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    Vitisin B
    Vitisin B
    Information
    CAS No. 184362-10-5 Price
    Catalog No.CFN93805Purity>=98%
    Molecular Weight517.45Type of CompoundPhenols
    FormulaC25H25O12Physical DescriptionPowder
    Download     COA    MSDS    SDFSimilar structuralComparison
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    Vitisin B Description
    Source: The fruits of Vitis thunbergii var. taiwaniana.
    Biological Activity or Inhibitors: 1. Vitisin B can stimulate osteoblastogenesis via estrogen receptor-mediated pathway.
    2. (-)-Vitisin B can significantly inhibit cell proliferation through inducing cell apoptosis in human HL-60 promyelocytic leukemia cells, it induces apoptosis of leukemia cells might be mediated through activation of JNK and Fas death-signal transduction.
    3. Vitisin B can inhibits migration through inhibition of PDGF signaling and enhancement of cell adhesiveness in cultured vascular smooth muscle cells.
    Solvent: Pyridine, Methanol, Ethanol, 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: service@chemfaces.com

    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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.9326 mL 9.6628 mL 19.3255 mL 38.6511 mL 48.3138 mL
    5 mM 0.3865 mL 1.9326 mL 3.8651 mL 7.7302 mL 9.6628 mL
    10 mM 0.1933 mL 0.9663 mL 1.9326 mL 3.8651 mL 4.8314 mL
    50 mM 0.0387 mL 0.1933 mL 0.3865 mL 0.773 mL 0.9663 mL
    100 mM 0.0193 mL 0.0966 mL 0.1933 mL 0.3865 mL 0.4831 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.
    Vitisin B References Information
    Citation [1]

    Integrative Medicine Research, 2015,May 4(1):76-7.

    Vitisin B stimulates osteoblastogenesis via estrogen receptor-mediated pathway[Reference: WebLink]
    Vitisin B stimulates osteoblastogenesis via estrogen receptor-mediated pathway
    Citation [2]

    Drug Chem Toxicol. 2013 Jul;36(3):313-9.

    Cytotoxicity of (-)-vitisin B in human leukemia cells.[Pubmed: 23030068 ]
    Vitis thunbergii var. taiwaniana (VTT) is an indigenous Taiwanese wild grape and is used as a folk medicine in Taiwan. VTT is rich in polyphenols, especially quercetin and resveratrol derivatives, which were demonstrated to exhibit inhibitory activities against carcinogenesis and prevent some neurodegenerative diseases. (-)-Vitisin B is one of the resveratrol tetramers extracted from VTT. In this study, we investigated the mechanisms of (-)-Vitisin B on the induction of apoptosis in human HL-60 promyelocytic leukemia cells. First, (-)-Vitisin B significantly inhibited cell proliferation through inducing cell apoptosis. This effect appeared to occur in a time- and dose-dependent manner. Cell-cycle distribution was also examined, and we found that (-)-Vitisin B significantly induced a sub-G1 population in a dose-dependent manner. In addition, (-)-Vitisin B exhibited stronger inhibitory effects on cell proliferation than resveratrol. Second, (-)-Vitisin B dose dependently induced apoptosis-related protein expressions, such as the cleavage form of caspase-3, caspase-8, caspase-9, poly(ADP ribose) polymerase, and the proapoptotic Bax protein. Third, (-)-Vitisin B treatment also resulted in increases in c-Jun N-terminal kinase (JNK) phosphorylation and Fas ligand (FasL) expression. Moreover, the (-)-Vitisin B-induced FasL expression and caspase-3 activation could be reversed by a JNK inhibitor. These results suggest that (-)-Vitisin B-induced apoptosis of leukemia cells might be mediated through activation of JNK and Fas death-signal transduction.
    Citation [3]

    Toxicol Appl Pharmacol. 2011 Oct 15;256(2):198-208.

    Vitisin B, a resveratrol tetramer, inhibits migration through inhibition of PDGF signaling and enhancement of cell adhesiveness in cultured vascular smooth muscle cells.[Pubmed: 21871475 ]
    Vascular smooth muscle cells (VSMCs) play an important role in normal vessel formation and in the development and progression of cardiovascular diseases. Grape plants contain resveratrol monomer and oligomers and drinking of wine made from grape has been linked to "French Paradox". In this study we evaluated the effect of Vitisin B, a resveratrol tetramer, on VSMC behaviors. Vitisin B inhibited basal and PDGF-induced VSMC migration. Strikingly, it did not inhibit VSMC proliferation but inversely enhanced cell cycle progression and proliferation. Among the tested resveratrol oligomers, Vitisin B showed an excellent inhibitory activity and selectivity on PDGF signaling. The anti-migratory effect by Vitisin B was due to direct inhibition on PDGF signaling but was independent of interference with PDGF binding to VSMCs. Moreover, the enhanced VSMC adhesiveness to matrix contributed to the anti-migratory effect by Vitisin B. Fluorescence microscopy revealed an enhanced reorganization of actin cytoskeleton and redistribution of activated focal adhesion proteins from cytosol to the peripheral edge of the cell membrane. This was confirmed by the observation that enhanced adhesiveness was repressed by the Src inhibitor. Finally, among the effects elicited by Vitisin B, only the inhibitory effect toward basal migration was partially through estrogen receptor activation. We have demonstrated here that a resveratrol tetramer exhibited dual but opposite actions on VSMCs, one is to inhibit VSMC migration and the other is to promote VSMC proliferation. The anti-migratory effect was through a potent inhibition on PDGF signaling and novel enhancement on cell adhesion.