Cyclooxygenase 1 and Cyclooxygenase 2 (COX-1 and COX-2)

Cyclooxygenase 1 and Cyclooxygenase 2 are two closely related enzymes that catalyze the conversion of arachidonic acid to prostaglandin H2, a key precursor for prostaglandins and thromboxanes[1][2][3]. COX-1 is constitutively expressed in most tissues and is primarily involved in protective physiological processes, such as maintaining gastric mucosal integrity and enabling platelet aggregation, while COX-2 is inducible and upregulated during inflammation, mediating pain, fever, and the inflammatory response[1][3][4][6]. Both are primary targets of nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen; COX-2 selective inhibitors (e.g., celecoxib) were developed to reduce gastrointestinal side effects but may increase cardiovascular risk[4][6]. Their differential expression and function have made both isozymes central to the development of anti-inflammatory, analgesic, and antipyretic therapies, though their inhibition is associated with significant adverse effects and complex roles in neuroinflammation and cancer[1][3][6][7].

Other names

Prostaglandin-endoperoxide synthase 1 (PTGS1)Prostaglandin-endoperoxide synthase 2 (PTGS2)Prostaglandin G/H synthase 1, 2Prostaglandin synthaseCOX enzymes

Inhibition of prostaglandin biosynthesis (by NSAIDs, COX inhibitors); Reduction of inflammation, pain, and fever (by attenuating prostaglandin signals); Inhibition of platelet aggregation (COX-1 blockade, especially with low-dose aspirin)