ViniferinCAS# 253435-07-3 |
- epsilon-Viniferin
Catalog No.:BCN4151
CAS No.:62218-08-0
- cis-ε-Viniferin
Catalog No.:BCN0640
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 253435-07-3 | SDF | Download SDF |
| PubChem ID | 5315232 | Appearance | Powder |
| Formula | C28H22O6 | M.Wt | 454.5 |
| Type of Compound | Phenols | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 5-[6-hydroxy-2-(4-hydroxyphenyl)-4-[(E)-2-(4-hydroxyphenyl)ethenyl]-2,3-dihydro-1-benzofuran-3-yl]benzene-1,3-diol | ||
| SMILES | C1=CC(=CC=C1C=CC2=CC(=CC3=C2C(C(O3)C4=CC=C(C=C4)O)C5=CC(=CC(=C5)O)O)O)O | ||
| Standard InChIKey | FQWLMRXWKZGLFI-DAFODLJHSA-N | ||
| Standard InChI | InChI=1S/C28H22O6/c29-20-7-2-16(3-8-20)1-4-18-11-24(33)15-25-26(18)27(19-12-22(31)14-23(32)13-19)28(34-25)17-5-9-21(30)10-6-17/h1-15,27-33H/b4-1+ | ||
| 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. | ||
| Description | 1. α-Viniferin has anti-oxidant and anticancer activities. 2. ɛ-Viniferin and vincristine can enhance the anti-tumor effects efficiently by inducing HepG2 cell apoptosis. 3. α-Viniferin strongly inhibits the activities of the two CYPs dose dependently. 4. α-Viniferin suppresses the expression of proinflammatory genes iNOS and COX-2 in the early stage of inflammation by inhibiting the Akt/PI3K-dependent NF-κB activation and inhibits the production of proinflammatory mediators NO and PGE2 in the late stage by stimulating Nrf2-mediated HO-1 signaling pathway in LPS-stimulated BV2 microglial cells. |
| Targets | NO | PGE | NOS | COX | NF-kB | PI3K | Akt | Nrf2 | HO-1 | P450 (e.g. CYP17) |
Viniferin Dilution Calculator
Viniferin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.2002 mL | 11.0011 mL | 22.0022 mL | 44.0044 mL | 55.0055 mL |
| 5 mM | 0.44 mL | 2.2002 mL | 4.4004 mL | 8.8009 mL | 11.0011 mL |
| 10 mM | 0.22 mL | 1.1001 mL | 2.2002 mL | 4.4004 mL | 5.5006 mL |
| 50 mM | 0.044 mL | 0.22 mL | 0.44 mL | 0.8801 mL | 1.1001 mL |
| 100 mM | 0.022 mL | 0.11 mL | 0.22 mL | 0.44 mL | 0.5501 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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Towards novel anti-tumor strategies for hepatic cancer: varepsilon-viniferin in combination with vincristine displays pharmacodynamic synergy at lower doses in HepG2 cells.[Pubmed:24341688]
OMICS. 2014 May;18(5):324-34.
Hepatocellular carcinoma is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. The efficacy of novel combination treatments are increasingly evaluated with use of integrative biology research and development (R&D) strategies and methodological triangulation. We investigated the anti-tumor effect of varepsilon-Viniferin alone, and the putative synergy of varepsilon-Viniferin with vincristine on the growth of HepG2 cells in vitro. Growth inhibition and apoptosis induction were determined by MTT assay and annexin V/propidium iodide (PI), respectively. Morphological changes and DNA fragmentation were investigated under electron microscopy and by agarose gel electrophoresis, respectively. The results collectively showed that treating cells with varepsilon-Viniferin and vincristine significantly inhibited cell viability at lower doses as compared to each agent applied alone. IC(50) values for varepsilon-Viniferin and vincristine were determined as 98.3 and 52.5 muM at 24 h, respectively. IC(50) value of varepsilon-Viniferin in combination with vincristine was 15.8+11.25 muM (mean/SD) at 24 h. The viability of cells treated with 17.9 muM vincristine alone for 24 h was 79.62%; it reduced to 26.53% when 25 muM varepsilon-Viniferin was added in combination with vincristine (p<0.05). We found that combination of drugs promoted the sensitivity of cells against to vincristine treatment. The effect of combined use was in support of a synergistic pharmacodynamic effect. Moreover, low doses of the combination regimen induced phosphatidyl re-localization, morphological changes, and DNA fragmentation, and therefore caused apoptotic death. This study thus suggests that low concentrations of varepsilon-Viniferin and vincristine can enhance the anti-tumor effects efficiently by inducing HepG2 cell apoptosis. Further studies in other model systems are warranted with a view to potential future applications in the clinic of such combination regimens and their putative mechanism of action in the observed synergy reported here.
Potent inhibitory effect of alpha-viniferin on human cytochrome P450.[Pubmed:24769006]
Food Chem Toxicol. 2014 Jul;69:276-80.
alpha-Viniferin isolated from Caragana chamlagu is a trimer of resveratrol, and has several biological activities, which include anti-inflammatory, anti-oxidant, anti-arthritis, and anti-tumor activities. Herb-drug interactions are the source of the most harmful complications in patients coadministered herbal and modern medicines, and are caused by modulation of the activities of drug metabolizing enzymes. Here, the authors investigated the inhibitory effects of alpha-Viniferin on the activities of 9 human cytochrome P450 (CYP) isoforms using a cocktail of probe substrates and LC-MS/MS in pooled human liver microsomes (HLMs). alpha-Viniferin strongly inhibited 7 of the 9 CYP isoforms (except CYP2A6 and CYP2E1). Furthermore, alpha-Viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC50 values of 0.93 and 1.2 muM, respectively. alpha-Viniferin strongly inhibited the activities of these two CYPs dose dependently, but not time-dependently. Lineweaver-Burk plots and secondary plots indicated a typical pattern of mix-mode inhibition for CYP2C19 and 3A4. This is the first investigation conducted on the inhibitory effect of alpha-Viniferin on CYP2C19 and 3A4 in HLMs to predict a potential herb-drug interaction.
Synthesis of epsilon-Viniferin Glycosides by Glucosyltransferase from Phytolacca americana and their Inhibitory Activity on Histamine Release from Rat Peritoneal Mast Cells.[Pubmed:26197540]
Nat Prod Commun. 2015 Jun;10(6):1017-8.
Glycosylation of (+)-epsilon-Viniferin was investigated using glucosyltransferase from Phytolacca americana (PaGT3) as a biocatalyst. (+)-epsilon-Viniferin was converted by PaGT3 into its 4b- and 13b-beta-D-glucosides, the inhibitory activities on histamine release from rat peritoneal mast cells of which were higher than that of (+)-epsilon-Viniferin.
Anti-inflammatory mechanism of alpha-viniferin regulates lipopolysaccharide-induced release of proinflammatory mediators in BV2 microglial cells.[Pubmed:24859013]
Cell Immunol. 2014 Jul;290(1):21-9.
alpha-Viniferin is an oligostilbene of trimeric resveratrol and has anticancer activity; however, the molecular mechanism underlying the anti-inflammatory effects of alpha-Viniferin has not been completely elucidated thus far. Therefore, we determined the mechanism by which alpha-Viniferin regulates lipopolysaccharide (LPS)-induced expression of proinflammatory mediators in BV2 microglial cells. Treatment with alpha-Viniferin isolated from Clematis mandshurica decreased LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2). alpha-Viniferin also downregulated the LPS-induced expression of proinflammatory genes such as iNOS and COX-2 by suppressing the activity of nuclear factor kappa B (NF-kappaB) via dephosphorylation of Akt/PI3K. Treatment with a specific NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), indirectly showed that NF-kappaB is a crucial transcription factor for expression of these genes in the early stage of inflammation. Additionally, our results indicated that alpha-Viniferin suppresses NO and PGE2 production in the late stage of inflammation through induction of heme oxygenase-1 (HO-1) regulated by nuclear factor erythroid 2-related factor (Nrf2). Taken together, our data indicate that alpha-Viniferin suppresses the expression of proinflammatory genes iNOS and COX-2 in the early stage of inflammation by inhibiting the Akt/PI3K-dependent NF-kappaB activation and inhibits the production of proinflammatory mediators NO and PGE2 in the late stage by stimulating Nrf2-mediated HO-1 signaling pathway in LPS-stimulated BV2 microglial cells. These results suggest that alpha-Viniferin may be a potential candidate to regulate LPS-induced inflammation.
