5,7-Diacetoxy-3,4',8-trimethoxyflavoneCAS# 5128-43-8 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 5128-43-8 | SDF | Download SDF |
PubChem ID | 13916287 | Appearance | Yellow powder |
Formula | C22H20O9 | M.Wt | 428.4 |
Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | [7-acetyloxy-3,8-dimethoxy-2-(4-methoxyphenyl)-4-oxochromen-5-yl] acetate | ||
SMILES | CC(=O)OC1=CC(=C(C2=C1C(=O)C(=C(O2)C3=CC=C(C=C3)OC)OC)OC)OC(=O)C | ||
Standard InChIKey | PKVJLPXCFDHGEY-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. |
5,7-Diacetoxy-3,4',8-trimethoxyflavone Dilution Calculator
5,7-Diacetoxy-3,4',8-trimethoxyflavone Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3343 mL | 11.6713 mL | 23.3427 mL | 46.6853 mL | 58.3567 mL |
5 mM | 0.4669 mL | 2.3343 mL | 4.6685 mL | 9.3371 mL | 11.6713 mL |
10 mM | 0.2334 mL | 1.1671 mL | 2.3343 mL | 4.6685 mL | 5.8357 mL |
50 mM | 0.0467 mL | 0.2334 mL | 0.4669 mL | 0.9337 mL | 1.1671 mL |
100 mM | 0.0233 mL | 0.1167 mL | 0.2334 mL | 0.4669 mL | 0.5836 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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N(6)-Substituted 5'-N-Methylcarbamoyl-4'-selenoadenosines as Potent and Selective A3 Adenosine Receptor Agonists with Unusual Sugar Puckering and Nucleobase Orientation.[Pubmed:28380296]
J Med Chem. 2017 Apr 27;60(8):3422-3437.
Potent and selective A3 adenosine receptor (AR) agonists were identified by the replacement of 4'-oxo- or 4'-thionucleosides with bioisosteric selenium. Unlike previous agonists, 4'-seleno analogues preferred a glycosidic syn conformation and South sugar puckering, as shown in the X-ray crystal structure of 5'-N-methylcarbamoyl derivative 3p. Among the compounds tested, N(6)-3-iodobenzyl analogue 3d was found to be the most potent A3AR full agonist (Ki = 0.57 nM), which was >/=800- and 1900-fold selective for A1AR and A2AAR, respectively. In the N(6)-cycloalkyl series, 2-Cl analogues generally exhibited better hA3AR affinity than 2-H analogues, whereas 2-H > 2-Cl in the N(6)-3-halobenzyl series. N(7) isomers 3t and 3u were much weaker in binding than corresponding N(9) isomers, but compound 3t lacked A3AR activation, appearing to be a weak antagonist. 2-Cl-N(6)-3-iodobenzyl analogue 3p inhibited chemoattractant-induced migration of microglia/monocytes without inducing cell death at =50 muM. This suggests the potential for the development of 4'-selenonucleoside A3AR agonists as novel antistroke agents.
Molecular mechanisms of 3,3'4,4',5-pentachlorobiphenyl-induced epithelial-mesenchymal transition in human hepatocellular carcinoma cells.[Pubmed:28284859]
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Polychlorinated biphenyls (PCBs) are classic persistent organic pollutants (POPs). Many studies have found a positive association between the progression of hepatocellular carcinoma (HCC) and PCBs exposure. However, the influence of PCBs on epithelial-mesenchymal transition (EMT) of HCC remains to be unclear. In this study, we explored the effect of PCB126 on EMT in HCC cells and its underlying mechanisms. The data showed that PCB126, exposing both Bel-7402 and SMMC-7721 cells for 48h, promoted EMT that was demonstrated by E-cadherin repression, up-regulation of N-cadherin and vimentin, and morphological alteration. We found that signal transducer and activator of transcription 3 (STAT3)/Snail1 signaling was activated after PCB126 exposure, and the addition of STAT3 inhibitor WP1066 blocked PCB126-induced down-regulation of E-cadherin as well as up-regulation of N-cadherin and vimentin. Moreover, PCB126 exposure increased pyruvate kinase M2 (PKM2) expression and its nuclear translocation, whereas treatment with PKM2 shRNA suppressed the activation of STAT3/Snail1 signaling and the alternation of EMT-related molecules (E-cadherin, N-cadherin and vimentin). Furthermore, this study indicated estrogen receptor (ER) and aryl hydrocarbon receptor (AhR) were involved in PCB126-induced effects on PKM2, STAT3/Snail1 signaling and EMT by according treatment using ER inhibitor ICI and AhR shRNA. Notably, PCB126-increased reactive oxygen species (ROS) production via AhR is associated with activation of PKM2/STAT3/Snail1 cascades and contributes to EMT. Taken together, these results indicated that PCB126 promotes EMT process of HCC cells via PKM2/STAT3/Snail1 signaling which is mediated by ER and AhR.
Design and synthesis of selective CDK8/19 dual inhibitors: Discovery of 4,5-dihydrothieno[3',4':3,4]benzo[1,2-d]isothiazole derivatives.[Pubmed:28302507]
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