ArticleNature cardiovascular research2024
Aficamten is a small-molecule cardiac myosin inhibitor designed to treat hypertrophic cardiomyopathy.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Safety and Efficacy of Mavacamten and Aficamten in Patients With Hypertrophic Cardiomyopathy.Journal of the American Heart Association · 2025Pooled it
- Towards a Quantitative Understanding of Aficamten Clinical Pharmacology: Pharmacokinetic-Cardiodynamic Modeling to Support Safety and Efficacy.CPT: pharmacometrics & systems pharmacology · 2026Trial
- A comprehensive review of small molecule drugs approved by the FDA in 2025: advance and prospect.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Mechanistic diversity within RLC-dependent myosin ATPase inhibitors differentiates EDG-7500, a diastolic-selective cardiac sarcomere modulator.JCI insight · 2026Article
- Contractile effects of Aficamten in the human atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Structure-Function Relationship as the Foundation for Cardiac Myosin Inhibition in Hypertrophic Cardiomyopathy.Circulation · 2026Article
- FDA-Approved Drugs Containing Amide Functionality in the Last Five Years (2021-2025): Pharmaceutical Use, Trends and Synthetic Approaches.Medicines (Basel, Switzerland) · 2026Review
- The E525K β-Myosin Mutation Causes Hypocontractility in Cardiomyocytes Without Altering Loaded Crossbridge Cycling.bioRxiv : the preprint server for biology · 2026Article
- Aficamten in symptomatic obstructive hypertrophic cardiomyopathy: the FOREST-HCM long-term study.European heart journal · 2026Article
- Changes in cardiac myosin acetylation disrupt the super-relaxed state in genotype-negative hypertrophic cardiomyopathy with type 2 diabetes.Cardiovascular diabetology · 2026Article
- Nitrogen-containing FDA-approved drugs in 2025: synthesis, significance and therapeutic applications.RSC advances · 2026Review
- Clinical Evaluation of Drug-Drug Interactions With Aficamten.Clinical and translational science · 2026Article
- PGM1 deficiency is linked to sarcomeric and mitochondrial dysfunction in patient-derived iPSC-cardiomyocytes.Journal of translational medicine · 2026Article
- Efficacy and Safety of Aficamten in Children and Adolescents With Obstructive Hypertrophic Cardiomyopathy: Study Design and Rationale of CEDAR-HCM.Circulation. Heart failure · 2026Article
- Novel Selective Cardiac Myosin-Targeted Inhibitors Alleviate Myocardial Ischaemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2026Article
- Unveiling the complexity of nonobstructive hypertrophic cardiomyopathy.Heart failure reviews · 2025Review
- Toward a Quantitative Understanding of Aficamten Clinical Pharmacology: Population Pharmacokinetic Modeling.CPT: pharmacometrics & systems pharmacology · 2025Article
- Understanding hypertrophic cardiomyopathy and its regulation by myosin drugs.Protein science : a publication of the Protein Society · 2025Article
- Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human β-cardiac myosin allosterically.Nature communications · 2025Article
- Cardiac Myosin Inhibitors in Hypertrophic Cardiomyopathy: From Sarcomere to Clinic.International journal of molecular sciences · 2025Review
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20 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is an inherited disease of the sarcomere resulting in excessive cardiac contractility. The first-in-class cardiac myosin inhibitor, mavacamten, improves symptoms in obstructive HCM. Here we present aficamten, a selective small-molecule inhibitor of cardiac myosin that diminishes ATPase activity by strongly slowing phosphate release, stabilizing a weak actin-binding state. Binding to an allosteric site on the myosin catalytic domain distinct from mavacamten, aficamten prevents the conformational changes necessary to enter the strongly actin-bound force-generating state. In doing so, aficamten reduces the number of functional myosin heads driving sarcomere shortening. The crystal structure of aficamten bound to cardiac myosin in the pre-powerstroke state provides a basis for understanding its selectivity over smooth and fast skeletal muscle. Furthermore, in cardiac myocytes and in mice bearing the hypertrophic R403Q cardiac myosin mutation, aficamten reduces cardiac contractility. Our findings suggest aficamten holds promise as a therapy for HCM.
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