ArticleNature communications2017
Small-molecule-biased formyl peptide receptor agonist compound 17b protects against myocardial ischaemia-reperfusion injury in mice.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Article
- FPR1-Driven Neutrophil-Endothelial Cell Axis Promotes Angiogenesis in PAOD.Circulation research · 2026Article
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Sex-Specific Associations Between Cadmium Exposure and Mortality Risk in Cardiovascular Disease Patients: A Cohort Study Integrating Molecular Mechanisms of Myocardial Dysfunction.Cardiovascular toxicology · 2026Article
- Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.Molecular biomedicine · 2026Review
- FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Monoclonal Antibody 5F1 Modulates Formyl Peptide Receptor 1 Conformation for Transmembrane Signaling.FASEB bioAdvances · 2025Article
- Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease.Acta pharmacologica Sinica · 2025Article
- Insights from precision-cut lung slices-investigating mechanisms and therapeutics for pulmonary hypertension.Respiratory research · 2025Review
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- Inflammaging and Immunosenescence in the Post-COVID Era: Small Molecules, Big Challenges.ChemMedChem · 2025Review
- Lipoxin ACardiovascular diabetology · 2024Article
- Novel formylpeptide receptor 1/2 agonist limits hypertension-induced cardiovascular damage.Cardiovascular research · 2024Article
- Beyond the numbers in treating hypertensive end-organ damage: role of formyl peptide receptor agonist Cmpd17b.Cardiovascular research · 2024Article
- Discovery and Optimization of Aryl Piperidinone Ureas as Selective Formyl Peptide Receptor 2 Agonists.ACS medicinal chemistry letters · 2024Article
- Enhancement of efferocytosis through biased FPR2 signaling attenuates intestinal inflammation.EMBO molecular medicine · 2023Article
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
- Ginsenoside Rb1 Improves Post-Cardiac Arrest Myocardial Stunning and Cerebral Outcomes by Regulating the Keap1/Nrf2 Pathway.International journal of molecular sciences · 2023Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effective treatment for managing myocardial infarction (MI) remains an urgent, unmet clinical need. Formyl peptide receptors (FPR) regulate inflammation, a major contributing mechanism to cardiac injury following MI. Here we demonstrate that FPR1/FPR2-biased agonism may represent a novel therapeutic strategy for the treatment of MI. The small-molecule FPR1/FPR2 agonist, Compound 17b (Cmpd17b), exhibits a distinct signalling fingerprint to the conventional FPR1/FPR2 agonist, Compound-43 (Cmpd43). In Chinese hamster ovary (CHO) cells stably transfected with human FPR1 or FPR2, Compd17b is biased away from potentially detrimental FPR1/2-mediated calcium mobilization, but retains the pro-survival signalling, ERK1/2 and Akt phosphorylation, relative to Compd43. The pathological importance of the biased agonism of Cmpd17b is demonstrable as superior cardioprotection in both in vitro (cardiomyocytes and cardiofibroblasts) and MI injury in mice in vivo. These findings reveal new insights for development of small molecule FPR agonists with an improved cardioprotective profile for treating MI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.