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 in vitro and aortic banding in vivo. Cardiomyocyte-specific mRNA translation changes were assessed in αMHC-Cre Ribo-tag mice. RMC-6272 demonstrated superior potency and specificity for mTORC1 compared to rapamycin and Torin1. RMC-6272 prevented pathological hypertrophic growth in vitro and suppressed mTORC1-dependent mRNA translation, particularly those encoding components of the translational machinery. Preventive RMC-6272 treatment preserved cardiac function under pressure overload, maintaining contractile dysfunction in mice. Therapeutic treatment improved function in established hypertrophy, demonstrating therapeutic potential even after disease onset.