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Description: Important polyunsaturated fatty acid found in fish oils. It serves as the precursor for the prostaglandin-3 and thromboxane-3 families. A diet rich in eicosapentaenoic acid lowers serum lipid concentration, reduces incidence of cardiovascular disorders, prevents platelet aggregation, and inhibits arachidonic acid conversion into the thromboxane-2 and prostaglandin-2 families. [PubChem]
Drug Type: Small Molecule; Nutraceutical; Approved
Pharmacology: Eicosanoids are chemical messengers derived from 20-carbon polyunsaturated fatty acids that play critical roles in immune and inflammatory responses. Both 20-carbon omega-6 fatty acids (arachidonic acid) and 20-carbon omega-3 fatty acids (EPA) can be found in cell membranes. During an inflammatory response, arachidonic acid and EPA are metabolized by enzymes known as cyclooxygenases and lipoxygenases to form eicosanoids. Increasing omega-3 fatty acid intake increases the EPA content of cell membranes and decreases the arachidonic acid content, resulting in higher proportions of eicosanoids derived from EPA. Physiologic responses to arachidonic acid-derived eicosanoids differ from responses to EPA-derived eicosanoids. In general, eicosanoids derived from EPA are less potent inducers of inflammation, blood vessel constriction, and clotting than eicosanoids derived from arachidonic acid.
Mechanism of Action: The anti-inflammatory, antithrombotic and immunomodulatory actions of EPA is probably due to its role in eicosanoid physiology and biochemistry. Most eicosanoids are produced by the metabolism of omega-3 fatty acids, specifically, arachidonic acid. These eicosanoids, leukotriene B4 (LTB4) and thromboxane A2 (TXA2) stimulate leukocyte chemotaxis, platelet aggregation and vasoconstriction. They are thrombogenic and artherogenic. On the other hand, EPA is metabolized to leukotriene B5 (LTB5) and thromboxane A3 (TXA3), which are eicosanoids that promote vasodilation, inhibit platelet aggregation and leukocyte chemotaxis and are anti-artherogenic and anti-thrombotic. The triglyceride-lowering effect of EPA results from inhibition of lipogenesis and stimulation of fatty acid oxidation. Fatty acid oxidation of EPA occurs mainly in the mitochondria. EPA is a substrate for Prostaglandin-endoperoxide synthase 1 and 2. It also appears to affect the function and bind to the Carbohydrate responsive element binding protein (ChREBP) and to a fatty acid receptor (G-coupled receptor) known as GP40.
Indication: EPA can be used for lowering elevated triglycerides in those who are hyperglyceridemic. In addition, EPA may play a therapeutic role in patients with cystic fibrosis by reducing disease severity and may play a similar role in type 2 diabetics in slowing the progression of diabetic nephropathy.
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Data Correlations | 1 study

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Genes category icon Genes
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644975 100 100
RGS1 92 92
CLC 90 90
IRAK3 83 83
ZNF200 82 82
ZNF614 80 80
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Biogroups category icon Biogroups
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G-alpha-S Pathway 100 100
Interferon Gamma Pathway 99 99
Death 99 99
Regulator of G protein signalling 99 99
Regulator of G protein signalling s… 99 99
Krueppel-associated box 98 98
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Individual Studies

  • Gene expression in PBMCs after fish oil supplementation

    Homo sapiens Homo sapiens | RNA Expression   RNA Expression

    Fasting venous blood samples were collected at baseline and after 26 weeks of supplementation with either 1.8 g EPA and DHA or HOSF.

    Source: NextBio Library/Immune response and infection
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Associated Researchers

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Thought leaders and organizations working on research involving eicosapentaenoic acid.

View All Author iconAuthors
  • Masaaki Soma
  • Marina A Lynch
  • Aileen M Lynch
  • Alice H Lichtenstein
  • Aedín M Minogue
View All Clinical trial sponsors icon Clinical Trials Sponsors
  • S.L.A. Pharma AG
  • University of Texas Southwestern Medical Center
  • Aalborg Hospital
  • Yamaguchi University Hospital
  • H. Lee Moffitt Cancer Center and Research Institute
View All Affiliations icon Organizations
  • Kyoto University
  • Kobe University
  • Tufts University
  • University of California
  • University of Oslo

Clinical Trials | 76 trials

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