16(s)hete

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. 16(S)-HETE inhibits proximal tubule ATPase activity by as much as 60% at a concentration of 2 μM.

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. 16(S)-HETE inhibits proximal tubule ATPase activity by as much as 60% at a concentration of 2 µM.[1]

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. (±)16-HETE is the racemic version of a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation. The biological activity of 16-HETE is stereospecific. 16(R)-HETE dose-dependently stimulates vasodilation of the rabbit kidney, however 16(S)-HETE does not affect perfusion pressure. At a concentration of 2 μM the (S)-enantiomer of 16-HETE inhibits proximal tubule ATPase activity by as much as 60%, whereas the (R)-isomer has negligible effects on ATPase activity.

1-Stearoyl-2-15(S)-HETE-sn-glycero-3-PC is a phospholipid that contains stearic acid at the sn-1 position and 15(S)-HETE at the sn-2 position. It is produced via oxidation of 1-stearoyl-2-arachidonoyl-sn-glycero-3-PC by 15-lipoxygenase (15-LO).

15(S)-HETE methyl ester is a synthetic derivative of 15(S)-HETE , a major arachidonic acid metabolite from the 15-lipoxygenase pathway. Methyl esters of lipids are commonly used in formulations of nutritional supplements.

19-HETE is one of the major cytochrome P450 (CYP450) metabolites of arachidonic acid that is released from the kidney in response to angiotensin II. When formed by the CYP2E1 isoform, 19-HETE is composed of 70% and 30% of the (S) and (R) stereoisomers, respectively. Both 19(S)- and 19(R)-HETE are potent vasodilators of renal preglomerular vessels. 19(S)-HETE stimulates both renal sodium-potassium ATPase and volume absorption in the rabbit proximal straight tubule.

5(S)-HETE, an endogenous metabolite found in the blood, is utilized in researching Rheumatoid Arthritis, Rhinitis, and Asthma [1] [2].

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.

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites.17-HETE is a cytochrome P450 (CYP450) metabolite of arachidonic acid that has stereospecific effects on sodium transport in the kidney.17(S)-HETE inhibits proximal tubule ATPase activity by as much as 70% at a concentration of 2 μM.

11(S)-HETE, an (S) enantiomer of 11(R)-HETE and a type of oxylipin, is non-enzymatically synthesized from arachidonic acid. Compared to its counterpart, 11(S)-HETE levels are found to be elevated in both isolated human plasma and serum, as well as in LPS-stimulated isolated human plasma. Notably, patients with allergic rhinitis exhibit a decrease in 11(S)-HETE levels in their serum following one year of double-mite subcutaneous immunotherapy (DM-SCIT), correlating with an enhanced quality of life, particularly in aspects related to rhinoconjunctivitis.

The compound is a mechanism-based inhibitor of cytochrome P450 ω-hydroxylase.

8(S)-HETE is a major lipoxygenase product in PMA-treated murine epidermis. It activates mouse keratinocyte protein kinase C with an IC50 of 100 μM. 8(S)-HETE also activates PPARα selectively at concentrations as low as 0.3 μM. Stereochemical assignment of the (S) enantiomer is based on comparison of chiral HPLC retention times to published results.

16-(S)-ML188 is a useful organic compound for research related to life sciences and the catalog number is T64738.

12(S)-HETE is the predominant lipoxygenase product of mammalian platelets. [1] It enhances tumor cell adhesion to endothelial cells, fibronectin, and the subendothelial matrix at 0.1μM181M.[2][3]

Iloprost is a second generation structural analog of prostacyclin (PGI2) with about ten-fold greater potency than the first generation stable analogs, typified by carbaprostacyclin. Iloprost binds with equal affinity to the recombinant human IP and EP1 receptors with a Ki value of 11 nM. Most preparations of iloprost contain 16(S) and 16(R) stereoisomers. 16(S)-Iloprost potently inhibits platelet aggregation with an IC50 value of 3.5 nM.

9(S)-HETE is an enantiomer which makes up 50% of (±)9-HETE . There are no reports of 9(S)-HETE occurring as an enzymatic lipoxygenation product. Whereas 12(S)-HETE promotes adhesion of several cell lines to endothelial cell monolayes, 9(S)-HETE and other positional HETEs are without effect. Stereochemical assignment of the (S) enantiomer is based on comparison of chiral HPLC retention times to published results.

1-Stearoyl-2-15(S)-HETE-sn-glycero-3-PE is a phospholipid that contains stearic acid at the sn-1 position and 15(S)-HETE at the sn-2 position. It is formed in human peripheral monocytes activated by the calcium ionophore A23187 by direct oxidation of 1-stearoyl-2-arachidonoyl-sn-glycero-3-PE by 15-LO. Phosphoethanolamine (PE) HETEs (PE-HETEs), including 1-stearoyl-2-15(S)-HETE-sn-glycero-3-PE, are the main source of esterified HETE in ionophore-activated monocytes.

5(S)-HETE lactone is a cyclic ester formed by acid-catalyzed nucleophilic addition of the C-5 hydroxyl to the C-1 carboxyl of 5(S)-HETE. The ability of (±)5-HETE lactone to inhibit rat basophilic leukemia cell 5-lipoxygenase (IC50 = 27 μM) may be entirely due to the 5(S) isomer, but the enantiomers have not been tested separately.