Cyclooxygenase-1 and cyclooxygenase-2 enzyme (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 to prostaglandins and thromboxanes, key mediators of inflammation, pain, fever, vascular homeostasis, and platelet aggregation[1][2][3][4][7]. COX-1 is constitutively expressed in most tissues and is primarily involved in protective physiological functions—such as maintaining gastrointestinal mucosal integrity, regulating renal blood flow, and producing thromboxane for normal platelet function[1][3][4][6]. COX-2 is an inducible isoform, expressed in response to inflammatory stimuli, and is mainly responsible for the pro-inflammatory synthesis of prostaglandins[1][2][4][7]. Inhibition of these enzymes by nonsteroidal anti-inflammatory drugs (NSAIDs) forms the basis of widely used therapies for pain, inflammation, and fever, but selective and non-selective COX inhibition is associated with significant safety concerns including gastrointestinal injury, increased cardiovascular risk, and renal complications[4][5][7]. Selective COX-2 inhibitors (coxibs) were developed to reduce gastrointestinal side effects but are linked to higher cardiovascular risk[5]. The COX enzymes are known by several alternative names, including prostaglandin-endoperoxide synthase (PTGS1 and PTGS2) and prostaglandin G/H synthase[2][3]. Both are validated and established drug targets in medicine, particularly for NSAIDs and related drug classes.

Other names

Prostaglandin-endoperoxide synthase 1 (PTGS1)Prostaglandin-endoperoxide synthase 2 (PTGS2)Prostaglandin G/H synthase 1/2Prostaglandin-endoperoxide H synthase 1/2Cyclo-oxygenase 1/2COX-1/COX-2

Inhibition of prostaglandin synthesis by blocking COX enzymatic activity Inhibition of thromboxane synthesis (especially by COX-1 inhibition) Reduction of inflammation and pain (especially by COX-2 inhibition) Antipyretic effect by lowering prostaglandin E2 in the hypothalamus Inhibition of platelet aggregation (via COX-1 inhibition)