Eicosanoid (None)

Eicosanoids are bioactive lipid mediators derived from arachidonic acid, produced locally at sites of tissue injury or infection through enzymatic oxidation pathways involving cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450s. They encompass several structurally related families—including prostaglandins, thromboxanes, leukotrienes, lipoxins, and others—that regulate key physiological processes such as initiation and resolution of inflammation; pain sensation; fever generation; vascular tone; platelet aggregation; smooth muscle contraction; reproductive events like labor induction; gastric mucosal protection; among others. Their dysregulation contributes significantly to acute/chronic inflammatory diseases (rheumatoid arthritis, asthma, IBD), cardiovascular pathology (hypertension, atherosclerosis), cancer progression/metastasis via tumor-promoting subtypes like PGE₂—and conversely some have anti-tumorigenic properties. Therapeutically relevant drugs modulate their synthesis/action rather than binding them directly—for example NSAIDs inhibit COXs reducing pro-inflammatory prostaglandin output but carry notable safety risks due to interference with homeostatic/protective roles elsewhere in the body.

Other names

EicosanoidsInflammatory lipid mediatorsPro-inflammatory eicosanoidsOxylipins

Drugs targeting this pathway act by: – Inhibiting biosynthetic enzymes such as cyclooxygenases (COX‑1, COX‑2) or lipoxygenases (LOX) to decrease production of pro-inflammatory eicosanoids. – Blocking specific cell-surface receptors for prostaglandins/leukotrienes on immune cells/smooth muscle/etc., thereby preventing downstream signaling events like vasodilation, pain sensitization, bronchoconstriction.