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Eicosanoid biosynthesis pathway enzyme

Molecular classification
Enzyme, Oxidoreductase, Monooxygenase
01

Overview

Eicosanoid biosynthesis pathway enzymes are a group of enzymes responsible for the conversion of polyunsaturated fatty acids—primarily arachidonic acid—into eicosanoids. The main classes include cyclooxygenases (COX‑1 and COX‑2), which produce prostaglandins and thromboxanes; lipoxygenases (such as 5-lipoxygenase), which generate leukotrienes and lipoxins; and cytochrome P450 monooxygenases that form epoxyeicosatrienoic acids and hydroxyeicosatetraenoic acids. These enzymes play central roles in regulating inflammation, immune responses, vascular tone, pain perception, fever generation, platelet aggregation, cell growth control, blood pressure regulation, reproductive processes such as labor induction or abortion prevention—and are implicated in numerous diseases including inflammatory disorders like arthritis or asthma as well as cancer and cardiovascular conditions. Drugs targeting these pathways include NSAIDs that inhibit COXs to reduce inflammation/pain/fever but may cause gastrointestinal or cardiovascular side effects; leukotriene modifiers used in asthma/allergy management; and experimental agents modulating CYP-derived metabolites. The term "Eicosanoid biosynthesis pathway enzyme" is not a single molecular target but rather refers collectively to several distinct enzyme families involved in this metabolic network[1][2][4][5].

Other names
Cyclooxygenase (COX)Lipoxygenase (LOX)Cytochrome P450 (CYP) enzymesProstaglandin-endoperoxide synthase5-LipoxygenasePhospholipase A2 (PLA2)
02

Mechanism of action

Inhibition of cyclooxygenases to reduce prostaglandin and thromboxane synthesis[1][2][4] Inhibition of lipoxygenases to reduce leukotriene production[4]

03

Biological functions

Signal transductionInflammation regulationImmune response modulationVascular tone regulation
04

Disease associations

InflammationCancerCardiovascular disease
05

Safety considerations

Gastrointestinal toxicity/uscoceration with COX inhibition[4]Increased cardiovascular risk with selective COX‑2 inhibitors[4]
06

Interacting drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs; e.g., aspirin, ibuprofen)

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