FPR3 (formyl peptide receptor 3) is a G-protein coupled receptor that functions as a pattern recognition receptor in innate immunity and plays diverse roles in cellular metabolism, inflammation, and cancer progression. Unlike FPR1 and FPR2, FPR3 shows restricted ligand specificity, binding bacterial N-formylated peptides from specific pathogens like L. monocytogenes and V. cholerae, but not the classical fMLF peptide 1. FPR3 also recognizes endogenous ligands including N-acetylated peptides from HEBP1 and ANXA1, and mitochondrial-derived humanin, facilitating tissue repair and anti-inflammatory responses 234. Mechanistically, ligand binding triggers conformational changes coupled to Gi protein signaling, inhibiting cAMP synthesis while activating phospholipase C-beta and PI3K pathways leading to calcium influx 1. In cancer contexts, FPR3 exhibits complex roles: it suppresses glycolysis and stemness in gastric cancer via calcium-NFATc1 signaling 5, yet promotes immunosuppressive tumor-associated macrophage formation through Wnt/PCP pathway activation 6. FPR3 also facilitates colon cancer metastasis by activating Wnt/β-catenin signaling and creating immunosuppressive microenvironments 7. Additionally, FPR3 promotes capsular contracture after rhinoplasty through PKA/Rap1/ERK1/2 and NF-κB pathways 8. The receptor undergoes tissue-specific transcriptional regulation via alternative promoters that emerged during primate evolution 9.