Here, we show for the first time that ITPP, a novel membrane‐permeant allosteric effector of haemoglobin that enhances the oxygen release capacity of RBC by lowering the affinity of Hb for oxygen, partially prevents post‐MI left ventricular dilation and impairment of contractility in the rat model of post‐MI heart failure, most important markers of heart failure progression and prognosis. The gene discussed is TPP1; the disease is myocardial infarction.