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Preservation of Post-Infarction Cardiac Structure and Function via Long-Term Oral Formyl Peptide Receptor Agonist Treatment.

García RA, Ito BR, Lupisella JA, Carson NA, Hsu MY, Fernando G, Heroux M, Bouvier M, Dierks E, Kick EK, Gordon DA, Chen J, Mintier G, Carrier M, St-Onge S, Shah H, Towne J, Bucardo MS, Ma X, Ryan CS, Wurtz NR, Ostrowski J, Villarreal FJ

Department of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.

Dysregulated inflammation following myocardial infarction (MI) promotes left ventricular (LV) remodeling and loss of function. Targeting inflammation resolution by activating formyl peptide receptors (FPRs) may limit adverse remodeling and progression towards heart failure. This study characterized the cellular and signaling properties of Compound 43 (Cmpd43), a dual FPR1/FPR2 agonist, and examined whether Cmpd43 treatment improves LV and infarct remodeling in rodent MI models. Cmpd43 stimulated FPR1/2-mediated signaling, enhanced proresolution cellular function, and modulated cytokines. Cmpd43 increased LV function and reduced chamber remodeling while increasing proresolution macrophage markers. The findings demonstrate that FPR agonism improves cardiac structure and function post-MI.

JACC Basic Transl Sci 2020;4(8):905-920.

Pubmed ID: 31909300

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