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MYK-461 (Mavacamten) Cardiac Myosin Modulator

Cat.No.S8861

Mavacamten (MYK-461, SAR439152) is a small-molecule modulator of cardiac myosin that targets the underlying sarcomere hypercontractility of hypertrophic cardiomyopathy (HCM), one of the most prevalent heritable cardiovascular disorders.
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Quality Control

Batch: Purity: 99.92%
99.92

Solubility

In vitro
Batch:

DMSO : 55 mg/mL (201.22 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 5 mg/mL

Water : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 273.33 Formula

C15H19N3O2

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 1642288-47-8 -- Storage of Stock Solutions

Synonyms SAR439152 SMILES CC(C)N1C(=O)C=C(NC1=O)NC(C)C2=CC=CC=C2

Read more about storage stability stock solution CAS number SMILES

Mechanism of Action

In vitro

Mavacamten (MYK-461) primarily reduces the steady-state ATPase activity by inhibiting the rate of phosphate release of β-cardiac myosin-S1. This compound modulates multiple steps of the myosin chemomechanical cycle. In addition to decreasing the rate-limiting step of the cycle (phosphate release), it reduces the number of myosin-S1 heads that can interact with the actin thin filament during transition from the weakly to the strongly bound state without affecting the intrinsic rate. It also decreases the rate of myosin binding to actin in the ADP-bound state and the ADP-release rate from myosin-S1 alone.

In vivo

In mice harboring heterozygous human mutations in the myosin heavy chain, early, chronic administration of Mavacamten (MYK-461) suppresses the development of ventricular hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertrophic and profibrotic gene expression.

References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT07120776 RECRUITING
Hypertrophic Obstructive Cardiomyopathy \(HOCM\); Left Ventricular Outflow Tract Obstruction; Myocardial Ischaemia
University of Manchester
2026-03-26
NCT07004972 ACTIVE_NOT_RECRUITING
Symptomatic Obstructive Hypertrophic Cardiomyopathy
Bristol-Myers Squibb
2025-09-04 PHASE4
NCT07600177 RECRUITING
Hypertrophic Cardiomyopathy (HCM)
Oregon Health and Science University
2026-05-05 PHASE4
NCT07077005 RECRUITING
Cardiomyopathy, Hypertrophic
Technical University of Munich
2025-11-01
NCT06112743 ACTIVE_NOT_RECRUITING
Cardiomyopathy, Hypertrophic
Bristol-Myers Squibb
2024-01-24 PHASE4
NCT07103655 NOT_YET_RECRUITING
Hypertrophic Cardiomyopathy (HCM)
Second Affiliated Hospital, Zhejiang University, School of Medicine
2026-01-01 PHASE4

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