Chemotactic factors from both Gram-positive and Gram-negative bacteria are short peptides with N-formyl methionine at the N-terminus (extensively reviewed in reference 1). These peptides are released from bacteria during infection and activate formyl peptide receptors (FPR), members of the G-protein coupled receptor (GPCR) superfamily. In humans, the FPR family consists mainly of three receptors, FPR1, FPR2/ALX (formerly FPRL1), and FPR3 (formerly FPRL2) which all couple to the G_i subtype of G-proteins and ultimately lead to the activation of phospholipase C and intracellular Ca²⁺ increase^1,2.

WKYMVM is a selective agonist of the Formyl peptide receptors (FPR2 and FPR3) and was discovered by screening peptide libraries for their ability to stimulate inositol phosphates in lymphocyte cell lines^3,4. FPR2 is expressed in the promyelocytic leukemia cell line HL-60 as well as in the chronic myelogenous leukemia cell line K562⁵.

WKYMVM triggered the activity of NADPH oxidase and generation of superoxide anions in human neutrophils⁶. In mouse dendritic cells, WKYMVM triggered Ca²⁺ signals in a pertussis toxin dependent manner, leading to increased phagocytosis via phospholipase D activation⁷.