Cyclooxygenase and Lipoxygenase (COX; LOX)

Cyclooxygenase (COX) and lipoxygenase (LOX) are enzyme families responsible for the conversion of arachidonic acid into eicosanoids, which include prostaglandins, thromboxanes, and leukotrienes[1][7][3][9]. These bioactive lipids regulate inflammation, immune responses, vascular tone, and other physiological processes. COX exists as two major isozymes—COX-1 (constitutive, involved in normal physiology) and COX-2 (inducible, often upregulated during inflammation and cancer)[7][9]. Lipoxygenases comprise several isoforms (e.g., 5-LOX, 12-LOX, 15-LOX) that produce leukotrienes and other lipid mediators involved in allergy, asthma, and inflammation[3][9]. Both COX and LOX are established drug targets: NSAIDs inhibit COX enzymes, reducing pain and inflammation, while leukotriene inhibitors target LOX pathways in asthma[2][7][9]. Dual COX/LOX inhibitors have been developed to address side effects and enhance efficacy but have encountered safety and efficacy challenges[4]. These enzymes are also implicated in the pathogenesis of cancer, cardiovascular, autoimmune, and neurodegenerative diseases[1][2][4][9].

Other names

Prostaglandin-endoperoxide synthase (PTGS)Prostaglandin G/H synthaseCOX-1 (PTGS1)COX-2 (PTGS2)LOX enzymes (various isoforms, e.g., 5-LOX, 12-LOX, 15-LOX)EC 1.13.11 family

Inhibition of COX blocks prostaglandin production, reducing inflammation and pain. Inhibition of LOX blocks leukotriene biosynthesis, reducing bronchoconstriction and inflammation. Dual inhibition suppresses both major pathways of eicosanoid synthesis, potentially providing broader efficacy and fewer side effects.