Prostaglandin-endoperoxide synthase 1 and Prostaglandin-endoperoxide synthase 2 (COX-1 and COX-2)

Prostaglandin-endoperoxide synthase 1 and 2 (COX-1 and COX-2) are closely related enzymes that catalyze the committed step in the conversion of arachidonic acid to prostaglandin H2, the precursor for prostanoids (including prostaglandins, thromboxanes, and prostacyclin)[1][3][4][5][6]. COX-1 is typically considered constitutive, playing roles in physiological homeostasis such as protecting the gastric mucosa and regulating platelet aggregation, while COX-2 is usually inducible, being upregulated in inflammation and contributing to pathological responses[5][6]. These enzymes are targets for NSAIDs and coxibs, therapeutically important for their anti-inflammatory, analgesic, and antipyretic properties, but associated with significant safety concerns when chronically inhibited or selectively targeted[4][5][6]. Overexpression or dysregulation is implicated in cancer and other diseases, and differential expression can serve as a useful biomarker in both research and clinical settings[5][6].

Other names

Cyclooxygenase-1 (COX-1)Cyclooxygenase-2 (COX-2)Prostaglandin G/H synthase 1 (PGHS-1)Prostaglandin G/H synthase 2 (PGHS-2)PTGS1PTGS2Prostaglandin-endoperoxide synthase 1Prostaglandin-endoperoxide synthase 2Prostaglandin synthase (PHS)Prostaglandin endoperoxide synthetase (PES)

NSAIDs: inhibit cyclooxygenase activity, blocking the conversion of arachidonic acid to prostaglandin H2, thus reducing pro-inflammatory prostanoid synthesis Antiplatelet effect (aspirin): irreversible inhibition of COX-1 in platelets, reducing thromboxane A2 synthesis and platelet aggregation Analgesic, antipyretic, anti-inflammatory effects: suppression of prostaglandin-mediated pain, fever, and inflammation COX-2 selective inhibitors: preferentially inhibit COX-2, reducing inflammation with less gastrointestinal toxicity