79551-81-8

Basic information

• Product Name: (5E,8E,11E)-14,15-dihydroxyicosa-5,8,11-trienoic acid
• Synonyms: (5E,8E,11E)-14,15-dihydroxyicosa-5,8,11-trienoic acid;14,15-Dihydroxyeicosatrienoic acid;14,15-dihydroxy-5,8,11-eicosatrienoic acid
• CAS NO: 79551-81-8
• Molecular Formula: C20H34O4
• Molecular Weight: 0
• Mol File: 79551-81-8.mol

Chemical Properties

• Boiling Point: 515.2°C at 760 mmHg
• Flash Point: 279.4°C
• Appearance: /
• Density: 1.025g/cm³
• Vapor Pressure: 9.1E-13mmHg at 25°C
• Refractive Index: 1.514
• CAS DataBase Reference: (5E,8E,11E)-14,15-dihydroxyicosa-5,8,11-trienoic acid(CAS DataBase Reference)
• NIST Chemistry Reference: (5E,8E,11E)-14,15-dihydroxyicosa-5,8,11-trienoic acid(79551-81-8)
• EPA Substance Registry System: (5E,8E,11E)-14,15-dihydroxyicosa-5,8,11-trienoic acid(79551-81-8)

Safety Data

• Hazardous Substances Data: 79551-81-8(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Industry:
14,15-DHET is used as a therapeutic agent for the treatment of hypertension, cardiovascular disease, and cancer due to its anti-inflammatory and vasodilatory effects. Its potential role in modulating inflammation and vascular function makes it a promising candidate for the development of novel therapeutic strategies to combat these conditions.
Used in Research Applications:
14,15-DHET is used as a research tool to study the molecular mechanisms underlying inflammation, vascular function, and cancer progression. Its involvement in various physiological and pathological processes makes it an important molecule for understanding the complex interplay between these processes and for identifying potential therapeutic targets.
Used in Drug Development:
14,15-DHET is used as a lead compound in the development of new drugs targeting hypertension, cardiovascular disease, and cancer. Its potent biological activities and potential therapeutic effects make it a valuable starting point for the design and synthesis of novel drug candidates with improved efficacy and safety profiles.

InChI:InChI=1/C20H34O4/c1-2-3-12-15-18(21)19(22)16-13-10-8-6-4-5-7-9-11-14-17-20(23)24/h4,6-7,9-10,13,18-19,21-22H,2-3,5,8,11-12,14-17H2,1H3,(H,23,24)/b6-4+,9-7+,13-10+

Upstream product

• 160031-48-1 (14S),(15S)-dihydroxyeicosatrienoic acid methyl ester 
• 159555-23-4 Methyl-β-D-glucofuranosidurono-6,3-lacton 
• 160031-38-9 Thiocarbonic acid O-((3S,3aS,5R,6R,6aS)-5-methoxy-2-oxo-6-phenoxythiocarbonyloxy-hexahydro-furo[3,2-b]furan-3-yl) ester O-phenyl ester 
• 98050-10-3 (2R,3R,5R)-5-Methoxy-2-pentyl-tetrahydro-furan-3-ol 
• 160031-47-0 (2R,3S,5R)-5-Methoxy-2-pentyl-tetrahydro-furan-3-ol 
• 1027550-50-0 (5Z,8Z,11Z)-(14S,15R)-15-Hydroxy-14-(4-methoxy-benzyloxy)-icosa-5,8,11-trienoic acid methyl ester 
• 17681-01-5 methyl β-D-glucofuranosidurono-6,3-lactone 
• 98064-06-3 (14R),(15R)-dihydroxyeicosatrienoic acid methyl ester 
• 1027051-55-3 (5Z,8Z,11Z)-(14R,15R)-15-Hydroxy-14-(4-methoxy-benzyloxy)-icosa-5,8,11-trienoic acid methyl ester 
• 160031-49-2 (14R),(15S)-dihydroxyeicosatrienoic acid methyl ester 
• 160031-50-5 (14S),(15R)-dihydroxyeicosatrienoic acid methyl ester 
• 197508-62-6 cis-14,15-epoxyeicosatrienoic acid 

Downstream Products

• 90080-09-4 14(R),15(S)-epoxyeicosatrienoic acid methyl ester 
• 110901-52-5 14(S),15(R)-epoxyeicosatrienoic acid methyl ester 

Relevant articles and documents

Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3β signaling

Acute kidney injury (AKI) causes severe morbidity and mortality for which new therapeutic strategies are needed. Docosahexaenoic acid (DHA), arachidonic acid (ARA), and their metabolites have various effects in kidney injury, but their molecular mechanisms are largely unknown. Here, we report that 14 (15)-epoxyeicosatrienoic acid [14 (15)-EET] and 19 (20)-epoxydocosapentaenoic acid [19 (20)-EDP], the major epoxide metabolites of ARA and DHA, respectively, have contradictory effects on kidney injury in a murine model of ischemia/ reperfusion (I/R)-caused AKI. Specifically, 14 (15)-EET mitigated while 19 (20)-EDP exacerbated I/R kidney injury. Manipulation of the endogenous 19 (20)-EDP or 14 (15)-EET by alteration of their degradation or biosynthesis with selective inhibitors resulted in anticipated effects. These observations are supported by renal histological analysis, plasma levels of creatinine and urea nitrogen, and renal NGAL. The 14 (15)-EET significantly reversed the I/R-caused reduction in glycogen synthase kinase 3β (GSK3β) phosphorylation in murine kidney, dose-dependently inhibited the hypoxia/reoxygenation (H/R)-caused apoptosis of murine renal tubular epithelial cells (mRTECs), and reversed the H/R-caused reduction in GSK3β phosphorylation in mRTECs. In contrast, 19 (20)-EDP dose-dependently promoted H/R-caused apoptosis and worsened the reduction in GSK3β phosphorylation in mRTECs. In addition, 19 (20)-EDP was more metabolically stable than 14 (15)-EET in vivo and in vitro. Overall, these epoxide metabolites of ARA and DHA function conversely in I/R-AKI, possibly through their largely different metabolic stability and their opposite effects in modulation of H/R-caused RTEC apoptosis and GSK3β phosphorylation. This study provides AKI patients with promising therapeutic strategies and clinical cautions.

vic-Diol chirons: Enantiospecific synthesis of 11,12- and 14,15-dihydroxyeicosatrienoic acids

A differentiated, six-carbon vicinal-diol chiron was prepared from D-glucurono-6,3-lactone and exploited in the asymmetric synthesis of the erythro/threo-isomers of the title eicosanoids.