Target intelligence / Profile preview

Arachidonic acid metabolic pathway (AA metabolic pathway (or AA pathway))

Target
AA metabolic pathway (or AA pathway)
Molecular classification
Enzyme (COX, LOX, CYP family enzymes), Metabolic pathway, Other (lipid mediator biosynthesis pathway)
01

Overview

The arachidonic acid metabolic pathway encompasses the release of arachidonic acid (AA) from cell membrane phospholipids, typically triggered by phospholipase A2, and its subsequent conversion by three principal enzymatic routes: cyclooxygenase (COX) to prostaglandins and thromboxanes; lipoxygenase (LOX) to leukotrienes and lipoxins; and cytochrome P450 (CYP) to epoxyeicosatrienoic acids and hydroxyeicosatetraenoic acids. These metabolites orchestrate diverse biological effects, including mediation of inflammation, immune responses, vascular tone, pain, and tissue homeostasis. Dysregulation of this pathway is implicated in inflammatory diseases, cardiovascular and metabolic disorders, neurodegeneration, and cancer. Numerous drugs target enzymes within this pathway to control inflammation and related conditions—making it a nexus of research and clinical intervention. However, as a pathway, it should not be classified as a single molecular target for structured drug or biomarker databases; its therapeutic significance lies in the individual molecular components, each with distinct biological roles and pharmacological relevance.

Other names
Arachidonic acid pathwayAA pathwayEicosanoid pathwayPUFA (polyunsaturated fatty acid) metabolism
02

Mechanism of action

Enzyme inhibition (block conversion of AA to prostaglandins, thromboxanes, or leukotrienes); Receptor antagonism (block eicosanoid receptors); Modulation of substrate availability (inhibit AA release)

03

Biological functions

Inflammation (pro- and anti-inflammatory mediator generation)Vascular tone regulationImmune response modulationCell proliferation and apoptosis (via eicosanoid signaling)Pain perceptionPlatelet aggregationResolution of inflammation and wound healing
04

Disease associations

Inflammation (e.g., asthma, arthritis)Cardiovascular disease (e.g., atherosclerosis, hypertension)Cancer (various types)Metabolic disease (obesity, diabetes, non-alcoholic fatty liver disease)Neurodegenerative disease (Alzheimer's disease, etc.)Allergy and autoimmune conditionsOther (pain, fibrosis, wound healing, infection)
05

Safety considerations

Gastrointestinal, cardiovascular, and renal risks (from COX inhibition/NSAIDs)Immunosuppression (with corticosteroids)Potential for increased cardiovascular events (COX-2 inhibitors)Disrupted wound healing or resolution of inflammation (with over-inhibition of pathway components)
06

Interacting drugs

Non-steroidal anti-inflammatory drugs (NSAIDs, e.g., aspirin, ibuprofen) inhibit COX enzymes

4 more in the full profile.

07

Biomarkers

Prostaglandin E2 and other prostaglandins (for inflammation and drug response)Leukotriene B4, C4, D4, E4 (for asthma and allergic diseases)Thromboxane B2Lipoxin A4 (in resolving inflammation and atherosclerosis)

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