or 5 to 2.5 mg) in patients who are on CAMZYOS treatment and intend to initiate a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor. Schedule clinical and echocardiographic assessment 4 weeks after inhibitor initiation, and do not up-titrate CAMZYOS until 12 weeks after inhibitor initiation. Avoid initiation of concomitant weak CYP2C19 and moderate CYP3A4 inhibitors in patients who are on stable treatment with 2.5 mg of CAMZYOS because a lower dose is not available.

Potential for CAMZYOS to Affect Plasma Concentrations of Other Drugs

CAMZYOS is an inducer of CYP3A4, CYP2C9, and CYP2C19. Concomitant use with CYP3A4, CYP2C9, or CYP2C19 substrates may reduce plasma concentration of these drugs. Closely monitor when CAMZYOS is used with concomitant CYP3A4, CYP2C9, or CYP2C19 substrates unless otherwise recommended in the Prescribing Information.

Certain Combined Hormonal Contraceptives (CHC): Progestin and ethinyl estradiol are CYP3A4 substrates. Concomitant use of CAMZYOS may decrease exposures of certain progestins, which may lead to contraceptive failure. CHCs containing a combination of ethinyl estradiol and norethindrone may be used with CAMZYOS, but if other CHCs are used, advise patients to add nonhormonal contraception (such as condoms) during concomitant use and 4 months after the last dose of CAMZYOS.

Drugs That Reduce Cardiac Contractility

Expect additive negative inotropic effects of CAMZYOS and other drugs that reduce cardiac contractility. Avoid concomitant use of CAMZYOS in patients on disopyramide, ranolazine, verapamil with a beta blocker, or diltiazem with a beta blocker as these medications and combinations increase the risk of left ventricular systolic dysfunction and heart failure symptoms and clinical experience is limited.

If concomitant therapy with a negative inotrope is initiated, or if the dose of a negative inotrope is increased, monitor LVEF closely until stable doses and clinical response have been achieved.

SPECIFIC POPULATIONS

Pregnancy

CAMZYOS may cause fetal harm when administered to a pregnant female. Advise pregnant females about the potential risk to the fetus with maternal exposure to CAMZYOS during pregnancy. There is a pregnancy safety study for CAMZYOS. If CAMZYOS is administered during pregnancy, or if a patient becomes pregnant while receiving CAMZYOS or within 4 months after the last dose of CAMZYOS, healthcare providers should report CAMZYOS exposure by contacting Bristol Myers Squibb at 1-800-721-5072 or www.bms.com.

Lactation

The presence of CAMZYOS in human or animal milk, the drug’s effects on the breastfed infant, or the effects on milk production are unknown. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for CAMZYOS and any potential adverse effects on the breastfed child from CAMZYOS or from the underlying maternal condition.

Females and Males of Reproductive Potential

Confirm absence of pregnancy in females of reproductive potential prior to initiation of CAMZYOS. Advise females of reproductive potential to use effective contraception during treatment with CAMZYOS and for 4 months after the last dose. CHCs containing a combination of ethinyl estradiol and norethindrone may be used with CAMZYOS. However, CAMZYOS may reduce the effectiveness of certain other combined hormonal contraceptives (CHC). If these CHCs are used, advise patients to add nonhormonal contraception (such as condoms) during concomitant use and for 4 months after the last dose of CAMZYOS.

INDICATION

CAMZYOS® (mavacamten) is indicated for the treatment of adults with symptomatic New York Heart Association (NYHA) class II-III obstructive hypertrophic cardiomyopathy (HCM) to improve functional capacity and symptoms.

CAMZYOS is available in 2.5 mg, 5 mg, 10 mg, and 15 mg capsules.

Please see US Full Prescribing Information, including Boxed WARNING.

References:

  1. Zaiser E, Sehnert AJ, Duenas A, Saberi S, Brookes E, Reaney M. Patient experiences with hypertrophic cardiomyopathy: a conceptual model of symptoms and impacts on quality of life. J Patient Rep Outcomes. 2020;4(1):102.
  2. Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy: a report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/CIR.0000000001250
  3. Naidu SS, ed. Hypertrophic Cardiomyopathy. London, Eng: Springer-Verlag; 2015.
  4. Jacoby DL, DePasquale EC, McKenna WJ. Hypertrophic cardiomyopathy: diagnosis, risk stratification and treatment. CMAJ. 2013;185(2):127-134.
  5. Borsari W, Davis L, Meiers E, Salberg L, Barbara McDonough. Living with hypertrophic cardiomyopathy: a patient’s perspective. Future Cardiol. 2022;18(1):43-50. doi:10.2217/fca-2021-0091
  6. Maron MS, Hellawell JL, Lucove JC, Farzaneh-Far R, Olivotto I. Occurrence of clinically diagnosed hypertrophic cardiomyopathy in the United States. Am J Cardiol. 2016;117(10):1651-1654.
  7. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation. 1995;92(4):785-789.
  8. Semsarian C, Ingles J, Maron MS, Maron BJ. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll Cardiol. 2015;65(12):1249-1254.
  9. Data on file. BMS-REF-MAVA-0025. Princeton, NJ: Bristol-Myers Squibb; 2022.
  10. Ho CY, Day SM, Ashley EA, et al. Genotype and lifetime burden of disease in hypertrophic cardiomyopathy: insights from the Sarcomeric Human Cardiomyopathy Registry (SHaRe). Circulation. 2018;138(14):1387-1398. doi:10.1161/CIRCULATIONAHA.117.033200
  11. Rowin EJ, Maron MS, Chan RH, et al. Interaction of adverse disease related pathways in hypertrophic cardiomyopathy. Am J Cardiol. 2017;120(12):2256-2264.
  12. MacIntyre C, Lakdawala NK. Management of atrial fibrillation in hypertrophic cardiomyopathy. Circulation. 2016;133(19):1901-1905.
  13. Maron BJ, Olivotto I, Bellone P, et al. Clinical profile of stroke in 900 patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2002;39(2):301-307.
  14. Palandri C, Santini L, Argirò A, et al. Pharmacological management of hypertrophic cardiomyopathy: from bench to bedside. Drugs. 2022;82(8):889-912. doi:10.1007/s40265-022-01728-w
  15. CAMZYOS [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2024.
  16. Garcia-Pavia P, Oreziak A, Masri A, et al. Long-term effect of mavacamten in obstructive hyptertrophic cardiomyopathy. Eur Heart J. 2024; ehae579. doi:10.1093/eurheartj/ehae579
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References:

  1. Zaiser E, Sehnert AJ, Duenas A, Saberi S, Brookes E, Reaney M. Patient experiences with hypertrophic cardiomyopathy: a conceptual model of symptoms and impacts on quality of life. J Patient Rep Outcomes. 2020;4(1):102.
  2. Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy: a report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/CIR.0000000001250
  3. Naidu SS, ed. Hypertrophic Cardiomyopathy. London, Eng: Springer-Verlag; 2015.
  4. Jacoby DL, DePasquale EC, McKenna WJ. Hypertrophic cardiomyopathy: diagnosis, risk stratification and treatment. CMAJ. 2013;185(2):127-134.
  5. Borsari W, Davis L, Meiers E, Salberg L, Barbara McDonough. Living with hypertrophic cardiomyopathy: a patient’s perspective. Future Cardiol. 2022;18(1):43-50. doi:10.2217/fca-2021-0091
  6. Maron MS, Hellawell JL, Lucove JC, Farzaneh-Far R, Olivotto I. Occurrence of clinically diagnosed hypertrophic cardiomyopathy in the United States. Am J Cardiol. 2016;117(10):1651-1654.
  7. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation. 1995;92(4):785-789.
  8. Semsarian C, Ingles J, Maron MS, Maron BJ. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll Cardiol. 2015;65(12):1249-1254.
  9. Data on file. BMS-REF-MAVA-0025. Princeton, NJ: Bristol-Myers Squibb; 2022.
  10. Ho CY, Day SM, Ashley EA, et al. Genotype and lifetime burden of disease in hypertrophic cardiomyopathy: insights from the Sarcomeric Human Cardiomyopathy Registry (SHaRe). Circulation. 2018;138(14):1387-1398. doi:10.1161/CIRCULATIONAHA.117.033200
  11. Rowin EJ, Maron MS, Chan RH, et al. Interaction of adverse disease related pathways in hypertrophic cardiomyopathy. Am J Cardiol. 2017;120(12):2256-2264.
  12. MacIntyre C, Lakdawala NK. Management of atrial fibrillation in hypertrophic cardiomyopathy. Circulation. 2016;133(19):1901-1905.
  13. Maron BJ, Olivotto I, Bellone P, et al. Clinical profile of stroke in 900 patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2002;39(2):301-307.
  14. Palandri C, Santini L, Argirò A, et al. Pharmacological management of hypertrophic cardiomyopathy: from bench to bedside. Drugs. 2022;82(8):889-912. doi:10.1007/s40265-022-01728-w
  15. CAMZYOS [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2024.
  16. Garcia-Pavia P, Oreziak A, Masri A, et al. Long-term effect of mavacamten in obstructive hyptertrophic cardiomyopathy. Eur Heart J. 2024; ehae579. doi:10.1093/eurheartj/ehae579
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