5(6)-DiHET is a fully racemic version of the enantiomeric forms biosynthesized from 5(6)-EET by epoxide hydrolases. [1] 5(6)-DiHET can be used to quantify 5(6)-EET due to the conversion of 5(6)-EET to 5(6)-δ-lactone in solution. [2] 5(6)-DiHET activates large conductance calcium-activated potassium (BK) channels in smooth muscle cells from rat small coronary arteries. [3 It is a substrate for sheep seminal vesicle COX, producing 5,6-dihydroxy prostaglandin E1 and F1α metabolites in vitro. [4] 5(6)-DiHET levels decrease in plasma in a high-fat diet-induced rat model of hyperlipidemia.[5]

Reference:
[1]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).
[2]. Rashid, M., Manivet, P., Nishio, H., et al. Identification of the binding sites and selectivity of sarpogrelate, a novel 5-HT2 antagonist, to human 5-HT2A, 5-HT2B and 5-HT2C receptor subtypes by molecular modeling. Life Sci. 73(2), 193-207 (2003).
[3]. Lu, T., Katakam, P.V.G., VanRollins, M., et al. Dihydroxyeicosatrienoic acids are potent activators of Ca2+-activated K+ channels in isolated rat coronary arterial myocytes. J. Physiol. 534(Pt 3), 651-667 (2001).
[4]. Oliw, E.H. Biosynthesis of 5,6-dihydroxyprostaglandin E1 and F1α from 5,6-dihydroxyeicosatrienoic acid by ram seminal vesicles. Biochim. Biophys. Acta. 795(2), 384-391 (1984).
[5]. Miao, H., Zhao, Y.-H., Vaziri, N.D., et al. Lipidomics biomarkers of diet-induced hyperlipidemia and its treatment with Poria cocos. J. Agric. Food Chem. 64(4), 969-979 (2016).