(±)8(9)-EET is a fully racemic version of the R/S enantiomeric forms biosynthesized from arachidonic acid .^1,2 (±)8(9)-EET is a major cytochrome P450 (CYP450) metabolite in the renal cortex.³ It activates PPARα in HEK293 cells when used at a concentration of 1 µM but inhibits NF-κB activity induced by IL-1β in a PPARα-dependent and -independent fashion.⁴ It is also a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 µM.⁵ (8S,9R)-EET (1 µg/kg), but not (8R,9S)-EET, reduces the glomerular filtration rate (GFR) through COX-dependent pre-glomerular vasoconstriction in rats.⁶