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Prostaglandin-endoperoxide synthase 1 (COX-1) and Prostaglandin-endoperoxide synthase 2 (COX-2) are enzyme isozymes that catalyze the key step in prostaglandin and thromboxane biosynthesis from arachidonic acid[1][2][3]. COX-1 is generally expressed constitutively in most tissues, where it mediates physiological functions such as platelet aggregation, gastric mucosal protection, and maintenance of vascular homeostasis[1][3]. COX-2 is typically inducible and upregulated during inflammation and certain pathological states, with a prominent role in mediating pain, fever, and mitogenic responses[3]. Both isoenzymes belong to the heme peroxidase enzyme family and share similar structures and reaction mechanisms[2][3]. Their pharmacological inhibition by nonsteroidal anti-inflammatory drugs (NSAIDs) is central to anti-inflammatory, analgesic, and antipyretic therapy, but is associated with notable therapeutic challenges, including gastrointestinal, cardiovascular, and renal adverse effects[2][3]. Overexpression or dysregulation of COX-1 and COX-2 is linked to cancers and chronic inflammatory diseases[3].
Inhibition of prostaglandin-endoperoxide synthase activity (enzyme inhibition) Selective inhibition of COX-2 isozyme (for COX-2 selective drugs), reducing production of pro-inflammatory prostaglandins
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