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    Atractylenolide II
    Information
    CAS No. 73069-14-4 Price $118 / 20mg
    Catalog No.CFN99945Purity>=98%
    Molecular Weight232.32Type of CompoundSesquiterpenoids
    FormulaC15H20O2Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Atractylenolide II Description
    Source: The rhizome of Atractylodes macrocephala Koidz.
    Biological Activity or Inhibitors: 1. Atractylenolide II has antimelanoma effect by inhibiting STAT3 signalling.
    2. Atractylenolide II has cytotoxic/apoptotic effects may via p38 activation ,ERK and Akt inactivation, p53 dependent.
    3. Atractylenolide II can inhibit platelets activities and thrombus formation.
    4. Atractylenolide II has antiinflammatory activity.
    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.

    PMID: 29149595

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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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    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.
    doi:10.1016/j.phymed.2017.12.030

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.3044 mL 21.522 mL 43.0441 mL 86.0882 mL 107.6102 mL
    5 mM 0.8609 mL 4.3044 mL 8.6088 mL 17.2176 mL 21.522 mL
    10 mM 0.4304 mL 2.1522 mL 4.3044 mL 8.6088 mL 10.761 mL
    50 mM 0.0861 mL 0.4304 mL 0.8609 mL 1.7218 mL 2.1522 mL
    100 mM 0.043 mL 0.2152 mL 0.4304 mL 0.8609 mL 1.0761 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.
    Atractylenolide II References Information
    Citation [1]

    Exp Dermatol. 2014 Nov;23(11):855-7.

    Inhibition of STAT3 signalling contributes to the antimelanoma action of atractylenolide II.[Pubmed: 25073716]
    Our previous studies showed that Atractylenolide II (AT-II) has antimelanoma effects in B16 melanoma cells. In this study, we investigated the involvement of STAT3 signalling in the antimelanoma action of Atractylenolide II. Daily administration of Atractylenolide II (12.5, 25 mg/kg, i.g.) for 14 days significantly inhibited tumor growth in a B16 xenograft mouse model and inhibited the activation/phosphorylation of STAT3 and Src in the xenografts. In B16 and A375 cells, Atractylenolide II (20, 40 μm) treatment for 48 h dose-dependently reduced protein expression levels of phospho-STAT3, phospho-Src, as well as STAT3-regulated Mcl-1 and Bcl-xL. Overexpression of a constitutively active variant of STAT3, STAT3C in A375 cells diminished the antiproliferative and apoptotic effects of Atractylenolide II. These data suggest that inhibition of STAT3 signalling contributes to the antimelanoma action of Atractylenolide II. Our findings shed new light on the mechanism of action underlying the antimelanoma effects of Atractylenolide II and provide further pharmacological basis for developing Atractylenolide II as a novel melanoma chemopreventive/chemotherapeutic agent.
    Citation [2]

    J. Am. Coll. Cardiol., 2015, 66(16):C44-C44.

    GW26-e1245 Atractylenolide II and Atractylenolide III Inhibit Platelets Activities and Thrombus Formation[Reference: WebLink]
    Atractylenolide II and Atractylenolide III Inhibit Platelets Activities and Thrombus Formation.
    Citation [3]

    J Ethnopharmacol. 2011 Jun 14;136(1):279-82.

    Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells.[Pubmed: 21524699]
    ETHNOPHARMACOLOGICAL RELEVANCE: Atractylenolide II (AT-II) is a sesquiterpene compound isolated from the dried rhizome of Atractylodes macrocephala (Baizhu in Chinese), which is traditionally prescribed for melanoma treatment by Chinese medicine practitioners. Our previous study showed that Atractylenolide II can inhibit B16 cells proliferation. Here we investigate the mechanistic basis for the anti-proliferative activity of Atractylenolide II in B16 melanoma cells. MATERIALS AND METHODS: Cell viability was examined by MTT assay. Cell cycle distribution and apoptosis were determined by flow cytometry. Protein expression was determined by Western blotting. RESULTS: Atractylenolide II treatment for 48 h dose-dependently inhibited cell proliferation with an IC(50) of 82.3 μM, and induced G1 phase cell cycle arrest. Moreover, treatment with 75 μM Atractylenolide II induced apoptosis. These observations were associated with the decrease of the expression of Cdk2, phosphorylated-Akt, phosphorylated-ERK and Bcl-2, the increase of the expression of phosphorylated-p38, phosphorylated-p53, p21, p27, and activation of caspases-8, -9 and -3. In addition, a chemical inhibitor of p53, PFTα, significantly decreased Atractylenolide II-mediated growth inhibition and apoptosis. CONCLUSIONS: We demonstrated that the G1-arresting and apoptotic effects of Atractylenolide II in B16 cells involve p38 activation as well as ERK and Akt inactivation, and the cytotoxic/apoptotic effects of Atractylenolide II are potentially p53 dependent. These findings provided chemical and pharmacological basis for the traditional application of Baizhu in melanoma treatment.
    Citation [4]

    Biomed Chromatogr. 2007 Mar;21(3):299-303.

    Determination of atractylenolide II in rat plasma by reversed-phase high-performance liquid chromatography.[Pubmed: 17236249]
    A method for quantitative determination of Atractylenolide II in rat plasma using reversed-phase high-performance liquid chromatography (RP-HPLC) coupled with UV spectrometry was established. From a variety of compounds and solvents tested, Atractylenolide III was selected as the internal standard (IS) and ethyl acetate was found to be the best solvent for extracting Atractylenolide II from plasma samples. RP-HPLC analysis of the extracts was performed on an analytical column (DIKMA ODS, 150 x 4.6 mm; i.d., 5 microm) equipped with a security guard pre-column system. There was good linearity over the range 0.05-5.0 microg/mL (r > 0.99). The recoveries were more than 90.0% in plasma, and the intra- and inter-day coefficients of variation were less than 10.0% in all cases. The limit of detection (LOD) was 0.025 microg/mL and the lower limit of quantification (LLOQ) was 0.05 microg/mL. The RP-HPLC method was applied to quantitate Atractylenolide II in rat plasma within 24 h in a pharmacokinetics study where experimental rats received a single dose of Atractylenolide II (60 mg/kg).
    Citation [5]

    Phytotherapy Research, 2007, 21(4):347-353.

    Antiinflammatory Principles of Atractylodes Rhizomes.[Reference: WebLink]
    The crude drug"jutsu"prepared from Atractylodes rhizomes has been used for antiinflammatory purposes in Oriental medicine. In fact, a preparation from A. japonica was found to show significant inhibition of the increased vascular permeability induced by acetic acid. Fractionation of the extract, monitoring by bioassay, resulted in the isolation of two active principles, (+)-eudesma-4 (14), 7 (11)-dien-8-one (VI) and atractylenolide I (VII). The structurally related principles Atractylenolide II and III (VIII and IX) also had the tendency to show antiinflammatory activity.