5(S)-Hydroperoxyeicosatetraenoic acid (5(S)-HpETE) is a monohydroperoxy polyunsaturated fatty acid (PUFA) generated by the enzymatic conversion of arachidonic acid via 5-lipoxygenase (5-LO). Subsequently, 5(S)-HpETE undergoes metabolism to form leukotriene A4 (LTA4), which serves as a pivotal intermediate in the synthesis of leukotrienes (LTs).

The lipoxins are trihydroxy fatty acids containing a 7,9,11,13-conjugated tetraene. Lipoxin A4 (LXA4) was first described as a metabolite of 15-HpETE and/or 15-HETE when added in vitro to isolated human leukocytes. The material obtained in this manner consists of at least four distinct isomers: 5(S), 6(S); 5(S), 6(R); and the 11-trans and 11-cis isomers of each of these. 6(S)-LXA4 is one of the original four metabolites first identified by Serhan, Nicolaou, and Samuelsson. It was considered to be an artifact by these authors because it lacked the potency of the 5(S),6(R) isomer with respect to contraction of isolated guinea pig lung parenchymal strips. It has not been possible to isolate natural LXA4 from humans or other mammals in amounts sufficient for determination of absolute stereochemistry. Most authors refer to LXA4 as the 5(S)

15(S)-HETrE is the hydroxy-trienoic acid resulting from 15-lipoxygenation of dihomo-γ-linolenic acid . It is an inhibitor of 5-LO in human PMNL with an IC50 value of 4.6 μM. In RBL cells, 15(S)-HETrE inhibits 5-LO, but is about 1/20 as potent as 15(S)-HpETE.

5(R)-HETE is a rare lipoxygenase product of arachidonic acid. Nearly all plant and animal 5-LOs produce 5(S)-HETE, but the presence of a 5(R)-LO and the synthesis of 5(R)-HpETE and 5(R)-HETE have been confirmed in oocytes of the bivalve mollusk, S. solidissima. 5(R)-HETE is more potent than the (S)-enantiomer as a chemotactic agent for human neutrophils.

15(S)-HpETE is a monohydroperoxy polyunsaturated fatty acid (PUFA) produced by the action of 15-lipoxygenase (15-LO) on arachidonic acid. It is either metabolized to 14,15-leukotriene A4 [1] or reduced to 15(S)-HETE by peroxidases.[2] [1] 15(S)-HpETE mediates a number of biological functions including the induction of c-fos and c-jun, and activation of AP-1. [3] 15(S)-HpETE inhibits prostacyclin synthesis in porcine aortic microsomes and bovine endothelial cells, and can cause the suicide inactivation of porcine 12-LO.[2][4][5]

12(S)-HpETE is a monohydroperoxy polyunsaturated fatty acid (PUFA) produced by the action of platelet or leukocyte 12-lipoxygenase (12-LO) on arachidonic acid. It activates human blood leukocyte 5-LO, resulting in the synthesis of 5(S)-HETE, leukotriene B4 (LTB4), and 5(S),12(S)-DiHETE. Rat lung metabolizes 12(S)-HpETE to 8,11,12- and 10,11,12-trihydroxyeicostrienoic acids. 12(S)-HpETE is the mediator of many biological functions, including induction of c-fos and c-jun, activation of AP-1, and endothelium-dependent vasoconstriction. It mediates the inhibitory synaptic response to FMRF-amide in Aplysia sensory neurons and inhibits Ca2+/calmodulin-dependent protein kinase II from rat brain cortex.