Editing Lipoxin (section)

===Further metabolism===
LXs are rapidly metabolized, mainly by macrophages, to inactive products by being oxidized at carbon 15 to form 15-[[Ketone|keto]] (also termed 15-oxo) LX products by a [[15-hydroxyprostaglandin dehydrogenase]]; 15-oxo-LXA<sub>4</sub> may be further metabolized to 13,14-dihydro-LXA<sub>4</sub> by an [[oxidoreductase]]. 15-Epi-LXA<sub>4</sub> and 15-epi-LXB<sub>4</sub> are more resistant to the dehydrogenation enzyme than their LX epimers.<ref name="pmid16046112"/> In consequence of the operation of this [[anabolic]] pathway, LXs have very short half-lives ''in vivo''. The epi-LXs have longer ''in vivo'' half-lives and thereby greater potencies than their LX epimers, and synthetic lipoxins that are metabolically resistant to this pathway have been prepared, used in animal models to study LX activities, and tested as potential therapeutic agents in animals and humans.<ref name="pmid25895638"/><ref name="pmid26457057"/>

Similar to various other AA metabolites such as [[LTA4|LTA<sub>4</sub>]] and [[5-oxo-eicosatetraenoic acid]], cells and tissues may convert LXs to 20-hydroxy products by [[omega oxidation]]; they also have been shown to ligate LXA<sub>4</sub> to [[glutathione]] to form [[cysteine|cysteinyl-lipoxins]], initially LXC<sub>4</sub>, which is then sequentially metabolized to LXD<sub>4</sub> and LXE<sub>4</sub>.<ref name="pmid7706749">{{cite journal |vauthors=Powell WS, Chung D, Gravel S |title=5-Oxo-6,8,11,14-eicosatetraenoic acid is a potent stimulator of human eosinophil migration |journal=J. Immunol. |volume=154 |issue=8 |pages=4123–32 |year=1995 |doi=10.4049/jimmunol.154.8.4123 |pmid=7706749 |s2cid=35712418 |doi-access=free }}</ref> The role of these pathways in limiting or contributing to the activity of the LXs has not been fully evaluated.