Mavacamten 10mg capsules
Requires a prescription from a doctor or prescriber
Mavacamten is a myosin inhibitor indicated for the treatment of adults with symptomatic New York Heart Association (NYHA) class II-III obstructive hypertrophic cardiomyopathy (HCM).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Mavacamten
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Mavacamten
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Mavacamten on the MHRA register
Camzyos 10mg capsules
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 24 · Randomised trials: 5 · 2020–2026
Showing the 50 most relevant studies, sorted by most relevant.
I. Olivotto, A. Oreziak, R. Barriales-Villa, et al.
Lancet, 2020
M. Desai, A. Owens, K. Wolski, et al.
JAMA cardiology, 2023
Ayesha Aman, Arfa Akram, Bisma Akram, et al.
Open Heart, 2025
Pavan Kumar Reddy Kalluru, S. Siddenthi, S. S. Valisekka, et al.
Heart international, 2025
Introduction Hypertrophic cardiomyopathy (HCM) is characterised by unusual thickening of the interventricular septum leading to dynamic left ventricular outflow tract obstruction, mitral valve regurgitation, impaired diastolic function and arrhythmias. Mavacamten (MYK-461) is a first-in-class, selective allosteric modulator of cardiac myosin adenosine triphosphatase and received US Food and Drug Administration (FDA) approval on 28 April 2022 to treat symptomatic obstructive HCM (oHCM). Methods A systematic search of Medline/PubMed and ClinicalTrials. gov was conducted using advanced search strategies with the terms 'mavacamten/MYK-461' and 'hypertrophic cardiomyopathy/HCM' to identify and include all clinical trials published to date. Results The clinical efficacy of mavacamten has been consistently demonstrated in the PIONEER-HCM, MAVERICK-HCM, EXPLORER-HCM, VALOR-HCM, EXPLORER-CN-HCM and HORIZON-HCM clinical trials - there was a notable decrease in the left ventricular outflow tract gradient. Apart from the MAVERICK experiment, which revealed no discernible change in functional class or peak volume of oxygen uptake (pVO2) in non-oHCM patients, improvements were reported in New York Heart Association functional class, pVO2 and quality-of-l ife metrics. Except for the PIONEER trial, which didn't report biomarker data such as N-terminal pro B-type natriuretic peptide (NT-proBNP) and troponins, mavacamten significantly reduced biomarkers in all investigations. Additionally, the VALOR trial showed that there was a reduced need for septal reduction therapy. Although systolic dysfunction is a major safety risk that requires careful monitoring, mavacamten was generally well tolerated. Conclusion Mavacamten offered a promising, non-invasive pharmacological therapy for patients with symptomatic oHCM, particularly for those who are not candidates for or who have failed conventional treatments.
Abstract licence: CC BY-NC
Zina Otmani, Noura Abdrabou, H. El-Sayed, et al.
Indian Heart Journal, 2025
Areeba Memon, Muhammad Omar Larik, Zoha Khan, et al.
Future Science OA, 2023
Carolina Bernardes, João Gomes Carvalho, Patrícia Rodrigues, et al.
Monaldi Archives for Chest Disease, 2025
Li Zheng, Xiaotong Gu, Yumiao Chen, et al.
Reviews in Cardiovascular Medicine, 2024
Mehrdad Rabiee Rad, Ghazal Ghasempour Dabaghi, Danial Habibi
The Egyptian Heart Journal, 2023
Network Meta-Analysis of, Mavacamten Aficamten, Imran Saleh, et al.
Bioscientia Medicina : Journal of Biomedicine and Translational Research, 2025
Background: Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterized by myocardial hypercontractility. Mavacamten and aficamten are first-in-class cardiac myosin inhibitors that have demonstrated efficacy in treating obstructive HCM. However, in the absence of direct head-to-head randomized controlled trials (RCTs), their comparative effectiveness and safety remain unquantified. We aimed to indirectly compare the efficacy and safety of mavacamten and aficamten in patients with obstructive HCM. Methods: We conducted a systematic review and Bayesian network meta-analysis of RCTs. We searched PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials from inception to December 2024. Eligible studies were RCTs comparing mavacamten or aficamten with placebo in adults with obstructive HCM. The primary efficacy outcomes were the change from baseline in post-exercise left ventricular outflow tract (LVOT) gradient and the change in peak oxygen consumption (pVO₂). The primary safety outcome was the incidence of left ventricular ejection fraction (LVEF) reduction to <50%. Results: Seven RCTs involving 1,025 patients were included. In the network meta-analysis, both aficamten (Mean Difference [MD], -50.8 mmHg; 95% Credible Interval [CrI], -61.2 to -40.4) and mavacamten (MD, -44.9 mmHg; 95% CrI, -53.7 to -36.1) were significantly more effective than placebo in reducing post-exercise LVOT gradient. The indirect comparison between the two agents did not reveal a statistically significant difference (MD, -5.9 mmHg; 95% CrI, -17.8 to 6.0). For pVO₂, both mavacamten and aficamten showed significant improvement over placebo, with no significant difference between them. The odds of LVEF dropping below 50% were numerically higher with mavacamten compared to aficamten, but the difference was not statistically significant (Odds Ratio [OR], 1.52; 95% CrI, 0.65 to 3.54). Conclusion: Mavacamten and aficamten are both highly effective in improving hemodynamic and functional parameters in patients with obstructive HCM. While our indirect comparison did not establish the superiority of one agent over the other, it provides foundational evidence for clinicians. Definitive conclusions await direct head-to-head clinical trials.
Abstract licence: CC BY-NC-SA
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
6-9 days
Mechanism
Myosin is a family of enzymes that can produce mechanical output by an ATP-mediated cyclic interaction with actin.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
85%
[L41680]…
Half-life
6-9 days
Protein binding
98%
[L41680]
Volume of distribution
9.5 L/kg
Metabolism
74%
[L41680]
Elimination
25 mg
[L41680]…
Clearance
4.9 mL/min/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L41680][L44106][L47466]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1031 interactions
In healthy subjects, doses of up to 25 mg have been administered for up to 25 days, with 3 of 8 participants treated at the 25-mg dose level experiencing 20% or greater reductions in LVEF. An infant's death was reported after accidental ingestion of three 15-mg capsules.
[L41680]
Systolic dysfunction is the most likely result of overdosage of CAMZYOS. Treatment of overdose with CAMZYOS consists of discontinuation of CAMZYOS treatment as well as medically supportive measures to maintain hemodynamic stability, including close monitoring of vital signs and LVEF and management of the clinical status of the patient.
Overdose in humans can be life-threatening and result in asystole refractory to any medical intervention.
[L41680]
Mavacamten was not genotoxic in a bacterial reverse mutation test (Ames test), a human in vitro lymphocyte clastogenicity assay, or a rat in vivo micronucleus assay. There was no evidence of carcinogenicity seen in a 6-month rasH2 transgenic mouse study at mavacamten doses of up to 2.0 mg/kg/day in males and 3.0 mg/kg/day in females, which resulted in exposures (AUC) that were 1.8- and 3-fold in males and females, respectively, compared to AUC exposures in humans at the MRHD.
[L41680]
In reproductive toxicity studies, there was no evidence of the effects of mavacamten on mating and fertility in male or female rats at doses up to 1.2 mg/kg/day, or on the viability and fertility of offspring of dams dosed up to 1.5 mg/kg/day. Plasma exposure (AUC) of mavacamten at the highest dose tested was the same as in humans at the MRHD.
[L41680]
The safety of mavacamten has been evaluated in rats and dogs at multiple dose levels (0.06 to 10 mg/kg/day) orally.
Noted toxicities, including echocardiographic findings, reduction in systolic function, cardiac dilation, and death, as well as increased heart weights in rats, were consistent with mavacamten’s mechanism of action and primary pharmacological activity. Other findings included cardiac osseous metaplasia in rats and QTc prolongation in dogs. Plasma exposures (AUC) at the NOAEL in rats and dogs were 0.1 and 0.3 times, respectively, human exposure (AUC) at the MRHD.
[L41680]
Mavacamten reduces sarcomere hypercontractility by acting as an allosteric and reversible modulator of the beta-cardiac isoform of myosin to reduce its ATPase activity, thus reducing actin-myosin cross bridging.[A248285] Specifically, mavacamten inhibits the phosphate release, the cycle's rate-limiting step, without affecting the ADP release rate in actin-bound myosin.[A247155]Also, mavacamten inhibits binding of ADP-bound myosin to actin as well as ADP release to prime the myosin head to initiate turnover.[A247120]Recently, it was also discovered when myosin is not in its active state to interact with actin, it exists in equilibrium between 2 energy sparing states: a disordered relaxed state, where interaction between actin and myosin by the thin filament regulatory proteins, and a super relaxed state, where significant myosin head-to-head interaction lengthen ATP turnover rate.[A248430][A248435]. Mavacamten's binding to myosin can shift the equilibrium toward the super relaxed state, effectively exerting both a basal and actin-activated ATP inhibition.[A248430][L41680]
In the EXPLORER-HCM trial, patients achieved reductions in mean resting and provoked (Valsalva) LVOT gradient by Week 4 which were sustained throughout the 30-week trial. At Week 30, the mean (SD) changes from baseline in resting and Valsalva LVOT gradients were -39 (29) mmHg and -49 (34) mmHg, respectively, for the CAMZYOS group and -6 (28) mmHg and -12 (31) mmHg, respectively, for the placebo group. The reductions in the Valsalva LVOT gradient were accompanied by decreases in LVEF, generally within the normal range. Eight weeks after discontinuation of CAMZYOS, mean LVEF and Valsalva LVOT gradients were similar to baseline.[L41680]
Echocardiographic measurements of the cardiac structure showed a mean (SD) reduction from baseline at Week 30 in left ventricular mass index (LVMI) in the mavacamten group (-7.4 [17.8] g/m2) versus an increase in LVMI in the placebo group (8.9 [15.3] g/m2). There was also a mean (SD) reduction from baseline in left atrial volume index (LAVI) in the mavacamten group(-7.5 [7.8] mL/m2) versus no change in the placebo group (-0.1 [8.7] mL/m2). The clinical significance of these findings is unknown.[L41680]
A reduction in a biomarker of cardiac wall stress, NT-proBNP, was observed by Week 4 and sustained through the end of treatment.
At Week 30 compared with baseline, the reduction in NT-proBNP after mavacamten treatment was 80% greater than for placebo (proportion of geometric mean ratio between the two groups, 0.20 [95% CI: 0.17, 0.24]). The clinical significance of these findings is unknown.[L41680]
In healthy volunteers receiving multiple doses of mavacamten, a concentration-dependent increase in the QTc interval was observed at doses up to 25 mg once daily. No acute QTc changes have been observed at similar exposures during single-dose studies. The mechanism of the QT prolongation effect is not known. A meta-analysis across clinical studies in HCM patients does not suggest clinically relevant increases in the QTc interval in the therapeutic exposure range. In HCM, the QT interval may be intrinsically prolonged due to the underlying disease, in association with ventricular pacing, or in association with drugs with the potential for QT prolongation commonly used in the HCM population. The effect of coadministration of mavacamten with QT-prolonging drugs or in patients with potassium channel variants resulting in a long QT interval has not been characterized.[L41680]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L41680]
Mavacamten exposures (AUC) increased up to 220% in patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment. The effect of severe (Child-Pugh C) hepatic impairment is unknown.
[L41680]
[L41680]
[L41680]
[A247155]
[L41680]
[L41680]
[A247155]
Assuming a one-compartment model, using simple allometric scaling of unbound blood clearance of mouse, rat, dog, and cynomolgus monkey, human plasma clearance of mavacamten is estimated to be 0.51 mL/min/kg.
[A247155]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC C01EB24
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Mavacamten
Additional database identifiers
Drugs Product Database (DPD)
23802
ChemSpider
57876199
PDB
XB2
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7577
GeneCards
MYH7
GenBank Gene Database
M58018
GenBank Protein Database
179510
UniProt Accession
MYH7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q105337531), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.