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    Dihydromethysticin
    Dihydromethysticin
    Information
    CAS No. 19902-91-1 Price
    Catalog No.CFN90332Purity>=98%
    Molecular Weight276.28Type of CompoundPhenols
    FormulaC15H16O5Physical DescriptionCryst.
    Download     COA    MSDS    SDFSimilar structuralComparison (Web)
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    Dihydromethysticin Description
    Source: The herbs of Piper methysticum
    Biological Activity or Inhibitors: 1. The induction of CYP3A23 by dihydromethysticin and desmethoxyyangonin involves transcription activation, probably through a pregnane X receptor (PXR).-independent or PXR-involved indirect mechanism.
    2. Dihydromethysticin non-competitively inhibits the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels.
    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: 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 3.6195 mL 18.0976 mL 36.1952 mL 72.3903 mL 90.4879 mL
    5 mM 0.7239 mL 3.6195 mL 7.239 mL 14.4781 mL 18.0976 mL
    10 mM 0.362 mL 1.8098 mL 3.6195 mL 7.239 mL 9.0488 mL
    50 mM 0.0724 mL 0.362 mL 0.7239 mL 1.4478 mL 1.8098 mL
    100 mM 0.0362 mL 0.181 mL 0.362 mL 0.7239 mL 0.9049 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.
    Dihydromethysticin References Information
    Citation [1]

    Planta Med. 1998 Jun;64(5):458-9.

    Kavain, dihydrokavain, and dihydromethysticin non-competitively inhibit the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels.[Pubmed: 9690349 ]
    The mode of action of the kava pyrones, kavain, dihydrokavain and Dihydromethysticin on the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to epitope 2 of voltage-dependent Na+ channels was investigated by performing saturation experiments in the presence and absence of these kava pyrones. The tested compounds significantly decreased the apparent total number of binding sites (Bmax) for [3H]-batrachotoxinin-A 20-alpha-benzoate (control: 0.5 pmol/mg protein, kava pyrones: 0.2-0.27 pmol/mg protein) with little change in the equilibrium constants (KD) for [3H]-batrachotoxin-A 20-alpha-benzoate (control: 28.2 nM, kava pyrones: 24-31 nM). The results indicate for the kava pyrones a non-competitive inhibition of the specific [3H]-batrachotoxinin-A 20-alpha-benzoate binding to receptor site 2 of voltage-gated Na+ channels.
    Citation [2]

    Drug Metab Dispos. 2004 Nov;32(11):1317-24.

    Desmethoxyyangonin and dihydromethysticin are two major pharmacological kavalactones with marked activity on the induction of CYP3A23.[Pubmed: 15282211]
    The induced expression, however, was markedly reduced or completely abolished if Dihydromethysticin, desmethoxyyangonin, or both were excluded from the mixtures. Interestingly, regardless of whether Dihydromethysticin or desmethoxyyangonin was used alone or together with other kavalactones, similar amounts of total kavalactones were needed to produce comparable induction, suggesting that the inductive activity of Dihydromethysticin and desmethoxyyangonin is additively/synergistically enhanced by other kavalactones. In addition, treatment with Dihydromethysticin, desmethoxyyangonin, or pregnenolone 16alpha-carbonitrile (PCN) markedly increased the levels of CYP3A23 mRNA, and inhibition of mRNA synthesis abolished the induction. In contrast to PCN, Dihydromethysticin and desmethoxyyangonin only slightly activated rat or human PXR. These findings suggest that the induction of CYP3A23 by Dihydromethysticin and desmethoxyyangonin involves transcription activation, probably through a PXR-independent or PXR-involved indirect mechanism.