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    Methysticin
    Methysticin
    Information
    CAS No. 20697-20-5 Price
    Catalog No.CFN90160Purity>=98%
    Molecular Weight274.27Type of CompoundPhenols
    FormulaC15H14O5Physical DescriptionCryst.
    Download     COA    MSDS    SDFSimilar structuralComparison (Web)
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    Methysticin Description
    Source: The herbs of Piper methysticum
    Biological Activity or Inhibitors: 1. Methysticin and yangonin show in vitro hepatotoxicity on human hepatocytes (HepG2) .
    2. Methysticin and 7,8-dihydroMethysticin contribute to CYP1A1 induction.
    3. Methysticin is a potent NF-kappaB inhibitor in kava with minimum toxicity.
    4. Methysticin possesses anticonvulsant and neuroprotective properties, possibly by interfering with frequency potentiation.
    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 3.646 mL 18.2302 mL 36.4604 mL 72.9208 mL 91.1511 mL
    5 mM 0.7292 mL 3.646 mL 7.2921 mL 14.5842 mL 18.2302 mL
    10 mM 0.3646 mL 1.823 mL 3.646 mL 7.2921 mL 9.1151 mL
    50 mM 0.0729 mL 0.3646 mL 0.7292 mL 1.4584 mL 1.823 mL
    100 mM 0.0365 mL 0.1823 mL 0.3646 mL 0.7292 mL 0.9115 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.
    Methysticin References Information
    Citation [1]

    Toxicol Sci. 2011 Dec;124(2):388-99.

    Methysticin and 7,8-dihydromethysticin are two major kavalactones in kava extract to induce CYP1A1.[Pubmed: 21908763]
    Kava is a plant traditionally used for making beverages in Pacific Basin countries and has been used for the treatment of nervous disorders in the United States. The pharmacological activity of kava is achieved through kavalactones in kava extract, which include kawain, 7,8-dihydrokawain, yangonin, 5,6-dehydrokawain, Methysticin, and 7,8-dihydroMethysticin. Recent studies have shown that kava extract induces hepatic CYP1A1 enzyme; however, the mechanisms of CYP1A1 induction have not been elucidated, and the kavalactones responsible for CYP1A1 induction have not yet been identified. Using a combination of biochemical assays and molecular docking tools, we determined the functions of kava extract and kavalactones and delineated the underlying mechanisms involved in CYP1A1 induction. The results showed that kava extract displayed a concentration-dependent effect on CYP1A1 induction. Among the six major kavalactones, Methysticin triggered the most profound inducing effect on CYP1A1 followed by 7,8-dihydroMethysticin. The other four kavalactones (yangonin, 5,6-dehydrokawain, kawain, and 7,8-dihydrokawain) did not show significant effects on CYP1A1. Consistent with the experimental results, in silico molecular docking studies based on the aryl hydrocarbon receptor (AhR)-ligand binding domain homology model also revealed favorable binding to AhR for Methysticin and 7,8-dihydroMethysticin compared with the remaining kavalactones. Additionally, results from a luciferase gene reporter assay suggested that kava extract, Methysticin, and 7,8-dihydroMethysticin were able to activate the AhR signaling pathway. Moreover, kava extract-, Methysticin-, and 7,8-dihydroMethysticin-mediated CYP1A1 induction was blocked by an AhR antagonist and abolished in AhR-deficient cells. These findings suggest that kava extract induces the expression of CYP1A1 via an AhR-dependent mechanism and that Methysticin and 7,8-dihydroMethysticin contribute to CYP1A1 induction. The induction of CYP1A1 indicates a potential interaction between kava or kavalactones and CYP1A1-mediated chemical carcinogenesis.
    Citation [2]

    Phytother Res. 2011 Mar;25(3):417-23.

    Kavalactones Yangonin and Methysticin induce apoptosis in human hepatocytes (HepG2) in vitro.[Pubmed: 20734326]
    While cases of severe kava hepatotoxicity have been reported, studies examining the toxicity of individual kavalactones are limited. The present study examined the in vitro hepatotoxicity of kavain, Methysticin and yangonin on human hepatocytes (HepG2) and the possible mechanism(s) involved. Cytotoxicity was assessed using lactate dehydrogenase (LDH) and ethidium bromide (EB) assays. The mode of cell death was analysed with acridine orange/ethidium bromide dual staining with fluorescence microscopy. Glutathione oxidation was measured using the ortho-phthalaldehyde (OPT) fluorescence assay. Kavain had minimal cytotoxicity, Methysticin showed moderate concentration-dependent toxicity and yangonin displayed marked toxicity with ~ 40% reduction in viability in the EB assay. Acridine orange/ethidium bromide staining showed the predominant mode of cell death was apoptosis rather than necrosis. No significant changes were observed in glutathione levels, excluding this as the primary mechanism of cell death in this model. Further studies may elucidate the precise apoptotic pathways responsible and whether toxic kavalactone metabolites are involved.
    Citation [3]

    Bioorg Med Chem Lett. 2009 Oct 1;19(19):5732-6.

    Identification of methysticin as a potent and non-toxic NF-kappaB inhibitor from kava, potentially responsible for kava's chemopreventive activity.[Pubmed: 19716299]
    Nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays an essential role in cancer development. The results of our recent chemopreventive study demonstrate that kava, a beverage in the South Pacific Islands, suppresses NF-kappaB activation in lung adenoma tissues, potentially a mechanism responsible for kava's chemopreventive activity. Methysticin is identified as a potent NF-kappaB inhibitor in kava with minimum toxicity. Other kava constituents, including four kavalactones of similar structures to Methysticin, demonstrate minimum activities in inhibiting NF-kappaB.
    Citation [4]

    Naunyn Schmiedebergs Arch Pharmacol. 1995 Apr;351(4):348-55.

    Effects of methysticin on three different models of seizure like events studied in rat hippocampal and entorhinal cortex slices.[Pubmed: 7630425]
    Methysticin is one of the constituents of Piper methysticum which possesses anticonvulsant and neuroprotective properties. Its effects on different in vitro seizure models were tested using extracellular recordings in rat temporal cortex slices containing the hippocampus and the entorhinal cortex. Elevating [K+]0 induced seizure-like events with tonic and clonic electrographic phases in area CA1. Lowering [Ca2+]0 caused recurrent seizure like episodes with large negative field potential shifts. Lowering Mg2+ induced short recurrent discharges in area CA3 and CA1 while ictaform events lasting for many seconds were induced in the subiculum, entorhinal and temporal neocortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the subiculum, entorhinal and temporal cortex changed their characteristics after one to two hours to late recurrent discharges. In a concentration-range from 10 to 100 microM Methysticin reversibly blocked all these types of epileptiform activity. Decreases in [Ca2+]0 and associated slow field potentials evoked by repetitive stimulation of the stratum radiatum or the alveus remained almost unaffected by Methysticin. A paired pulse stimulus paradigm used to test for effects of Methysticin on synaptically evoked transient field potentials in normal medium revealed interference with mechanisms involved in frequency potentiation. While responses to alvear stimulation were largely unaffected, the responses to a paired pulse stimulus to stratum radiatum were depressed over the whole range of tested stimulus intervals. The findings suggest that Methysticin has effects on different patterns of epileptiform activity possibly by interfering with processes responsible for frequency potentiation.