A new cardioprotective drug for acute treatment of myocardial infarction

Informations projet

CardioProtectMI

N° de convention de subvention: 101144395

DOI

10.3030/101144395

Projet clôturé

Date de signature de la CE 27 Février 2024

Date de début 1 Février 2024

Date de fin 31 Janvier 2026

Financé au titre de

• The European Innovation Council (EIC)

Coût total

€ 3 770 625,00

Contribution de l’UE

€ 2 499 999,00

Coordonné par

RESOTHER PHARMA A/S
Denmark

Periodic Reporting for period 2 - CardioProtectMI (A new cardioprotective drug for acute treatment of myocardial infarction)

Période du rapport: 2025-02-01 au 2026-01-31

Résumé du contexte et des objectifs généraux du projet

Ischemic Heart Disease kills more than 1.7M people/year in the EU, the vast majority via a heart attack (Myocardial
Infarction - MI). Heart failure (HF) is the major cause of death after MI with a prevalence of >26M individuals globally.
While current treatment involving restoration of blood flow to the heart saves the MI patient´s life it also causes additional
damage to the heart through an inflammatory reaction (reperfusion injury).
ResoTher’s leading drug candidate, RTP-026, is an immunomodulating therapeutic aimed at resolving inflammation
triggered during MI, thereby reducing damage to the heart and significantly decreasing risk of HF and death. Pre-clinical
data suggests RTP-026 could reduce post-MI HF by >20%. A Phase I study has been conducted to determine safety and
tolerability of RTP-026 in Healthy Volunteers. With the EIC we aim to validate RTP-026 clinical effectiveness by means
of a Phase IIa patient proof of principle study and Phase IIb proof of concept study.

Travail effectué depuis le début du projet jusqu’à la fin de la période considérée dans le rapport et principaux résultats atteints jusqu’à présent

In the course of the EIC project, significant progress has been made in advancing RTP-026 within clinical development, with a particular focus on the execution of a Phase 2a study in patients with ST-elevation myocardial infarction (STEMI) undergoing primary PCI.

The clinical trial protocol was successfully developed, approved by relevant regulatory authorities, and implemented across participating clinical sites. Site initiation activities were completed, and the Phase 2a study was initiated, enabling clinical evaluation of RTP-026 in the target patient population.

During the reporting period, recruitment and dosing were completed for the first cohort (Group A), and recruitment for the second cohort (Group B) was initiated following a favourable interim safety evaluation. In total, 54 out of the planned 64 patients were enrolled within the project period, corresponding to 84% of target enrolment. Interim safety data across both cohorts indicate an acceptable tolerability profile, with no major safety concerns identified.

Patient recruitment proved more challenging than initially anticipated. To address this, protocol adjustments were implemented, including refinement of inclusion criteria and expansion of screening capacity at clinical sites. These measures improved recruitment feasibility and supported continued study progress.

Overall, the project has achieved substantial progress toward its main objective of generating clinical safety and translational data for RTP-026 in STEMI patients. The results provide a solid foundation for completion of the Phase 2a study and progression to the next stage of clinical development.

Progrès au-delà de l’état des connaissances et impact potentiel prévu (y compris l’impact socio-économique et les conséquences sociétales plus larges du projet jusqu’à présent)

The project has advanced RTP-026 as a novel therapeutic approach targeting resolution of inflammation in acute myocardial infarction. Unlike conventional strategies that aim to suppress inflammatory responses or focus solely on reperfusion, RTP-026 is designed to actively promote the endogenous resolution phase of inflammation, representing a differentiated mechanism of action in the STEMI setting.

Through the execution of the Phase 2a clinical study, the project has generated first clinical safety and translational data supporting the feasibility of this approach in STEMI patients undergoing primary PCI. These results contribute to bridging the gap between preclinical evidence on Annexin-A1 mediated pathways and clinical application in cardiovascular disease.

In addition, the project has provided insights into patient selection and trial feasibility, including optimisation of inclusion criteria and recruitment strategies in a contemporary STEMI population. These learnings are directly relevant for the design of subsequent clinical studies and represent an advancement in the practical implementation of inflammation-targeted therapies in acute cardiovascular care.

Further development will require completion of the Phase 2a study, generation of full clinical data, and progression to Phase 2b trials to evaluate efficacy and confirm clinical benefit.