Biologically Active Small Molecules

13(R)-HODE is the opposite enantiomer of the 13(S)-HODE produced when linoleic acid is incubated with soybean LO. The presence of 13(R)-HODE in the supernatants and membranes of cultured bovine endothelial cells has been attributed to COX metabolism.

A chiral enantiomer of 13,14-epoxy fluprostenol isopropyl ester whose pharmacology has not been studied extensively to date.

A chiral enantiomer of 13,14-epoxy fluprostenol isopropyl ester whose pharmacology has not been studied extensively to date.

A chiral enantiomer of 13,14-epoxy fluprostenol isopropyl ester whose pharmacology has not been studied extensively to date.

13(S)-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(S)-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(S)-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.

A neutral, more lipophilic form of the free acid.

A neutral, more lipophilic form of the free acid.

A neutral, more lipophilic form of the free acid.

13(S)-HODE is produced by incubation of linoleic acid with plant and mammalian LOs. It has been shown to inhibit the adhesion of tumor cells to the endothelium at concentrations around 1 &microM, and down regulates the expression of the

13(S)-HODE is the LO metabolite of linoleic acid. 13(S)-HODE modulates the PAF, LTB4, and fMLP-induced calcium influx in human PMNL.