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    Bakkenolide A
    CAS No. 19906-72-0 Price $218 / 20mg
    Catalog No.CFN98579Purity>=98%
    Molecular Weight234.34Type of CompoundMiscellaneous
    FormulaC15H22O2Physical DescriptionCryst.
    Download Manual    COA    MSDSSimilar structuralComparison
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    Biological Activity
    Description: 1. Bakkenolide A has antifeedant and growth inhibitory effects on neonate variegated cutworms.
    2. Bakkenolide A inhibits leukemia by regulation of HDAC3 and PI3K/Akt-related signaling pathways.
    Targets: HDAC | IkB | IL Receptor | Caspase | TNF-α | PI3K | Akt | GSK-3 | IKK
    Bakkenolide A Description
    Source: The herbs of Petasites japonicus F. Schmidt
    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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

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    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

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    doi: 10.3390/molecules22111829.

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    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.2673 mL 21.3365 mL 42.673 mL 85.3461 mL 106.6826 mL
    5 mM 0.8535 mL 4.2673 mL 8.5346 mL 17.0692 mL 21.3365 mL
    10 mM 0.4267 mL 2.1337 mL 4.2673 mL 8.5346 mL 10.6683 mL
    50 mM 0.0853 mL 0.4267 mL 0.8535 mL 1.7069 mL 2.1337 mL
    100 mM 0.0427 mL 0.2134 mL 0.4267 mL 0.8535 mL 1.0668 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.
    Bakkenolide A References Information
    Citation [1]

    J Mass Spectrom. 2012 Aug;47(8):962-8.

    Determination of bakkenolide A in rat plasma using liquid chromatography/tandem mass spectrometry and its application to a pharmacokinetic study.[Pubmed: 22899504]
    A sensitive rapid analytical method was established and validated to determine the Bakkenolide A (BA) in rat plasma. This method was further applied to assess the pharmacokinetics of Bakkenolide A in rats receiving a single dose of Bakkenolide A. Intra- and inter-day accuracies for Bakkenolide A were 93-112% and 103-104%, respectively, and the inter-day precision was less than 15%. After a single oral dose of 20 mg/kg of Bakkenolide A, the mean peak plasma concentration (C(max) ) of Bakkenolide A was 234.7 ± 161 ng/mL at 0.25 h. The area under the plasma concentration-time curve (AUC(0-24 h) ) was 535.8 ± 223.7 h·ng/mL, and the elimination half-life (T(1/2) ) was 5.0 ± 0.36 h. In case of intravenous administration of Bakkenolide A at a dosage of 2 mg/kg, the area under the plasma concentration-time curve (AUC(0-24 h) ) was 342 ± 98 h⋅ng/mL, and the elimination half-life (T(1/2) ) was 5.8 ± 0.7 h. Based on the results, the oral bioavailability of Bakkenolide A in rats at 20 mg/kg is 15.7%.
    Citation [2]

    J.Appl. Entomol.,2010,107(1-5):524-9.

    Antifeedant and growth inhibitory effects of bakkenolide-A and other sesquiterpene lactones on the variegated cutworm, Peridroma saucia Huebner (Lep., Noctuidae). [Reference: WebLink]
    When added to artificial diets, the sesquiterpene lactone Bakkenolide A deterred feeding of neonate variegated cutworms in a choice test, and inhibited larval growth in a no-choice bioassay. In both bioassays, Bakkenolide A was more active against this polyphagous pest than several other sesquiterpene lactones previously shown to be active against other insects. In the choice test, older larvae (second instar) were found to be less sensitive to the antifeedant effect of Bakkenolide A than younger ones (first instar). Bakkenolide A also reduced larval growth and survival of second instar larvae when applied topically. Bioactivity of bakkenolide-A via topical application was also greater than that of other sesquiterpene lactones tested.
    Citation [3]

    Biomed. Pharmacother.,2016 Oct;83:958-66.

    Bakkenolide A inhibits leukemia by regulation of HDAC3 and PI3K/Akt-related signaling pathways.[Pubmed: 27522258 ]
    Leukemia has been the third type of cancer killing many people across the world. Bakkenolide A (Bak), extracted from Petasites tricholobus, has been suggested to against cancer and display protective effects on inflammatory cytokines formation. And increasing evidences suggest that histone deacetylase 3 (HDAC3) plays vital roles in cancer formation and persistence via cell death, apoptosis and inflammation. But the function of Bakkenolide A in regulating leukemia is not understood yet, particularly via HDAC3. Here, we found that HDAC3 is up-regulated in clinical samples of leukemia compared with adjacent normal tissues. Then the expression of HDAC3 was knocked down via RNA interference in K562 cells. And inhibition of HDAC3 expression is able to improve leukemia invasion, migration and proliferation. Further, we also found HDAC3 bound to IκBα, affecting subsequent inflammation response. Moreover, Bakkenolide A was found to inhibit inflammation, induce apoptosis and cell death in leukemia cells via PI3K-regulated signaling pathway, down-regulating IKKs expression and suppressing in proinflammatory cytokines of IL-1β, IL-18 and TNF-α. Up-regulation of Caspase3/7 was observed in cells of HDAC3-knockdown and Bakkenolide A treatment, inducing leukemia cell apoptosis. Also, the expression of Akt and GSK were activated by HDAC3-knockdown and Bakkenolide A-treatment. Thus, these results indicated that Bakkenolide A-mediated HDAC3 sensitization in leukemia cells seem to be associated with activation of effector IKKs, Akt/GSK, and caspases through induction of the PI3K pathway, leading to inflammation, cell death, and apoptosis.