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The *cyclooxygenases* (**COXs**) are key enzymes responsible for converting arachidonic acid into prostanoids—including prostaglandins and thromboxanes—which mediate inflammation, pain sensation, fever response, platelet aggregation/clotting processes, gastric mucosal protection, kidney function regulation, among other physiological roles.[3][6] There are two main isoforms in humans—COX‑1 (*prostaglandin-endoperoxide synthase 1*, PTGS1), which is constitutively expressed in most tissues for homeostatic functions; and COX‑2 (*prostaglandin-endoperoxide synthase 2*, PTGS2), which is inducible at sites of inflammation.[6][7] Pharmaceutical inhibitors targeting these enzymes—most notably NSAIDs—are widely used for their anti-inflammatory analgesic effects but carry risks related to gastrointestinal integrity (mainly via COX‑1) as well as cardiovascular safety concerns when selectively inhibiting only COX‑2.[8]
Drugs targeting cyclooxygenases act by: - Reversibly or irreversibly inhibiting the enzymatic activity of COX‑1 and/or COX‑2. - Blocking conversion of arachidonic acid to prostaglandins and thromboxanes. - Reducing synthesis of mediators involved in inflammation, pain, fever, and platelet aggregation.
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