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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWBMS 986235 is a formyl peptide receptor 2 (FPR2) agonist.1 It selectively induces calcium mobilization in HEK293 cells overexpressing human FPR2 over FPR1 (EC50s = 0.41 and 2,800 nM, respectively). BMS 986235 inhibits chemotaxis of HL-60 human promyeloblast cells and induces phagocytosis of opsonized zymosan by isolated mouse peritoneal macrophages. In vivo, BMS 986235 inhibits neutrophil infiltration into the lungs in a mouse model of LPS-induced lung inflammation. BMS 986235 reduces left ventricle remodeling, scar length, and heart mass in a mouse model of myocardial infarction when administered at a dose of 0.3 mg/kg on days 4-28 post-occlusion. It also reduces right and left ventricle damage and inflammation in a mouse model of Duchenne muscular dystrophy.2
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1. Discovery of BMS-
2. Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy. Cell Death Dis. 16(1), 505 (2025).