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However, reperfusion can cause cardiomyocyte hypercontracture. Recently, cardiac myosin-targeted inhibitors (CMIs), such as Mavacamten (MYK-461) and Aficamten (CK-274), have been developed to treat patients with cardiac hypercontractility. These CMIs are well tolerated and safe in clinical trials. We hypothesised that, by limiting hypercontraction, CMIs may reduce hypercontracture and protect hearts in the setting of ischaemia and reperfusion (IR).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We investigated the ability of MYK-461 and CK-274 to inhibit hypercontracture of adult rat cardiomyocytes (ARVC)\n                      <jats:italic>in vitro<\/jats:italic>\n                      following ATP depletion. A suitable dose of CMIs for subsequent\n                      <jats:italic>in vivo<\/jats:italic>\n                      IR studies was identified using cardiac echocardiography of healthy male Sprague Dawley rats. Rats were anaesthetized and subject to coronary artery ligation for 30\u00a0min followed by 2\u00a0h of reperfusion. Prior to reperfusion, CMI or vehicle was administered intraperitoneally. Ischaemic preconditioning (IPC) was used as a positive control group. Infarct size was assessed by tetrazolium chloride staining and extent of hypercontracture was assessed by histological staining.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Treatment with CMIs inhibited ARVC hypercontracture\n                      <jats:italic>in vitro<\/jats:italic>\n                      . MYK-461 (2\u00a0mg\/kg) and CK-274 (0.5\u00a0mg\/kg to 2\u00a0mg\/kg) significantly reduced infarct size vs. vehicle. IR caused extensive contraction band necrosis, which was reduced significantly by IPC but not by CMIs, likely due to assay limitations. GDC-0326, an inhibitor of PI3K\u03b1, abrogated CK-274-mediated protection following IR injury. GDC-0326 reduced phosphorylation of AKT when administered together with CK-274.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study identifies CMIs as novel cardioprotective agents in the setting of IR injury.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s10557-024-07663-0","type":"journal-article","created":{"date-parts":[[2025,1,4]],"date-time":"2025-01-04T01:48:35Z","timestamp":1735955315000},"page":"39-52","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Novel Selective Cardiac Myosin-Targeted Inhibitors Alleviate Myocardial Ischaemia\u2013Reperfusion Injury"],"prefix":"10.1007","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5826-328X","authenticated-orcid":false,"given":"Nur Liyana Mohammed","family":"Yusof","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7791-9320","authenticated-orcid":false,"given":"Derek M.","family":"Yellon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5182-4980","authenticated-orcid":false,"given":"Sean M.","family":"Davidson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,1,4]]},"reference":[{"issue":"14","key":"7663_CR1","doi-asserted-by":"publisher","first-page":"1674","DOI":"10.1016\/j.jacc.2016.01.069","volume":"67","author":"GW Stone","year":"2016","unstructured":"Stone GW, Selker HP, Thiele H, et al. 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