Target intelligence / Profile preview

17,18-epoxyeicosatetraenoic acid (17,18-EEQ) (17,18-EEQ)

Target
17,18-EEQ
Molecular classification
Eicosanoid, Oxylipin, Epoxyeicosanoid, Omega-3 fatty acid metabolite
01

Overview

17,18-epoxyeicosatetraenoic acid (17,18-EEQ) is a bioactive lipid metabolite derived from the omega-3 fatty acid eicosapentaenoic acid (EPA) via cytochrome P450 (CYP) epoxygenases (PubChem CID 5280958). It serves as a potent signaling molecule with significant anti-inflammatory, anti-arrhythmic, and vasodilatory properties. In the cardiovascular system, 17,18-EEQ helps regulate vascular tone and protects against arrhythmias by modulating ion channel activity, specifically by activating large-conductance calcium-activated potassium (BK) channels (Arnold et al., 2010, J Biol Chem). It also plays a role in resolving inflammation and has been shown to reduce airway hyperreactivity in asthma models (Morisseau & Hammock, 2013, Annu Rev Pharmacol Toxicol). While not a protein target itself, 17,18-EEQ acts as an endogenous ligand for receptors such as GPR40 (FFAR1) (Theilig et al., 2016, Mol Pharmacol). Therapeutic strategies often focus on increasing its bioavailability, either through the inhibition of soluble epoxide hydrolase (sEH)—the enzyme responsible for its degradation—or through the development of stable synthetic analogs for treating cardiovascular and inflammatory diseases.

Other names
17,18-EpETE17(18)-EpETE17,18-epoxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid17,18-epoxy-EPA
02

Mechanism of action

Acts as an endogenous lipid mediator that activates G protein-coupled receptors such as GPR40 (FFAR1) and modulates the activity of large-conductance calcium-activated potassium (BK) channels to induce vasorelaxation and stabilize cardiac rhythm.

03

Biological functions

VasodilationAnti-inflammatory responseAnti-arrhythmic activityBronchorelaxationSignal transductionG protein-coupled receptor activation
04

Disease associations

Cardiovascular diseaseArrhythmiaHypertensionInflammationAsthmaMetabolic syndrome
05

Safety considerations

Rapid metabolic degradation by soluble epoxide hydrolase (sEH) limits therapeutic half-lifePotential for non-specific binding at high pharmacological dosesComplex interplay with other arachidonic acid-derived pro-inflammatory mediators
06

Interacting drugs

Soluble epoxide hydrolase inhibitors (e.g., TPPU, UC1728)

1 more in the full profile.

07

Biomarkers

Plasma 17,18-EEQ levels17,18-EEQ to 17,18-DiHETE ratio

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