15(R)-HpETE and 15(R)-HETE lack some of the activity attributed to their S stereoisomers but can be further metabolized to bioactive products viz., the 15(R) class of lipoxins (also termed epi-lipoxins).

They appear to act as hormone-like autocrine and paracrine signaling agents that are involved in regulating inflammatory and perhaps other responses.

In this terminology S refers to the absolute configuration of the chirality of the hydroxy functional group at carbon position 15.

[11] When pretreated with aspirin, however, COX-1 is inactive while COX-2 attacks arachidonic acid to produce almost exclusively 15(R)-HETE along with its presumed precursor 15(R)-HpETE.

[54][55][56][57] These growth-stimulating effects could contribute to the progression of the cited cancer types in animal models or even humans[48][49] and the excess fibrosis that causes the narrowing of pulmonary arteries in hypoxia-induced pulmonary hypertension[51] or narrowing of portal arteries in the portal hypertension accompanying liver cirrhosis.

[58] 15(S)-HETE may also act through BLT2 to stimulate an immediate contractile response in rat pulmonary arteries[59] and its angiogenic effect on human umbilical[55] and dermal[54] vascular endothelial cells.

[66] The decline in the level of 15(S)-HpETE-forming enzymes and consequential fall in cellular 15-HETE production that occurs in human prostate cancer cells may be one mechanism by which this and perhaps other human cancer cells (e.g. those of the colon, rectum, and lung) avoid the apoptosis-inducing actions of 15(S)-HpETE and/or 15(S)-HETE and thereby proliferate and spread.

[69][70][66][71][72] 15(S)-HpETE and 15(S)-HETE inhibit angiogenesis and the growth of cultured human chronic myelogenous leukemia K-562 cells by a mechanism that is associated with the production of reactive oxygen species.

[55][73][74] Several bifunctional electrophilic breakdown products of 15(S)-HpETE, e.g. 4-hydroxy-2(E)-nonenal, 4-hydroperoxy-2(E)-nonenal, 4-oxo-2(E)-nonenal, and cis-4,5-epoxy-2(E)-decanal, are mutagens in mammalian cells and thereby may contripute to the development and/or progression of human cancers.

[38] In cultured human monocytes of the THP1 cell line, 15-oxo-ETE inactivates IKKβ (also known as IKK2) thereby blocking this cell's NF-κB-mediated pro-inflammatory responses (e.g. lipopolysaccharide-induced production of TNFα, interleukin 6, and IL1B) while concurrently activating anti-oxidant responses upregulated through the anti-oxidant response element (ARE) by forcing cytosolic KEAP1 to release NFE2L2 which then moves to the nucleus, binds ARE, and induces production of, e.g. hemoxygenase-1, NADPH-quinone oxidoreductase, and possibly glutamate-cysteine ligase modifier.

These ketones are highly reactive with nucleophiles, adducting to, for example, the cysteines in transcription and transcription-related regulatory factors and enzymes to form their alkylated and thereby often inactivated products.

This 15-oxo-ETE action may prove to inhibit the remodeling of blood vessels and reduce the growth of the cited cell types and cancers.

At sub-micromolar concentrations, 15-oxo-ETE has weak chemotaxis activity for human monocytes and could serve to recruit this white blood cell into inflammatory responses.

[80] LXA4, LXB4, AT-LXA4, and AT-LXB4 are specialized proresolving mediators, i.e. they potently inhibit the progression and contribute to the resolution of diverse inflammatory and allergic reactions.

The production of eoxins by Reed-Sternburg cells has also led to suggestion that they are involve in the lymphoma of Hodgkins disease.