15(S)-HETE Chemical Properties

Boiling point:

487.7±45.0 °C(Predicted)

Density 

0.984±0.06 g/cm3(Predicted)

Flash point:

14℃

storage temp. 

-20°C

solubility 

0.1 M Na2CO3: 2 mg/ml; DMF: Miscible; DMSO: Miscible; Ethanol: Miscible; PBS (pH 7.2): 0.8 mg/ml

pka

4.75±0.10(Predicted)

form 

Liquid.

BRN 

2470466

Safety Information

Hazard Codes 

F,Xi

Risk Statements 

11-36/37/38

Safety Statements 

7-16-26-36

RIDADR 

UN 1170 3/PG 2

WGK Germany 

3

MSDS

• Language:English Provider:SigmaAldrich

15(S)-HETE Usage And Synthesis

Description

15(S)-HETE is a major arachidonic acid metabolite from the 15-lipoxygenase pathway. In mammals, 15(S)-HETE is synthesized in the respiratory epithelium, leukocytes, and reticulocytes. 15(S)-HETE is present in μg/ml concentrations in the nasal secretions of allergic rhinitis.

Uses

15(S)-HETE is a major arachidonic acid metabolite from the 15-lipoxygenase pathway. In mammals, 15(S)-HETE is synthesized in the respiratory epithelium, leukocytes, and reticulocytes. 15(S)-HETE is present in μg/ml concentrations in the nasal secretions of allergic rhinitis.

Uses

15(S)-HETE is an arachidonic acid metabolite with immunosuppressive activity.

Definition

ChEBI: An optically active form of 15-HETE having 15(S)-configuration..

General Description

15(S)-HETE is a product of the arachidonic acid pathway. It is synthesized by the human lungs and airway epithelial cells. 15(S)-HETE is a potent mucosecretagogue in human airways. It is a metabolite of 15-lipoxygenase. 15(S)-HETE is an endogenous ligand for peroxisome proliferator-activated receptor γ (PPARγ).

Biochem/physiol Actions

Metabolite of arachidonic acid via the 15-lipoxygenase pathway that may be involved in pulmonary anti-inflammatory responses through the inhibition of 5-lipoxygenase. 15(S)-HETE suppresses the incorporation of thymidine and biosynthesis of prostaglandin E2 in tumor cell cultures. Treatment of colon cancer cells with 15(S)-HETE inhibited cell proliferation and induced apoptosis, which was preceded by an increase in TGF-beta-inducible early gene (TIEG) and a decrease in Bcl-2.

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