Cyclooxygenase 1 (prostaglandin-endoperoxide synthase 1) and Cyclooxygenase 2 (prostaglandin-endoperoxide synthase 2) (COX-1 and COX-2)

Cyclooxygenase 1 and Cyclooxygenase 2 are closely related, membrane-bound enzymes that catalyze the oxygenation of arachidonic acid to form prostaglandin endoperoxides, the precursors for prostaglandins and thromboxanes, which are lipid signaling molecules with diverse roles in inflammation, hemostasis, vascular tone, and gastroprotection[1][3][9]. COX-1 is constitutively expressed in most tissues and is responsible for maintaining physiological "housekeeping" functions, such as gastric mucosal protection and platelet aggregation, whereas COX-2 is inducible by inflammatory stimuli, growth factors, and some cytokines and is principally involved in inflammation, pain, and fever[2][5][8]. Both isoforms are targeted by nonsteroidal anti-inflammatory drugs (NSAIDs), but COX-2-selective inhibitors (coxibs) have been developed to reduce the gastrointestinal side effects associated with non-selective inhibition[2][4][9]. Inhibition of these enzymes plays a major role in the management of pain and inflammation but is associated with notable safety challenges, particularly regarding gastrointestinal and cardiovascular risks[2][4][5].

Other names

COX-1COX-2Prostaglandin-endoperoxide synthase 1 (PTGS1)Prostaglandin-endoperoxide synthase 2 (PTGS2)Prostaglandin G/H synthase 1Prostaglandin G/H synthase 2

Nonselective inhibition of COX-1 and COX-2 (classical NSAIDs): decreases synthesis of prostaglandins and thromboxanes by blocking the conversion of arachidonic acid.\nSelective inhibition of COX-2 (coxibs): reduces the pathophysiological production of pro-inflammatory prostaglandins with less impact on gastric protection and platelet function.