Anti-inflammatory peptide. By activating the G-protein coupled receptor formyl peptide receptor 2 (FPR2), this peptide markedly activates neutrophils, resulting in cytosolic calcium increase, superoxide anion production, and chemotactic cellular migration. In vivo, when tested on a auto-antibody-injected model, its administration strongly blocks the clinical phenotype of rheumatoid arthritis (RA). Mechanistically, this peptide inhibits inflammatory cytokine synthesis from the joints and neutrophil recruitment into the joint area. It may serve as a novel potential therapeutic agent for the control of RA via FPR2. Expressed by the venom gland.