Lipoxin A4 (LXA4; 5S, 6R, 15S-trihydroxy-7E, 9E, 11Z, 13E-eicosatetraenoic acid) and lipoxin B4 (LXB4; 5S, 14R, 15S-trihydroxy-6E, 8Z, 10E, 12E-eicosatetraenoic acid) were the first lipid SPMs to be discovered (Chiang and Serhan 2017). They are produced from the conversion of omega-6 (ω-6) arachidonic acid (AA) by lipoxygenase (LOX) through unicellular and transcellular biosynthesis pathways. In transcellular biosynthesis, LXs are synthesized by12-LOX derived through platelet-leukocyte interaction while unicellular biosynthesis pathways involve a series of LOXs-15-lipoxygenase, 5-lipoxygenase, and epoxide hydrolase reactions. In addition to the lipoxygenase-initiated biosynthesis, two distinct lipoxins biosynthesis pathways have been elucidated; aspirin-triggered and statin-triggered routes. Aspirin induces the production of a lipoxin named “aspirin-triggered " (AT) 15-epi-LX through acetylation of serine residue of cyclooxygenase-2 (COX-2), acetylated COX-2 transforms AA into 15R-HETE, which serves as a substrate for 5-LOX (Chiang et al. 2005). Statins, widely used as potent cholesterol-lowering agents, have also been found to enhance the conversion of arachidonate to 15-epi-LX (Planaguma et al. 2010). Epi-lipoxins, trihydroxy metabolites of arachidonic acid, are 15R-epimers of their respective lipoxins, 15-epi-LXA4, LXA4, and 15-epi-LXB4, LXB4 (Romano et al. 2015).