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    Natural Products
    Dihydrokavain
    Dihydrokavain
    Information
    CAS No. 587-63-3 Price $288 / 20mg
    Catalog No.CFN90536Purity>=98%
    Molecular Weight232.27Type of CompoundPhenols
    FormulaC14H16O3Physical DescriptionPowder
    Download     COA    MSDS    SDFSimilar structuralComparison (Web)  (SDF)
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    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 / $85.2 / In-stock
    Other Packaging *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap
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    Dihydrokavain

    Dihydrokavain
    Product Name Dihydrokavain
    CAS No.: 587-63-3
    Catalog No.: CFN90536
    Molecular Formula: C14H16O3
    Molecular Weight: 232.27 g/mol
    Purity: >=98%
    Type of Compound: Phenols
    Physical Desc.: Powder
    Targets: GABA Receptor | Sodium channel
    Source: The roots of Piper methysticum Forst.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $288 / 20mg
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  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
    Related Libraries
  • Inhibitors Compound Library
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  • Biological Activity
    Description: Dihydrokavain may play an important role in regulation of GABAergic neurotransmission, it non-competitively inhibits the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels. Dihydrokavain may treat sleep disturbances, as well as stress and anxiety.
    Targets: GABA Receptor | Sodium channel
    In vitro:
    Planta Med. 2002 Dec;68(12):1092-6.
    Kavalactones and dihydrokavain modulate GABAergic activity in a rat gastric-brainstem preparation.[Pubmed: 12494336]

    METHODS AND RESULTS:
    Using an in vitro neonatal rat gastric-brainstem preparation, the activity of majority neurons recorded in the nucleus tractus solitarius (NTS) of the brainstem were significantly inhibited by GABA A receptor agonist, muscimol (30 microM), and this inhibition was reversed by selective GABA A receptor antagonist, bicuculline (10 microM). Application of kavalactones (300 microg/ml) and Dihydrokavain (300 microM) into the brainstem compartment of the preparation also significantly reduced the discharge rate of these NTS neurons (39 % and 32 %, respectively, compared to the control level), and this reduction was partially reversed by bicuculline (10 microM). Kavalactones or Dihydrokavain induced inhibitory effects were not reduced after co-application of saclofen (10 microM; a selective GABA B receptor antagonist) or naloxone (100 nM; an opioid receptor antagonist). Pretreatment with kavalactones (300 microg/ml) or Dihydrokavain (300 microM) significantly decreased the NTS inhibitory effects induced by muscimol (30 microM), approximately from 51 % to 36 %.
    CONCLUSIONS:
    Our results demonstrated modulation of brainstem GABAergic mechanism by kavalactones and Dihydrokavain, and suggested that these compounds may play an important role in regulation of GABAergic neurotransmission.
    Dihydrokavain Description
    Source: The roots of Piper methysticum Forst.
    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.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.3053 mL 21.5267 mL 43.0533 mL 86.1067 mL 107.6334 mL
    5 mM 0.8611 mL 4.3053 mL 8.6107 mL 17.2213 mL 21.5267 mL
    10 mM 0.4305 mL 2.1527 mL 4.3053 mL 8.6107 mL 10.7633 mL
    50 mM 0.0861 mL 0.4305 mL 0.8611 mL 1.7221 mL 2.1527 mL
    100 mM 0.0431 mL 0.2153 mL 0.4305 mL 0.8611 mL 1.0763 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.
    Protocol
    Kinase Assay:
    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]

    METHODS AND RESULTS:
    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).
    CONCLUSIONS:
    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.
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