Powder: -20°C for 3 years | In solvent: -80°C for 1 year
20-HETE (20-hydroxy Arachidonic Acid) is a CYP450 metabolite and a potent vasoconstrictor and it is an endogenous inhibitor of the large-conductance Ca2+-activated K+ channel in renal arterioles. 20-HETE increases NADPH oxidase, ROS, and NF-κB activity, and it also inhibits endothelial NO synthase and inhibits apoptosis of pulmonary artery smooth muscle cells[1][2]. 20-HETE constricts smooth muscles, stimulates smooth muscle proliferation and migration.
Pack Size | Availability | Price/USD | Quantity |
---|---|---|---|
25 mg | Inquiry | $ 2,120.00 | |
50 mg | Inquiry | $ 2,780.00 | |
100 mg | Inquiry | $ 3,700.00 |
Description | 20-HETE (20-hydroxy Arachidonic Acid) is a CYP450 metabolite and a potent vasoconstrictor and it is an endogenous inhibitor of the large-conductance Ca2+-activated K+ channel in renal arterioles. 20-HETE increases NADPH oxidase, ROS, and NF-κB activity, and it also inhibits endothelial NO synthase and inhibits apoptosis of pulmonary artery smooth muscle cells[1][2]. 20-HETE constricts smooth muscles, stimulates smooth muscle proliferation and migration. |
In vitro | 20-HETE promotes platelet-derived growth factor-stimulated vascular smooth muscle cell migration via pathways that involve MEK and phosphatidylinositol 3-kinase activation[2]. 20-HETE induces the phosphorylation of ERK1/2, a MAPK that plays a pivotal role in the proliferation induced by the activation of receptor tyrosine kinases and G protein-coupled receptors. 20-HETE (1-1000 nM) reduces the diameter of isolated perfused small renal arteries of the rat by approximately 15% tetraethylammonium (1 mM) blocked the vasoconstrictor response to 20-HETE (100 nM)[1]. Addition of 20-HETE to the bath (1-100 nM), reduces the frequency of opening of the large-conductance Ca2+-activated K+ channel recorded using cell-attached patches on vascular smooth muscle cells (VSM)[1]. |
In vivo | In Sprague-Dawley rats, administration of the 20-HETE inhibitor HET0016 or the 20-HETE antagonist 20-HEDE preventes DHT-induced increases in blood pressure as well as abrogates DHT-induced increases in the media-to-lumen ratio (M/L), media thickness, and collagen IV deposition in renal interlobar arteries. 20-HETE is a key regulator of microvascular remodeling in hypertension; its effect is independent of blood pressure elevation and androgen levels[2]. 20-HETE contributes to DHT-induced vascular remodeling independent of blood pressure elevation[2]. In Cyp4a14-/- mice, which display androgen-driven and 20-HETE-dependent hypertension, treatment with the 20-HETE antagonist abolishes remodeling of renal resistance arteries measured as media thickness and M/L. |
Synonyms | 20-hydroxy Arachidonic Acid |
Molecular Weight | 320.47 |
Formula | C20H32O3 |
CAS No. | 79551-86-3 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
DMSO: 3.2 mg/mL (9.99 mM)
Ethanol: 6.67 mg/mL (20.81 mM), Sonification is recommended.
You can also refer to dose conversion for different animals. More
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20-HETE 79551-86-3 Others 20-hydroxy Arachidonic Acid 20 HETE 20HETE inhibitor inhibit