ArticleJournal of molecular and cellular cardiology plus2026
RMC-6272, a selective third-generation bi-steric mTORC1 inhibitor, improves cardiac function in pressure overload-induced cardiac hypertrophy.
Article in Journal of molecular and cellular cardiology plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pathological remodeling in cardiomyocytes during heart failure is driven by excessive activation of mTORC1. Preclinical studies in mice demonstrated that reducing mTORC1 activity protects against cardiac dysfunction and hypertrophic remodeling. However, clinical application of current mTOR inhibitors is limited by incomplete mTORC1 inhibition and off-target effects, including suppression of mTORC2-mediated pro-survival signaling. To address these challenges, the therapeutic effects of the third-generation bi-steric mTORC1 inhibitor RMC-6272 was tested in pressure overload induced heart failure models. The potency and selectivity of RMC-6272 were evaluated in isolated cardiomyocytes. Hypertrophy was induced by phenylephrine
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