Prostaglandin-endoperoxide synthase 1 and 2 (COX-1 and COX-2 (also PTGS1 and PTGS2))

Prostaglandin-endoperoxide synthases—commonly known as cyclooxygenases—are enzymes responsible for the conversion of arachidonic acid into prostaglandins and thromboxanes, which are key mediators in inflammation, pain signaling, platelet aggregation, gastrointestinal protection, renal function regulation, and other physiological processes. There are two main isoforms in humans: **Cyclooxygenase 1** (*PTGS1*, *COX‐1*) is constitutively expressed throughout most tissues where it produces baseline levels of protective prostaglandins involved in maintaining gastric mucosal integrity, supporting renal blood flow under stress conditions, and promoting normal platelet function. **Cyclooxygenase 2** (*PTGS2*, *COX‐2*) is primarily inducible—its expression increases dramatically during inflammatory states under the influence of cytokines or growth factors—and is responsible for generating large amounts of pro-inflammatory prostaglandins at sites of injury or infection. Both isoforms share high sequence homology but differ significantly in their regulatory mechanisms and tissue distribution. Pharmacological inhibition by NSAIDs targets these enzymes to reduce pain and inflammation; however nonselective inhibition can lead to gastrointestinal side effects while selective inhibition may increase cardiovascular risks.

Other names

Cyclooxygenase 1Cyclooxygenase 2Prostaglandin G/H synthaseProstaglandin-endoperoxide synthetasePHS (prostaglandin synthase/synthetase)

Inhibition of cyclooxygenase activity to block conversion of arachidonic acid to prostaglandins/thromboxane; reduces inflammation, pain, fever; antiplatelet effect for some agents like aspirin by irreversibly inhibiting COX‑1 in platelets.