Cyclooxygenase and Lipoxygenase enzymes (COX and LOX)

**Cyclooxygenase (COX) enzymes**—comprising COX-1 and COX-2 isoforms—*catalyze the conversion of arachidonic acid to prostaglandins and thromboxanes*, mediators of inflammation, pain, fever, and hemostasis. **Nonsteroidal anti-inflammatory drugs (NSAIDs)** alleviate symptoms by inhibiting COX activity[3][5]. **Lipoxygenase (LOX) enzymes** encompass several isoforms (e.g., 5-LOX, 12-LOX, 15-LOX) and *oxygenate polyunsaturated fatty acids* to form hydroperoxy derivatives, which are then converted to leukotrienes, lipoxins, and other signaling mediators. LOX enzymes are key to inflammatory and allergic processes, with drugs targeting their activity used in asthma and allergy management[1][4]. Both enzyme families are targets for drug discovery in inflammation, cancer, cardiovascular disease, and respiratory disorders, but are best analyzed individually for clarity and specificity in clinical or research settings[6][4][2][1].

Other names

Prostaglandin-endoperoxide synthaseProstaglandin G/H synthaseLOXarachidonate 5-lipoxygenasearachidonate 12-lipoxygenasearachidonate 15-lipoxygenase

Cyclooxygenase inhibitors block prostaglandin and thromboxane synthesis, reducing inflammation, pain, fever, and platelet aggregation. Lipoxygenase inhibitors block leukotriene biosynthesis, reducing bronchoconstriction and immune cell recruitment in allergy and asthma.