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

Cyclooxygenase enzyme 1 and 2 are membrane-bound oxidoreductases that catalyze the conversion of arachidonic acid into prostaglandins, which are lipid mediators involved in inflammation, pain signaling, fever response, platelet aggregation, maintenance of gastric mucosal integrity, and regulation of renal blood flow. There are two main isoforms encoded by separate genes: COX‑1 is constitutively expressed in most tissues where it performs housekeeping functions such as protecting the stomach lining and supporting platelet function; COX‑2 is primarily inducible at sites of inflammation or injury but also has physiological roles in certain tissues. Both isoforms are major therapeutic targets for nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin and ibuprofen. Selective inhibition strategies have been developed to reduce gastrointestinal side effects associated with nonselective NSAID use; however, selective COX‑2 inhibitors carry increased cardiovascular risks. The balance between efficacy in reducing pain/inflammation and safety concerns remains a central issue in drug development targeting these enzymes[1][5][6].

Other names

Prostaglandin-endoperoxide synthase 1 (PTGS1)Prostaglandin-endoperoxide synthase 2 (PTGS2)CyclooxygenasesCOX enzymesCyclo-oxygenase enzymes

– Inhibition of prostaglandin synthesis by blocking the conversion of arachidonic acid to prostaglandins via COX active site inhibition[5][6] – Irreversible acetylation/inhibition for aspirin on COX enzymes[5]