Mutations in β-cardiac myosin, the predominant motor protein for human heart contraction,
can alter power output and cause cardiomyopathy. However, measurements of the intrinsic …

We used transient biochemical and structural kinetics to elucidate the molecular mechanism
of mavacamten, an allosteric cardiac myosin inhibitor and a prospective treatment for …

Morbidity and mortality associated with heart disease is a growing threat to the global
population, and novel therapies are needed. Mavacamten (formerly called MYK-461) is a …

Mavacamten, formerly known as MYK-461 is a recently discovered novel small-molecule
modulator of cardiac myosin that targets the underlying sarcomere hypercontractility of …

Thin filament hypertrophic cardiomyopathy (HCM) mutations increase myofilament Ca2+
sensitivity and alter Ca2+ handling and buffering. The myosin inhibitor mavacamten …

Background Recent studies suggest that mavacamten (Myk461), a small myosin‐binding
molecule, decreases hypercontractility in myocardium expressing hypertrophic …

Hypertrophic cardiomyopathies (HCMs) are the leading cause of acute cardiac failure in
young individuals. Over 300 mutations throughout β-cardiac myosin, including in the motor …

Background and Purpose Heart failure can reflect impaired contractile function at the
myofilament level. In healthy hearts, myofilaments become more sensitive to Ca2+ as cells …

Hypertrophic cardiomyopathy (HCM) is primarily caused by mutations in β-cardiac myosin
and myosin-binding protein-C (MyBP-C). Changes in the contractile parameters of myosin …

Cardiac myosin binding protein-C (cMyBP-C) is a structural and regulatory component of
cardiac thick filaments. It is observed in electron micrographs as seven to nine transverse …