1,4,6-Trihydroxy-5-methoxy-7-prenylxanthoneCAS# 160623-47-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 160623-47-2 | SDF | Download SDF |
PubChem ID | 71307362 | Appearance | Yellow powder |
Formula | C19H18O6 | M.Wt | 342.4 |
Type of Compound | Xanthones | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | 1,4,6-trihydroxy-5-methoxy-7-(3-methylbut-2-enyl)xanthen-9-one | ||
SMILES | CC(=CCC1=C(C(=C2C(=C1)C(=O)C3=C(C=CC(=C3O2)O)O)OC)O)C | ||
Standard InChIKey | XOFZQNNUVXEIJS-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. |
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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. |
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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. |
1,4,6-Trihydroxy-5-methoxy-7-prenylxanthone Dilution Calculator
1,4,6-Trihydroxy-5-methoxy-7-prenylxanthone Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.9206 mL | 14.6028 mL | 29.2056 mL | 58.4112 mL | 73.014 mL |
5 mM | 0.5841 mL | 2.9206 mL | 5.8411 mL | 11.6822 mL | 14.6028 mL |
10 mM | 0.2921 mL | 1.4603 mL | 2.9206 mL | 5.8411 mL | 7.3014 mL |
50 mM | 0.0584 mL | 0.2921 mL | 0.5841 mL | 1.1682 mL | 1.4603 mL |
100 mM | 0.0292 mL | 0.146 mL | 0.2921 mL | 0.5841 mL | 0.7301 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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Structural and Functional State of Erythrocyte Membranes in Mice at Different Stages of Experimental Parkinson's Disease Induced by Administration of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP).[Pubmed:28382410]
Bull Exp Biol Med. 2017 Mar;162(5):597-601.
We studied some structural and functional parameters of erythrocyte membranes in mice at the late presymptomatic and early symptomatic stages of experimental Parkinson's disease induced by administration of MPTP (hemolysis, microviscosity of different regions of the lipid bilayer, LPO intensity, activity of antioxidant enzymes, and kinetic properties of acetylcholinesterase). At the presymptomatic stage, significant deviations of the studied parameters from the normal were observed; they were similar in direction and magnitude to those in humans with Parkinson's disease. At the early symptomatic stage, most parameters tended to normal. Microviscosity of bulk lipids increased at the presymptomatic stage and decreased after appearance of clinical symptoms. This dynamics probably reflects activation of compensatory mechanisms aimed at inhibition of oxidative stress triggered by the development of the pathological process.
Fatty acid-binding protein 4 regulates fatty infiltration after rotator cuff tear by hypoxia-inducible factor 1 in mice.[Pubmed:28382782]
J Cachexia Sarcopenia Muscle. 2017 Oct;8(5):839-850.
BACKGROUND: Fatty infiltration in skeletal muscle is directly linked to loss of muscle strength and is associated with various adverse physical outcomes such as muscle atrophy, inflammation, insulin resistance, mobility impairments, and even mortality in the elderly. Aging, mechanical unloading, muscle injury, and hormonal imbalance are main causes of muscle fat accumulation, and the fat cells are derived from muscle stem cells via adipogenic differentiation. However, the pathogenesis and molecular mechanisms of fatty infiltration in muscles are still not fully defined. Fatty acid-binding protein 4 (FABP4) is a carrier protein for fatty acids and is involved in fatty acid uptake, transport, and lipid metabolism. Rotator cuff tear (RCT) usually occurs in the elderly and is closely related with fatty infiltration in injured muscle. To investigate potential mechanisms for fatty infiltration other than adipogenic differentiation of muscle stem cells, we examined the role of FABP4 in muscle fatty infiltration in an RCT mouse model. METHODS: In the RCT model, we evaluated the expression of FABP4 by qRT-PCR, western blotting, and immunohistochemical analyses. Histological changes such as inflammation and fat accumulation in the injured muscles were examined immunohistochemically. To evaluate whether hypoxia induces FABP4 expression, the levels of FABP4 mRNA and protein in C3H10T1/2 cells after hypoxia were examined. Using a transient transfection assay in 293T cells, we assessed the promoter activity of FABP4 by hypoxia-inducible factors (HIFs). Additionally, we evaluated the reduction in FABP4 expression and fat accumulation using specific inhibitors for HIF1 and FABP4, respectively. RESULTS: FABP4 expression was significantly increased after RCT in mice, and its expression was localized in the intramuscular fatty region. Rotator cuff tear-induced FABP4 expression was up-regulated by hypoxia. HIF1alpha, which is activated by hypoxia, augmented the promoter activity of FABP4, together with HIF1beta. Hypoxia-induced FABP4 expression was significantly decreased by HIF1 inhibitor treatment. Furthermore, in RCT model mice, fat accumulation was remarkably reduced by FABP4 inhibitor treatment. CONCLUSIONS: This study shows that RCT induces FABP4 expression, leading to fat accumulation in injured muscle. FABP4 transcription is regulated by the direct binding of HIF1 to the FABP4 promoter in the hypoxic condition induced by RCT. Fat accumulation in injured muscle was reduced by the inhibition of FABP4. Ultimately, in the RCT model, we identified a novel mechanism for fatty infiltration by FABP4, which differs from adipogenic differentiation of muscle stem cells, and we found that fatty infiltration might be regulated by inhibition of HIF1 or FABP4.
Novel substrates for the automated and manual assay of endo-1,4-beta-xylanase.[Pubmed:28384512]
Carbohydr Res. 2017 Jun 5;445:14-22.
endo-1,4-beta-Xylanase (EC 3.2.1.8) is employed across a broad range of industries including animal feed, brewing, baking, biofuels, detergents and pulp (paper). Despite its importance, a rapid, reliable, reproducible, automatable assay for this enzyme that is based on the use of a chemically defined substrate has not been described to date. Reported herein is a new enzyme coupled assay procedure, termed the XylX6 assay, that employs a novel substrate, namely 4,6-O-(3-ketobutylidene)-4-nitrophenyl-beta-4(5)-O-glucosyl-xylopentaoside. The development of the substrate and associated assay is discussed here and the relationship between the activity values obtained with the XylX6 assay versus traditional reducing sugar assays and its specificity and reproducibility were thoroughly investigated.