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    Desmethoxy yangonin
    Desmethoxy yangonin
    Information
    CAS No. 15345-89-8 Price $188 / 20mg
    Catalog No.CFN90149Purity>=98%
    Molecular Weight228.24Type of CompoundPhenols
    FormulaC14H12O3Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Desmethoxy yangonin Description
    Source: The roots of Piper methysticum Forst
    Biological Activity or Inhibitors: 1. Desmethoxy yangonin protects LPS or LPS/D-GalN-induced damages in cell or liver tissues mainly through de-regulating IKK/NFκB and Jak2/STAT3 signaling pathways.
    2. The induction of CYP3A23 by dihydromethysticin and Desmethoxy yangonin involves transcription activation, probably through a PXR-independent or PXR-involved indirect mechanism.
    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 4.3814 mL 21.9068 mL 43.8135 mL 87.6271 mL 109.5338 mL
    5 mM 0.8763 mL 4.3814 mL 8.7627 mL 17.5254 mL 21.9068 mL
    10 mM 0.4381 mL 2.1907 mL 4.3814 mL 8.7627 mL 10.9534 mL
    50 mM 0.0876 mL 0.4381 mL 0.8763 mL 1.7525 mL 2.1907 mL
    100 mM 0.0438 mL 0.2191 mL 0.4381 mL 0.8763 mL 1.0953 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.
    Desmethoxy yangonin References Information
    Citation [1]

    PLoS One. 2013 Oct 15;8(10):e77626.

    A plant kavalactone desmethoxy yangonin prevents inflammation and fulminant hepatitis in mice.[Pubmed: 24143247]
    An active compound of the plant rhizomes, Desmethoxy yangonin (DMY), was identified in this study for its novel effect against endotoxin lipopolysaccharide (LPS)-stimulated inflammation in murine macrophages and LPS/D-galactosamine (LPS/D-GalN)-induced fulminant hepatitis in mice. Desmethoxy yangonin was observed to significantly inhibit proliferation and activation of T cells ex vivo and the activity of several pro-inflammatory mediators in vitro. Desmethoxy yangonin also protected LPS/D-GalN-induced acute hepatic damages in mice through inhibiting aminotransferases activities and infiltrations of inflammatory macrophages, neutrophils and pathogenic T cells into the liver tissues. In addition, pretreatment with Desmethoxy yangonin significantly improved the survival rate of LPS/D-GalN-treated mice to 90% (9/10), compared to LPS/D-GalN-treated group (40%, 4/10). UPLC/MS platform-based comparative metabolomics approach was used to explore the serum metabolic profile in fulminant hepatic failure (FHF) mice with or without the Desmethoxy yangonin pretreatment. The results showed that LPS/D-GalN-induced hepatic damage is likely through perturbing amino acid metabolism, which leads to decreased pyruvate formation via catalysis of aminotransferases, and Desmethoxy yangonin treatment can prevent to a certain degree of these alterations in metabolic network in mouse caused by LPS/D-GalN. Mechanistic investigation demonstrated that Desmethoxy yangonin protects LPS or LPS/D-GalN-induced damages in cell or liver tissues mainly through de-regulating IKK/NFκB and Jak2/STAT3 signaling pathways.
    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]
    This study was undertaken to test the ability of purified kavalactones to induce CYP3A23 and activate PXR. Rat hepatocytes were treated with Desmethoxy yangonin, dihydrokawain, dihydromethysticin, kawain, methysticin, or yangonin, and the expression of CYP3A23 was monitored. Among the kavalactones, only Desmethoxy yangonin and dihydromethysticin markedly induced the expression of CYP3A23 (approximately 7-fold). A similar magnitude of induction was detected with combined six kavalactones at a noninductive concentration when individually used. The induced expression, however, was markedly reduced or completely abolished if dihydromethysticin, Desmethoxy yangonin, or both were excluded from the mixtures. Interestingly, regardless of whether dihydromethysticin or Desmethoxy yangonin 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 Desmethoxy yangonin is additively/synergistically enhanced by other kavalactones. In addition, treatment with dihydromethysticin, Desmethoxy yangonin, 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 Desmethoxy yangonin only slightly activated rat or human PXR. These findings suggest that the induction of CYP3A23 by dihydromethysticin and Desmethoxy yangonin involves transcription activation, probably through a PXR-independent or PXR-involved indirect mechanism.