(±)13 hode

13(S)HODE Ethanolamide is a biochemical used to inhibit the adhesion of tumor cells

(S)-Coriolic acid (13(S)-HODE) is an important intracellular signaling agent generated by the reaction of linoleic acid with plant and mammalian lipoxygenases. It is involved in cell proliferation and differentiation in various biological systems and inhibits the adhesion of tumor cells to the vascular endothelium, while down-regulating IRGpIIb/IIIa receptor expression at around 1 μM. Additionally, (S)-Coriolic acid is a metabolite of 15-lipoxygenase (15-LOX) and often acts as an endogenous ligand to activate PPARγ. It induces mitochondrial dysfunction and airway epithelial damage.

(±)13-HODE is one of the two racemic monohydroxy fatty acids resulting from the non-enzymatic oxidation of linoleic acid. It is the principle hydroxylated fatty acid in human psoriatic skin scales, with a mean concentration of 17 ng/mg.[1]

(±)13-HODE cholesteryl ester, initially extracted from atherosclerotic lesions, is produced via Cu2+-catalyzed oxidation of LDL. Subsequent studies revealed that 15-LO from rabbit reticulocytes and human monocytes could metabolize cholesteryl linoleate (a major LDL component) to 13-HODE cholesteryl ester.

1-Palmitoyl-2-13(S)-HODE-sn-glycero-3-PC (13-HODE-PC) is an oxidized phospholipid with Palmitic acid at the sn-1 position and 13(S)-HODE at the sn-2 position. This compound can compete with 125I-NO2-LDL (5 g/ml) for binding to CD36-transfected 293 cells, with an IC50 value exceeding 200 μM.

13(R)-HODE cholesteryl ester was originally extracted from atherosclerotic lesions. It remains uncertain whether the oxidized fatty acid portion of the molecule results from enzymatic lipoxygenation or from random lipid peroxidation. 13(R)-HODE cholesteryl ester can be used as a standard for analysis of chiral HODE cholesteryl esters.

13(R)-HODE is the opposite enantiomer of 13(S)-HODE produced when linoleic acid is incubated with soybean lipoxygenase. Its presence in supernatants and membranes of cultured bovine endothelial cells has been attributed to COX metabolism. 13(R)-HODE is a weak (IC50 = 2.7 μM) inhibitor of U-46619-induced platelet aggregation.

13(S)-HODE is the lipoxygenase metabolite of linoleic acid. 13(S)-HODE modulates the platelet-activating factor, leukotriene B4, and formyl-Met-Leu-Phe-induced calcium influx in human polymorphonuclear leukocytes. The mechanism by which 13(S)-HODE elicits its inhibitory effect is still unclear. The use of biotinylated 15(S)-HETE as a probe for detecting binding proteins and/or receptors that specifically bind 15(S)-HETE provides a basis for similar use of 13(S)-HODE-biotin.

(±)9-HODE is one of the two racemic monohydroxy fatty acids resulting from the non-enzymatic oxidation of linoleic acid. Approximately equal proportions of both isomers are found in mitochondrial and plasma membranes of rabbit reticulocytes. [1][2] Oxidized LDL contains significant amounts of esterified 9- and 13-HpODEs and HODEs. [3][4]

13-Hydroxyoctadecadienoic acid (13-HODE), an endogenous metabolite produced by the lipoxygenase pathway of Linoleic acid, promotes prostacyclin synthesis by facilitating the release of arachidonic acid (AA) from phospholipids [1].

9-OxoODE, formed through the oxidation of the allylic hydroxyl group in both 9(S)-HODE and 9(R)-HODE, is present in rabbit reticulocyte plasma and mitochondrial membranes as both 9- and 13-oxoODEs, constituting approximately 2% of the total linoleate residues. The majority of these oxidized linoleate residues are esterified to membrane lipids.