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    Natural Products
    CAS No. 253435-07-3 Price
    Catalog No.CFN92854Purity>=98%
    Molecular Weight454.1Type of CompoundPhenols
    FormulaC28H22O6Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    * Packaging according to customer requirements(5mg, 10mg, 20mg and more). We shipped via FedEx, DHL, UPS, EMS and others courier.
    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / Inquiry
    Other Packaging *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap
    Our products had been exported to the following research institutions and universities, And still growing.
  • University of Virginia (USA)
  • Vin?a Institute of Nuclear Scie... (Serbia)
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  • Nanjing University of Chinese M... (China)
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    Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
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    Related Libraries
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  • Biological Activity
    Description: α-Viniferin has anti-oxidant and anticancer activities, it strongly inhibits the activities of the two CYPs dose dependently. 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. ɛ-Viniferin and vincristine can enhance the anti-tumor effects efficiently by inducing HepG2 cell apoptosis.
    Targets: NO | PGE | NOS | COX | NF-kB | PI3K | Akt | Nrf2 | HO-1 | P450 (e.g. CYP17)
    In vitro:
    OMICS. 2014 May;18(5):324-34.
    Towards novel anti-tumor strategies for hepatic cancer: ɛ-viniferin in combination with vincristine displays pharmacodynamic synergy at lower doses in HepG2 cells.[Pubmed: 24341688]
    We investigated the anti-tumor effect of ɛ-Viniferin alone, and the putative synergy of ɛ-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 ɛ-Viniferin and vincristine significantly inhibited cell viability at lower doses as compared to each agent applied alone. IC(50) values for ɛ-Viniferin and vincristine were determined as 98.3 and 52.5 μM at 24 h, respectively. IC(50) value of ɛ-Viniferin in combination with vincristine was 15.8+11.25 μM (mean/SD) at 24 h. The viability of cells treated with 17.9 μM vincristine alone for 24 h was 79.62%; it reduced to 26.53% when 25 μM ɛ-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.
    This study thus suggests that low concentrations of ɛ-Viniferin and vincristine can enhance the anti-tumor effects efficiently by inducing HepG2 cell apoptosis.
    Nat Prod Commun. 2015 Jun;10(6):1017-8.
    Synthesis of ε-Viniferin Glycosides by Glucosyltransferase from Phytolacca americana and their Inhibitory Activity on Histamine Release from Rat Peritoneal Mast Cells.[Pubmed: 26197540]

    Glycosylation of (+)-ε-Viniferin was investigated using glucosyltransferase from Phytolacca americana (PaGT3) as a biocatalyst. (+)-ε-Viniferin was converted by PaGT3 into its 4b- and 13b-β-D-glucosides, the inhibitory activities on histamine release from rat peritoneal mast cells of which were higher than that of (+)-ε-Viniferin.
    Viniferin Description
    Source: The herbs of Gnetum montanum
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to:

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.2022 mL 11.0108 mL 22.0216 mL 44.0432 mL 55.054 mL
    5 mM 0.4404 mL 2.2022 mL 4.4043 mL 8.8086 mL 11.0108 mL
    10 mM 0.2202 mL 1.1011 mL 2.2022 mL 4.4043 mL 5.5054 mL
    50 mM 0.044 mL 0.2202 mL 0.4404 mL 0.8809 mL 1.1011 mL
    100 mM 0.022 mL 0.1101 mL 0.2202 mL 0.4404 mL 0.5505 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Cell Immunol. 2014 Jul;290(1):21-9.
    Anti-inflammatory mechanism of α-viniferin regulates lipopolysaccharide-induced release of proinflammatory mediators in BV2 microglial cells.[Pubmed: 24859013]
    α-Viniferin is an oligostilbene of trimeric resveratrol and has anticancer activity; however, the molecular mechanism underlying the anti-inflammatory effects of α-Viniferin has not been completely elucidated thus far. Therefore, we determined the mechanism by which α-Viniferin regulates lipopolysaccharide (LPS)-induced expression of proinflammatory mediators in BV2 microglial cells.
    Treatment with α-Viniferin isolated from Clematis mandshurica decreased LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2). α-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-κB) via dephosphorylation of Akt/PI3K. Treatment with a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), indirectly showed that NF-κB is a crucial transcription factor for expression of these genes in the early stage of inflammation. Additionally, our results indicated that α-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 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. These results suggest that α-Viniferin may be a potential candidate to regulate LPS-induced inflammation.
    Food Chem Toxicol. 2014 Jul;69:276-80.
    Potent inhibitory effect of alpha-viniferin on human cytochrome P450.[Pubmed: 24769006]
    α-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 α-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). α-Viniferin strongly inhibited 7 of the 9 CYP isoforms (except CYP2A6 and CYP2E1). Furthermore, α-Viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC50 values of 0.93 and 1.2 μM, respectively. α-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 α-Viniferin on CYP2C19 and 3A4 in HLMs to predict a potential herb-drug interaction.