Reducing heart failure risk after myocardial infarction
Ischaemic heart disease remains one of Europe’s leading causes of death, claiming more than 1.7 million lives annually. Although rapid restoration of blood flow after myocardial infarction has dramatically improved survival, the process itself can trigger damaging inflammatory responses known as reperfusion injury. This secondary damage increases the risk of heart failure, a major long-term consequence affecting millions worldwide.
A different approach to cardioprotection
Inflammation is an essential part of the healing process after myocardial infarction. The challenge is that in severe cases the inflammatory response becomes excessive and contributes to additional tissue damage. The EIC-funded CardioProtectMI project is developing a new therapeutic strategy designed not to suppress inflammation entirely, but to rebalance it and promote healing after heart attack. It focuses on RTP-026(opens in new window), an investigational immunomodulatory therapy developed by ResoTher Pharma. “Unlike conventional anti-inflammatory approaches, RTP-026 aims to regulate the body’s immune response following reperfusion therapy,” explains project coordinator, founder of ResoTher Pharma Thomas Jonassen. This concept of pharmacological resolution distinguishes RTP-026 from earlier cardioprotective strategies that attempted broad suppression of inflammation. By shifting the inflammatory response towards resolution, the treatment is expected to limit infarct expansion, accelerate recovery and preserve heart function. Preclinical studies suggest the therapy could reduce incidence of post-infarction heart failure by more than 20 %, potentially delivering substantial clinical benefits and expected annual healthcare savings exceeding EUR 450 million.
Advancing RTP-026 into clinical evaluation
During the project, RTP-026 progressed from preclinical development into patient-focused clinical evaluation. A Phase I study established safety and tolerability in healthy volunteers, paving the way for Phase II studies in patients with myocardial infarction. Key milestones included finalisation and regulatory approval of the Phase IIa protocol, completion of site initiation visits and the launch of clinical recruitment across participating centres. Clinical teams received specialised training to ensure consistency in trial procedures, safety monitoring and data collection. Following completion of two study cohorts involving 64 participants, researchers decided to advance RTP-026 into a larger Phase IIb study. This decision was supported by encouraging safety and pharmacological findings. “We could already see after the first cohort that exposure levels were within the expected therapeutic range with no fatal cases or rehospitalisations due to major adverse cardiovascular events,” notes Jonassen. Preliminary imaging data also indicated potential protection of heart tissue after reperfusion. The goal is to reduce final infarct size, one of the strongest predictors of long-term outcomes after myocardial infarction. Smaller infarcts are associated with lower risks of heart failure, rehospitalisation and mortality.
Transforming cardiovascular care
Overall, CardioProtectMI highlights the growing importance of inflammation resolution as a therapeutic target in cardiovascular medicine. Current treatments primarily restore blood flow mechanically, but few options directly address the inflammatory consequences of reperfusion injury. If successful, RTP-026 could become a first-in-class therapy integrated into standard myocardial infarction care pathways. Looking ahead, the consortium plans to launch a larger Phase IIb study in 2026, supported by newly secured funding. Clinical development is expected to continue through 2027, with study readouts anticipated in 2028.