Target intelligence / Profile preview

Cyclooxygenase and lipoxygenase pathway enzyme (COX and LOX)

Target
COX and LOX
Molecular classification
Enzyme
01

Overview

Cyclooxygenase and lipoxygenase pathway enzymes are two major families of iron-containing oxidative enzymes involved in the metabolism of arachidonic acid and related polyunsaturated fatty acids into bioactive lipid mediators known as eicosanoids[4][5][1]. Cyclooxygenases (COX; prostaglandin-endoperoxide synthase, PTGS) catalyze the conversion of arachidonic acid to prostaglandin H2 (PGH2), a precursor to prostanoids such as prostaglandins, prostacyclin, and thromboxanes, which play central roles in inflammation, pain, fever, platelet aggregation, and other physiological processes[5][2][3][6]. Two main COX isoforms exist in humans: COX-1 (constitutively expressed, physiologic homeostasis) and COX-2 (inducible, inflammation and disease contexts)[2][5][6]. Lipoxygenases (LOX) comprise a family of enzymes that oxygenate polyunsaturated fatty acids such as arachidonic acid, resulting in hydroperoxy derivatives that are further converted to leukotrienes, lipoxins, and hydroxyeicosatetraenoic acids (HETEs), key mediators in inflammation, allergy, asthma, and immune regulation[1][2][4]. Several LOX isoforms exist, defined by their regioselectivity (e.g., 5-LOX, 12-LOX, 15-LOX), each producing distinct sets of lipid mediators[4][1]. Both COX and LOX pathways are well-established therapeutic targets. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit COX activity to manage pain and inflammation, while leukotriene pathway modulators (e.g., zileuton, montelukast) target LOX products for asthma and allergy treatment[5][2]. Key safety challenges include gastrointestinal toxicity, cardiovascular risk (COX inhibitors), and hepatotoxicity (LOX inhibitors)[5].

Other names
prostaglandin-endoperoxide synthase (for cyclooxygenase)PTGS (for cyclooxygenase)COX (for cyclooxygenase)lipoxygenase (for lipoxygenase)LOX (for lipoxygenase)
02

Mechanism of action

Inhibition of prostaglandin synthesis (NSAIDs, COX inhibitors), Inhibition of leukotriene synthesis (LOX inhibitors), Selective COX-2 inhibition

03

Biological functions

Lipid mediator synthesisEicosanoid biosynthesisInflammationCell signaling
04

Disease associations

InflammationCancerCardiovascular diseaseOther
05

Safety considerations

Gastrointestinal toxicity (NSAIDs)Cardiovascular risk (COX-2 selective inhibitors)Increased bleeding riskRenal effectsHepatotoxicity (some LOX inhibitors)
06

Interacting drugs

Aspirin

6 more in the full profile.

07

Biomarkers

Overexpression of COX-2 in tumorsLeukotriene levels in asthma

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