15(R)-Lipoxin A4  (Synonyms: 15-epi-LXA4)

15 (R)-Lipoxin A4 (15-epi-LXA4) is a specialized pro-resolving mediator and an acetylated derivative of COX2. 15 (R)-Lipoxin A4 is present in neurons. 15 (R)-Lipoxin A4 induces the SPM synthases ALOX12 and ALOX15, as well as the pro-resolving receptor ALX. 15 (R)-Lipoxin A4 inhibits protein kinases, including JNK1/2/3, Lyn, STAT-3 and STAT-6. 15 (R)-Lipoxin A4 enhances the release of pro-resolving mediators. 15 (R)-Lipoxin A4 alleviates the pro-inflammatory phenotype of tendon-derived stromal cells. 15 (R)-Lipoxin A4 promotes the resolution of neuroinflammation. 15 (R)-Lipoxin A4 is applicable to research related to achilles tendinitis, achilles tendon rupture and Alzheimer’s disease^[1][2].

15 (R)-Lipoxin A4 (10 nM; 24 h) reduces the levels of proinflammatory eicosanoids and increases the levels of specific pro-resolving mediators in IL-1β-stimulated tendon matrix cells derived from tendinopathy^[1].
15 (R)-Lipoxin A4 (10 nM; 24 h) reduces the levels of proinflammatory eicosanoids and increases the levels of pro-resolving mediators in tendon stromal cells derived from allergic rhinitis following stimulation with IL-1β^[1].
15 (R)-Lipoxin A4 (10 nM; 24 h) upregulates the expressions of pro-resolving biosynthetic enzymes ALOX12, ALOX15 and receptor ALX in tendon stromal cells derived from tendinopathy and allergic rhinitis that are stimulated by IL-1β, and the mRNA level of ALOX15 increases significantly in both cell types^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

352.47

C₂₀H₃₂O₅

171030-11-8

Liquid

Colorless to light yellow

CCCCC[C@@H](O)/C=C/C=C\C=C\C=C\[C@@H](O)[C@@H](O)CCCC(O)=O

Room temperature in continental US; may vary elsewhere.

Solution, -20°C, 2 years

• [1]. Dakin SG, et al. 15-Epi-LXA₄ and MaR1 counter inflammation in stromal cells from patients with Achilles tendinopathy and rupture. FASEB J. 2019;33(7):8043-8054.  [Content Brief]

  [2]. Lee JY, et al. Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer's Disease. Nat Commun. 2018;9(1):1479. Published 2018 Apr 16.  [Content Brief]