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14,15-EE-8(Z)-E Sale

(Synonyms: 14,15Epoxyeicosa8(Z)enoic Acid) 目录号 : GC40425

A potent vasodilator

14,15-EE-8(Z)-E Chemical Structure

Cas No.:519038-93-8

规格 价格 库存 购买数量
25μg
¥652.00
现货
50μg
¥1,234.00
现货
100μg
¥2,346.00
现货
500μg
¥10,415.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

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产品描述

Epoxyeicosatrienoic acids (EETs), such as 11(12)-EET and 14(15)-EET, are cytochrome P450 metabolites of arachidonic acid that have been identified as endothelium-derived hyperpolarizing factors with vasodilator activity. 14,15-EE-8(Z)-E is a structural analog of 14(15)-EET that demonstrates potent vasodilator agonist activity in bovine coronary arteries similar to that of 14(15)-EET.

Chemical Properties

Cas No. 519038-93-8 SDF
别名 14,15Epoxyeicosa8(Z)enoic Acid
Canonical SMILES CCCCC[C@H]1O[C@H]1CCCC/C=C\CCCCCCC(=O)O
分子式 C20H36O3 分子量 324.5
溶解度 DMF: 10 mg/ml,DMSO: 10 mg/ml,Ethanol: 10 mg/ml,PBS (pH 7.2): 0.5 mg/ml 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 3.0817 mL 15.4083 mL 30.8166 mL
5 mM 0.6163 mL 3.0817 mL 6.1633 mL
10 mM 0.3082 mL 1.5408 mL 3.0817 mL
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Research Update

Epoxyeicosatrienoic Acid and Prostanoid Crosstalk at the Receptor and Intracellular Signaling Levels to Maintain Vascular Tone

Int J Mol Sci 2022 May 25;23(11):5939.PMID:35682616DOI:PMC9180422

Epoxyeicosatrienoic acids (EETs) are signaling lipids produced by the cytochrome P450-(CYP450)-mediated epoxygenation of arachidonic acid. EETs have numerous biological effects on the vascular system, but aspects including their species specificity make their effects on vascular tone controversial. CYP450 enzymes require the 450-reductase (POR) for their activity. We set out to determine the contribution of endothelial CYP450 to murine vascular function using isolated aortic ring preparations from tamoxifen-inducible endothelial cell-specific POR knockout mice (ecPOR-/-). Constrictor responses to phenylephrine were similar between control (CTR) and ecPOR-/- mice. Contrastingly, sensitivity to the thromboxane receptor agonist U46619 and prostaglandin E2 (PGE2) was increased following the deletion of POR. Ex vivo incubation with a non-hydrolyzable EET (14,15-EE-8(Z)-E, EEZE) reversed the increased sensitivity to U46619 to the levels of CTR. EETs had no effect on vascular tone in phenylephrine-preconstricted vessels, but dilated vessels contracted with U46619 or PGE2. As U46619 acts through RhoA-dependent kinase, this system was analyzed. The deletion of POR affected the expression of genes in this pathway and the inhibition of Rho-GTPase with SAR407899 decreased sensitivity to U46619. These data suggest that EET and prostanoid crosstalk at the receptor level and that lack of EET production sensitizes vessels to vasoconstriction via the induction of the Rho kinase system.