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

Cyclooxygenase 1 and Cyclooxygenase 2 (COX-1 and COX-2) are closely related enzymes that catalyze the conversion of arachidonic acid into prostaglandins and thromboxanes, mediators essential for inflammation, pain, fever, blood clotting, and gastric mucosal integrity. COX-1 is constitutively expressed, providing homeostatic prostaglandin production for platelet aggregation, renal blood flow, and gastroprotection, whereas COX-2 is inducible, predominantly during inflammation or in neoplastic tissues[1][4][5][8][7]. Both enzymes are homodimeric, membrane-bound oxidoreductases targeted by NSAIDs and coxibs, widely used for their anti-inflammatory, analgesic, antipyretic, and antithrombotic properties. Selective inhibition of COX-1 or COX-2 can result in substantial therapeutic benefits as well as notable adverse effects, especially concerning gastrointestinal and cardiovascular safety[4][5][2][6].

Other names

Prostaglandin-endoperoxide synthase 1 (PTGS1, for COX-1)Prostaglandin-endoperoxide synthase 2 (PTGS2, for COX-2)COX isoformscyclooxygenase isoenzymes

Inhibition of prostaglandin and thromboxane synthesis via blockade of cyclooxygenase active site (NSAIDs, both nonselective and COX-2 selective) Covalent acetylation (aspirin, irreversible inhibition) Competitive inhibition (other NSAIDs and coxibs) Selective COX-2 inhibition (celecoxib, etoricoxib)