Prostaglandin-endoperoxide synthase (COX enzyme complex) (COX)

Prostaglandin-endoperoxide synthase, commonly called cyclooxygenase (COX), is a key enzyme complex that catalyzes the conversion of arachidonic acid to prostaglandin H2, the precursor of various prostanoids including prostaglandins, prostacyclin, and thromboxane[1][2][3][5]. This enzyme is crucial in the regulation of inflammation, pain, and hemostasis. There are two major isoforms: COX-1, which is constitutively expressed and involved in physiological processes such as gastrointestinal protection and platelet function; and COX-2, which is inducible and primarily involved in inflammatory responses[2][3][5]. Pharmaceutical inhibitors of COX, including nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors, are widely used for treatment of pain, fever, and inflammation but are associated with significant GI and cardiovascular risks[1][3][4][7]. COX enzymes are well-established therapeutic targets in medicine and are implicated in numerous diseases, including inflammation, cancer, and cardiovascular disorders[2][8]. For precise drug development and research, the term "prostaglandin-endoperoxide synthase" and its gene symbols PTGS1 (COX-1) and PTGS2 (COX-2) are preferred, though "COX" is widely used in clinical and pharmacological contexts[1]. **Note:** The submitted name "Cyclooxygenase enzyme complex" is somewhat imprecise. While "cyclooxygenase" and "COX" accurately refer to the target, for canonical clarity the names "Prostaglandin-endoperoxide synthase" (PTGS), COX-1, and COX-2 should be used for specific isoenzymes[1][2][5].

Other names

CyclooxygenaseProstaglandin H synthaseProstaglandin-endoperoxide synthaseProstaglandin G/H synthasePHSPESPTGSCOX-1COX-2

Nonselective inhibition of COX-1 and COX-2 reduces synthesis of prostanoids, decreasing inflammation, pain, and fever (e.g., ibuprofen, naproxen) - Selective COX-2 inhibition reduces inflammation and pain with lower risk of GI adverse effects (e.g., celecoxib, rofecoxib) - Irreversible acetylation and inhibition (aspirin) - Reversible, competitive inhibition (most NSAIDs)