ArticleThe Journal of biological chemistry2017
Omecamtiv Mecarbil Enhances the Duty Ratio of Human β-Cardiac Myosin Resulting in Increased Calcium Sensitivity and Slowed Force Development in Cardiac Muscle.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 94 citations in OpenAlex.
- Targeting cardiac myosin in HFrEF: mechanism, clinical evidence, and the role of omecamtiv mecarbil.Journal of cardiothoracic surgery · 2026Review
- The hypertrophic cardiomyopathy mutation G768R makes cardiac myosin a high duty ratio motor.bioRxiv : the preprint server for biology · 2026Article
- Impact of salt concentration and free magnesium on human beta-cardiac myosin reveal important details about the conserved mechanochemical mechanism.The Journal of biological chemistry · 2026Article
- Article
- Review
- Thick-Filament-Based Regulation and the Determinants of Force Generation.Biomedicines · 2025Article
- Mechanistic insights into effects of the cardiac myosin activator omecamtiv mecarbil from mechanokinetic modelling.Frontiers in physiology · 2025Article
- Differential effects of myosin activators on myocardial contractile function in nonfailing and failing human hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- Pharmacodynamics of single-dose omecamtiv mecarbil administered intravenously in clinically healthy cats.Open veterinary journal · 2024Article
- Myosin Isoform-Dependent Effect of Omecamtiv Mecarbil on the Regulation of Force Generation in Human Cardiac Muscle.International journal of molecular sciences · 2024Article
- Omecamtiv mecarbil and Mavacamten target the same myosin pocket despite opposite effects in heart contraction.Nature communications · 2024Article
- Tail length and E525K dilated cardiomyopathy mutant alter human β-cardiac myosin super-relaxed state.The Journal of general physiology · 2024Article
- The dynamics of actin protrusions can be controlled by tip-localized myosin motors.The Journal of biological chemistry · 2024Article
- From amoeboid myosin to unique targeted medicines for a genetic cardiac disease.Frontiers in physiology · 2024Review
- Omecamtiv Mecarbil in the treatment of heart failure: the past, the present, and the future.Frontiers in cardiovascular medicine · 2024Review
- Tail Length and E525K Dilated Cardiomyopathy Mutant Alter Human β-Cardiac Myosin Super-Relaxed State.bioRxiv : the preprint server for biology · 2023Article
- Omecamtiv mecarbil and Mavacamten target the same myosin pocket despite antagonistic effects in heart contraction.bioRxiv : the preprint server for biology · 2023Article
- Effect of the Novel Myotrope Danicamtiv on Cross-Bridge Behavior in Human Myocardium.Journal of the American Heart Association · 2023Article
- Estimation of crossbridge-state during cardiomyocyte beating using second harmonic generation.Life science alliance · 2023Article
- Virus-free transfection, transient expression, and purification of human cardiac myosin in mammalian muscle cells for biochemical and biophysical assays.Scientific reports · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The small molecule drug omecamtiv mecarbil (OM) specifically targets cardiac muscle myosin and is known to enhance cardiac muscle performance, yet its impact on human cardiac myosin motor function is unclear. We expressed and purified human β-cardiac myosin subfragment 1 (M2β-S1) containing a C-terminal Avi tag. We demonstrate that the maximum actin-activated ATPase activity of M2β-S1 is slowed more than 4-fold in the presence of OM, whereas the actin concentration required for half-maximal ATPase was reduced dramatically (30-fold). We find OM does not change the overall actin affinity. Transient kinetic experiments suggest that there are two kinetic pathways in the presence of OM. The dominant pathway results in a slow transition between actomyosin·ADP states and increases the time myosin is strongly bound to actin. However, OM also traps a population of myosin heads in a weak actin affinity state with slow product release. We demonstrate that OM can reduce the actin sliding velocity more than 100-fold in the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.