Bilobetin

CAS# 521-32-4

Bilobetin

2D Structure

Catalog No. BCN5661----Order now to get a substantial discount!

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Quality Control of Bilobetin

3D structure

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Bilobetin

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Chemical Properties of Bilobetin

Cas No. 521-32-4 SDF Download SDF
PubChem ID 5315459 Appearance Yellow powder
Formula C31H20O10 M.Wt 552.5
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms 4'-O-Methylamentoflavone; 4',5,5'',7,7''-Pentahydroxy 4'''-methoxy 3''',8-biflavone
Solubility Soluble in acetonitrile; slightly soluble in water
Chemical Name 8-[5-(5,7-dihydroxy-4-oxochromen-2-yl)-2-methoxyphenyl]-5,7-dihydroxy-2-(4-hydroxyphenyl)chromen-4-one
SMILES COC1=C(C=C(C=C1)C2=CC(=O)C3=C(C=C(C=C3O2)O)O)C4=C(C=C(C5=C4OC(=CC5=O)C6=CC=C(C=C6)O)O)O
Standard InChIKey IWEIJEPIYMAGTH-UHFFFAOYSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Bilobetin

1 Juniperus sp. 2 Taxus sp. 3 Thuja sp.

Biological Activity of Bilobetin

DescriptionBilobetin treatment ameliorates hyperlipidaemia, lipotoxicity and insulin resistance in rats by stimulating PPARα-mediated lipid catabolism.
TargetsPPAR | cAMP
In vivo

Bilobetin ameliorates insulin resistance by PKA-mediated phosphorylation of PPARα in rats fed a high-fat diet.[Pubmed: 22091731]

Br J Pharmacol. 2012 Apr;165(8):2692-706.

The amelioration of insulin resistance by Bilobetin is closely related to its hypolipidaemic effect. The aim of the present study was to determine the insulin-sensitizing mechanism of Bilobetin by elucidating its effect on lipid metabolism.
METHODS AND RESULTS:
Rats fed a high-fat diet were treated with Bilobetin for either 4 or 14 days before applying a hyperinsulinaemic-euglycaemic clamp. Triglyceride and fatty acids labelled with radioactive isotopes were used to track the transportation and the fate of lipids in tissues. The activity of lipid metabolism-related enzymes and β-oxidation rate were measured. Western blot was used to investigate the phosphorylation, translocation and expression of PPARα in several tissues and cultured cells. The location of amino acid residues subjected to phosphorylation in PPARα was also studied. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity. Threonine-129-alanine and/or serine-163-alanine mutations on the PPARα genes and PKA inhibitors prevented the effects of Bilobetin on PPARα. However, cells overexpressing PKA appeared to stimulate the phosphorylation, nuclear translocation and activity of PPARα.
CONCLUSIONS:
Bilobetin treatment ameliorates hyperlipidaemia, lipotoxicity and insulin resistance in rats by stimulating PPARα-mediated lipid catabolism. PKA activation is crucial for this process.

Bilobetin Dilution Calculator

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Preparing Stock Solutions of Bilobetin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.81 mL 9.0498 mL 18.0995 mL 36.1991 mL 45.2489 mL
5 mM 0.362 mL 1.81 mL 3.6199 mL 7.2398 mL 9.0498 mL
10 mM 0.181 mL 0.905 mL 1.81 mL 3.6199 mL 4.5249 mL
50 mM 0.0362 mL 0.181 mL 0.362 mL 0.724 mL 0.905 mL
100 mM 0.0181 mL 0.0905 mL 0.181 mL 0.362 mL 0.4525 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Bilobetin

Bilobetin ameliorates insulin resistance by PKA-mediated phosphorylation of PPARalpha in rats fed a high-fat diet.[Pubmed:22091731]

Br J Pharmacol. 2012 Apr;165(8):2692-706.

BACKGROUND AND PURPOSE: The amelioration of insulin resistance by Bilobetin is closely related to its hypolipidaemic effect. The aim of the present study was to determine the insulin-sensitizing mechanism of Bilobetin by elucidating its effect on lipid metabolism. EXPERIMENTAL APPROACH: Rats fed a high-fat diet were treated with Bilobetin for either 4 or 14 days before applying a hyperinsulinaemic-euglycaemic clamp. Triglyceride and fatty acids labelled with radioactive isotopes were used to track the transportation and the fate of lipids in tissues. The activity of lipid metabolism-related enzymes and beta-oxidation rate were measured. Western blot was used to investigate the phosphorylation, translocation and expression of PPARalpha in several tissues and cultured cells. The location of amino acid residues subjected to phosphorylation in PPARalpha was also studied. KEY RESULTS: Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in beta-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARalpha accompanied by elevated cAMP level and PKA activity. Threonine-129-alanine and/or serine-163-alanine mutations on the PPARalpha genes and PKA inhibitors prevented the effects of Bilobetin on PPARalpha. However, cells overexpressing PKA appeared to stimulate the phosphorylation, nuclear translocation and activity of PPARalpha. CONCLUSIONS AND IMPLICATIONS: Bilobetin treatment ameliorates hyperlipidaemia, lipotoxicity and insulin resistance in rats by stimulating PPARalpha-mediated lipid catabolism. PKA activation is crucial for this process.

Description

Bilobetin, an active component of Ginkgo biloba, can reduce blood lipids and improve the effects of insulin. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity.

Keywords:

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