Resolvin E1-d4

Resolvin E1-d4 (RvE1-d4) is intended for use as an internal standard for the quantification of RvE1 (Item No. 10007848) by GC- or LC-MS. RvE1 is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1 It is produced from eicosapentaenoic acid (EPA; Item No. 90110 | 90110.1 | 21908) via an 18-HEPE epoxide intermediate, which is formed by aspirin-acetylated COX-2-mediated oxidation of EPA and 5-lipoxygenase (5-LO), by leukotriene A4 (LTA4) hydrolase in human polymorphonuclear (PMN) neutrophils. RvE1 activates chemokine-like receptor 1 (CMKLR1; EC50 = 0.137 nM in a reporter assay). RvE1 (20 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of peritonitis induced by zymosan A (Item No. 21175). It increases survival and prevents decreases in colon length in a mouse model of TNBS-induced colitis when administered at a dose of 50 µg/kg.2 RvE1 (50 µg/kg) inhibits ovalbumin-induced increases in eosinophil and total cell numbers, as well as IL-13 and IgE levels in bronchoalveolar lavage fluid (BALF) in an ovalbumin-sensitized mouse model of asthma.3WARNING This product is not for human or veterinary use.

[1] SUNGWHAN F OH. Pro-resolving actions and stereoselective biosynthesis of 18S E-series resolvins in human leukocytes and murine inflammation.[J]. Journal of Clinical Investigation, 2011, 121 2: 569-581. DOI: 10.1172/jci42545
[2] MAKOTO ARITA. Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis.[J]. Proceedings of the National Academy of Sciences of the United States of America, 2005, 102 21: 7671-7676. DOI: 10.1073/pnas.0409271102
[3] HARUKA AOKI . Resolvin E1 dampens airway inflammation and hyperresponsiveness in a murine model of asthma[J]. Biochemical and biophysical research communications, 2008, 367 2: Pages 509-515. DOI: 10.1016/j.bbrc.2008.01.012
[4] DAVID MERIWETHER. Apolipoprotein A-I mimetics mitigate intestinal inflammation in COX2-dependent inflammatory bowel disease model.[J]. Journal of Clinical Investigation, 2019, 129 9: 3670-3685. DOI: 10.1172/jci123700