ArticleJournal of the American Heart Association2018
Impact of the Myosin Modulator Mavacamten on Force Generation and Cross-Bridge Behavior in a Murine Model of Hypercontractility.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Mechanistic diversity within RLC-dependent myosin ATPase inhibitors differentiates EDG-7500, a diastolic-selective cardiac sarcomere modulator.JCI insight · 2026Article
- The CabioRxiv : the preprint server for biology · 2026Article
- Mavacamten in the Treatment of Obstructive Hypertrophic Cardiomyopathy: from Pathophysiology To Real World Data.Current cardiology reports · 2025Review
- Myocardium From Patients With ATTR Amyloidosis Produces Less Force Secondary to Increased Fibrosis.JACC. Basic to translational science · 2025Article
- Review
- cMyBP-C in hypertrophic cardiomyopathy: gene therapy and small-molecule innovations.Frontiers in cardiovascular medicine · 2025Review
- Tracking single hiPSC-derived cardiomyocyte contractile function using CONTRAX an efficient pipeline for traction force measurement.Nature communications · 2024Article
- Myosin-Catalyzed ATP Hydrolysis in the Presence of Disease-Causing Mutations: Mavacamten as a Way to Repair Mechanism.The journal of physical chemistry. B · 2024Article
- Assessing Cardiac Contractility From Single Molecules to Whole Hearts.JACC. Basic to translational science · 2024Review
- Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.Pediatric discovery · 2024Review
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
- Discovery of a novel cardiac-specific myosin modulator using artificial intelligence-based virtual screening.Nature communications · 2023Article
- Hypertrophic Cardiomyopathy: Genetic Foundations, Outcomes, Interconnections, and Their Modifiers.Medicina (Kaunas, Lithuania) · 2023Review
- Mavacamten, a precision medicine for hypertrophic cardiomyopathy: From a motor protein to patients.Science advances · 2023Review
- New Approved Drugs Appearing in the Pharmaceutical Market in 2022 Featuring Fragments of Tailor-Made Amino Acids and Fluorine.Molecules (Basel, Switzerland) · 2023Review
- cMyBP-C ablation in human engineered cardiac tissue causes progressive Ca2+-handling abnormalities.The Journal of general physiology · 2023Article
- Muscle Mechanics and Thick Filament Activation: An Emerging Two-Way Interaction for the Vertebrate Striated Muscle Fine Regulation.International journal of molecular sciences · 2023Review
- Review of Mavacamten for Obstructive Hypertrophic Cardiomyopathy and Future Directions.Drug design, development and therapy · 2023Review
- Mechanism based therapies enable personalised treatment of hypertrophic cardiomyopathy.Scientific reports · 2022Article
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Background Recent studies suggest that mavacamten (Myk461), a small myosin-binding molecule, decreases hypercontractility in myocardium expressing hypertrophic cardiomyopathy-causing missense mutations in myosin heavy chain. However, the predominant feature of most mutations in cardiac myosin binding protein-C ( cMyBPC ) that cause hypertrophic cardiomyopathy is reduced total cMyBPC expression, and the impact of Myk461 on cMyBPC -deficient myocardium is currently unknown. Methods and Results We measured the impact of Myk461 on steady-state and dynamic cross-bridge ( XB ) behavior in detergent-skinned mouse wild-type myocardium and myocardium lacking cMyBPC (knockout (KO)). KO myocardium exhibited hypercontractile XB behavior as indicated by significant accelerations in rates of XB detachment (k
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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.