Cyclooxygenase and lipoxygenase pathways (COX for cyclooxygenase and LOX for lipoxygenase)

The **cyclooxygenase (COX) and lipoxygenase (LOX) pathways** describe two principal enzyme-mediated routes for the metabolism of arachidonic acid (a polyunsaturated fatty acid liberated from membrane phospholipids) to a broad array of bioactive lipids known as **eicosanoids**. COX enzymes convert arachidonic acid into prostaglandins, prostacyclin, and thromboxane, which regulate inflammation, vasodilation, and platelet function. LOX enzymes generate hydroperoxy derivatives further converted into leukotrienes and lipoxins, key mediators of inflammation, immune response, and allergy. Both COX and LOX are proven drug targets in pain, inflammation, cancer, and cardiovascular therapy. Their inhibition forms the mechanism behind NSAIDs, COX-2-selective drugs, and leukotriene inhibitors used clinically. However, their products are critical for physiologic homeostasis, so pharmacologic manipulation is linked with notable safety concerns including GI, cardiovascular, and renal adverse effects. For structured database use, the canonical targets should be listed individually: - "Cyclooxygenase-1" (COX-1/PTGS1) - "Cyclooxygenase-2" (COX-2/PTGS2) - "5-Lipoxygenase" (ALOX5) - "12-Lipoxygenase," "15-Lipoxygenase," etc. The entry as provided ("Cyclooxygenase and lipoxygenase pathways") is a **pathway, not a singular molecular target**. For drug target annotation, use specific enzyme names.

Other names

Cyclooxygenase pathway (COX pathway)Lipoxygenase pathway (LOX pathway)Eicosanoid biosynthesis pathwaysArachidonic acid metabolic pathways

Inhibition of prostanoid synthesis (NSAIDs block COX to reduce prostaglandin production, thereby decreasing inflammation and pain). Leukotriene inhibition (inhibitors of LOX block formation of leukotrienes, used in asthma and allergies). Prevention of platelet aggregation and thrombosis (COX-1 inhibition).