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Related Experiment Video

Updated: Oct 22, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Selective FPR2 Agonism Promotes a Proresolution Macrophage Phenotype and Improves Cardiac Structure-Function Post

Ricardo A García1,2, John A Lupisella1, Bruce R Ito2

  • 1Department of Cardiovascular and Fibrosis Drug Discovery, Bristol Myers Squibb, Princeton, New Jersey, USA.

JACC. Basic to Translational Science
|September 1, 2021
PubMed
Summary

A novel drug targeting formyl peptide receptor 2 (FPR2) improved healing and survival after heart attack (myocardial infarction) in animal models. This therapeutic approach may offer new options for treating heart disease.

Keywords:
BRET, bioluminescence resonance energy transferEC50, half maximal effective concentrationFPR2FPR2, formyl peptide receptor 2HFHF, heart failureI/R, ischemia-reperfusionIL, interleukinKO, knockoutLPS, lipopolysaccharideLV, left ventricle/ventricularMCP, monocyte chemoattractant proteinMIMI, myocardial infarctionSAA, serum amyloid ATNF, tumor necrosis factorWT, wild-typeformyl peptide receptor 2heart failuremRNA, messenger RNAmyocardial infarctionresolution

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Dysregulated inflammation post-myocardial infarction (MI) impairs heart healing and leads to adverse remodeling.
  • Formyl peptide receptor 2 (FPR2) plays a role in inflammatory responses.

Purpose of the Study:

  • To characterize and evaluate the efficacy of a selective FPR2 agonist, BMS-986235, in improving post-MI outcomes.
  • To investigate the molecular and cellular mechanisms underlying BMS-986235's effects.

Main Methods:

  • In vitro cellular assays were used to assess BMS-986235's effects on G protein activation, β-arrestin recruitment, phagocytosis, neutrophil apoptosis, chemotaxis, and gene expression (IL-10, MCP-1).
  • Rodent models of myocardial infarction (MI) were used to evaluate the in vivo effects of BMS-986235 on survival, cardiac remodeling, scar size, wall thickness, myocardial viability, and ejection fraction.
  • Macrophage phenotype was assessed by measuring arginase-1 mRNA and CD206 levels.

Main Results:

  • BMS-986235 demonstrated G protein activation, β-arrestin recruitment, enhanced phagocytosis, neutrophil apoptosis, and modulated inflammatory gene expression in cellular assays.
  • In mice, BMS-986235 treatment improved survival, reduced cardiac and scar areas, and preserved ventricular wall thickness.
  • Treatment promoted a pro-resolution macrophage phenotype and, in rats, preserved myocardium, attenuated cardiac remodeling, and improved ejection fraction post-MI.

Conclusions:

  • Selective FPR2 agonism with BMS-986235 effectively promotes beneficial post-MI healing and limits adverse cardiac remodeling.
  • FPR2 agonism preserves cardiac function and improves survival in preclinical models of myocardial infarction.
  • BMS-986235 represents a potential innovative therapeutic strategy for improving outcomes after heart attack.