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Cyclooxygenase enzymes (COX, officially prostaglandin-endoperoxide synthase) are key mediators in the conversion of arachidonic acid into prostaglandins and thromboxanes, which regulate inflammation, pain, fever response, and platelet aggregation. COX-1 is constitutively expressed and maintains physiological functions such as gastric mucosal integrity and renal blood flow, whereas COX-2 is primarily inducible and mediates inflammatory responses. Both isoforms are targeted by NSAIDs, which provide anti-inflammatory and analgesic effects but can also lead to notable adverse effects such as gastrointestinal toxicity and increased cardiovascular risk. COX-2 is often overexpressed in cancers, making it a therapeutic and prognostic target
Nonselective COX inhibition (aspirin, ibuprofen, naproxen): blocks both COX-1 and COX-2 - Selective COX-2 inhibition (celecoxib, etoricoxib): blocks only COX-2 - Irreversible acetylation (aspirin): permanently inactivates COX
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