Kazinol U

Kazinol U
Product Name Kazinol U
CAS No.: 1238116-48-7
Catalog No.: CFN97839
Molecular Formula: C20H22O4
Molecular Weight: 326.39 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: Estrogen receptor | NF-kB | IkB | NO | NOS | IFN-γ | IL Receptor | IKK | Progestogen receptor
Source: The barks of Broussonetia papyrifera.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Kazinol U may have therapeutic value in delaying pancreatic β-cell destruction in type 1 diabetes by blocking the NF-κB pathway in pancreatic β-cells reduces cell damage. Kazinol U shows estrogenic activity with ligand-activity of estrogen receptor, transcriptional activity of estrogen -responsive element-reporter genes, it may have beneficial effects in the treatment of menopausal symptoms.
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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

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.
  • Molecules.2019, 24(10):E1930
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  • Food Addit Contam Part A Chem Anal Control Expo Risk Assess.2020, 37(9):1437-1448.
  • Pharmacia2022, 69(3): 883-890.
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    Bioorg Med Chem Lett. 2010 Jun 15;20(12):3764-7.
    New estrogenic compounds isolated from Broussonetia kazinoki.[Pubmed: 20493686 ]

    METHODS AND RESULTS:
    Two new and two known compounds were identified as estrogenic constituents from Broussonetia kazinoki. Their structures were elucidated as broussonin A (1), tupichinol C (2), Kazinol U (3), and (+)-(2R) kazinol I (4). They showed estrogenic activity with ligand-binding activity of estrogen receptor, transcriptional activity of estrogen-responsive element-luciferase reporter genes. They also control the cellular gene expression levels of estrogen-responsive genes.
    CONCLUSIONS:
    Phytoestrogens from B. kazinoki may have beneficial effects in the treatment of menopausal symptoms.
    Biol Pharm Bull. 2011;34(7):1026-31.
    A prenylated flavan from Broussonetia kazinoki prevents cytokine-induced β-cell death through suppression of nuclear factor-κB activity.[Pubmed: 21720008]
    The generation of nitric oxide (NO) via inducible NO synthase (iNOS) and reactive oxygen species plays a key role in cytokine-mediated pancreatic β-cell damage. Oxidative stress due to reactive oxygen species activates the nuclear factor-κB (NF-κB) transcription factor, which regulates iNOS expression. In this regard, suppression of the NF-κB pathway is a novel strategy for protecting β-cells from damage.
    METHODS AND RESULTS:
    This study was performed to explore the effects of Kazinol U, a prenylated flavan from Broussonetia kazinoki, on the NF-κB activation pathway in interleukin-1β (IL-1β)- and interferon-γ (IFN-γ)-treated β-cells. The cytotoxic effects of cytokines were completely abolished when RINm5F cells or islets were pretreated with Kazinol U. Kazinol U inhibited the nuclear translocation and DNA binding of NF-κB subunits, which correlated with the inhibitory effects on IκB kinase (IKK) phosphorylation and IκBα degradation. In addition, Kazinol U suppressed NO and hydrogen peroxide production and apoptotic cell death by cytokines in RINm5F cells. The protective effects of Kazinol U were further demonstrated by normal insulin secretion of cytokine-treated islets in response to glucose.
    CONCLUSIONS:
    Taken together, these results suggest that using Kazinol U to block the NF-κB pathway in pancreatic β-cells reduces cell damage. Therefore, Kazinol U may have therapeutic value in delaying pancreatic β-cell destruction in type 1 diabetes.
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