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tetranor-12(S)-HETE Sale

(Synonyms: tetranor-12(S)-Hydroxyeicosatetraenoic Acid) 目录号 : GC45024

A peroxisome metabolite of 12(S)-HETE

tetranor-12(S)-HETE Chemical Structure

Cas No.:121842-79-3

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25μg
¥2,262.00
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50μg
¥4,300.00
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100μg
¥8,137.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

12(S)-HETE is a product of arachidonic acid metabolism through the 12-lipoxygenase pathway. It is primarily found in platelets, leukocytes, and to a lesser extent in smooth muscle cells. It enhances tumor cell adhesion to endothelial cells, fibronectin, and the subendothelial matrix. tetranor-12(S)-HETE is the major β-oxidation product resulting from peroxisomal metabolism of 12(S)-HETE in numerous tissues, and Lewis lung carcinoma cells. No biological function has yet been determined for tetranor-12(S)-HETE. Some data indicate it may play a role in controlling the inflammatory response in injured corneas. In some diseases (e.g., Zellweger's Syndrome) peroxisomal abnormalities result in the inability of cells to metabolize 12(S)-HETE, which may be responsible for symptoms of the disease. The tetranor derivative of 12(S)-HETE is available as a research tool for the elucidation of the metabolic fate of its parent compound.

Chemical Properties

Cas No. 121842-79-3 SDF
别名 tetranor-12(S)-Hydroxyeicosatetraenoic Acid
Canonical SMILES CCCCC/C=C\C[C@H](O)/C=C/C=C\CCC(O)=O
分子式 C16H26O3 分子量 266.4
溶解度 0.1 M Na2CO3: 2 mg/ml,DMF: 25 mg/ml,DMSO: 25 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): .5 mg/ml 储存条件 Store at -20°C
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1 mM 3.7538 mL 18.7688 mL 37.5375 mL
5 mM 0.7508 mL 3.7538 mL 7.5075 mL
10 mM 0.3754 mL 1.8769 mL 3.7538 mL
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Research Update

Lack of association of ALOX12 and ALOX15B polymorphisms with psoriasis despite altered urinary excretion of 12(S)-hydroxyeicosatetraenoic acid

Br J Dermatol 2015 Feb;172(2):337-44.PMID:24975552DOI:10.1111/bjd.13225

Background: Pro- and anti-inflammatory metabolites of arachidonic acid - eicosanoids - participate in skin homeostasis, affecting the growth and differentiation of keratinocytes. Alterations of 12-lipoxygenase (LOX) and 15-LOX and their metabolites have been described in the epidermis of patients with psoriasis, but systemic production of 12-LOX and 15-LOX eicosanoids has not been studied in the disease. Objectives: To ascertain the frequencies of the genetic variants ALOX12 rs1126667 and ALOX15 rs11568070 in cases and controls, and to compare urinary metabolites of 12(S)-hydroxyeicosatetraenoic acid (HETE) between patients with psoriasis and healthy controls. Methods: Patients with psoriasis (n = 200) were stratified depending on the severity of their dermal lesions. Genotyping was performed using a 5'-nuclease real-time assay. The concentrations of 12(S)-HETE, its metabolites and 15(S)-HETE were determined in urine samples using high-performance liquid chromatography-tandem mass spectrometry. Results: tetranor-12(S)-HETE metabolite excretion was significantly higher in urine of patients with psoriasis, while excretion of 12(S)-HETE was decreased. Neither 12(S)-HETE nor tetranor-12(S)-HETE correlated with the type of disease or severity score. No difference in urinary 15(S)-HETE was found between the study groups. Genotype distribution of the ALOX12 rs1126667 or ALOX15 rs11568070 polymorphisms did not discriminate for the disease or its severity. Conclusions: Systemic metabolism of 12(S)-HETE is accelerated in psoriasis because excretion of the tetranor-12(S)-HETE inactivation product is elevated. No correlation with the severity or extent of psoriasis is detectable. We propose that in patients with psoriasis, 12(S)-HETE to tetranor-12(S)-HETE conversion could be at least a marker for this disease, in which inflammation of the skin can induce microsomal beta-oxidation of this eicosanoid.