Atractylenolide II

Atractylenolide II
Product Name Atractylenolide II
CAS No.: 73069-14-4
Catalog No.: CFN99945
Molecular Formula: C15H20O2
Molecular Weight: 232.32 g/mol
Purity: >=98%
Type of Compound: Sesquiterpenoids
Physical Desc.: Powder
Targets: STAT | Src | CDK | Akt | ERK | Bcl-2/Bax | p38MAPK | Caspase | p53 | p21
Source: The rhizomes of Atractylodes macrocephala Koidz.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $70/20mg
Atractylenolide II has antiinflammatory activity, it can inhibit platelets activities and thrombus formation. Atractylenolide II has cytotoxic/apoptotic effects may via p38 activation ,ERK and Akt inactivation, p53 dependent, it also has antimelanoma effect by inhibiting STAT3 signalling.
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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.

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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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    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.
    Biomed Chromatogr. 2007 Mar;21(3):299-303.
    Determination of atractylenolide II in rat plasma by reversed-phase high-performance liquid chromatography.[Pubmed: 17236249]

    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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).
    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.
    METHODS AND RESULTS:
    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).
    CONCLUSIONS:
    The structurally related principles Atractylenolide II and III (VIII and IX) also had the tendency to show antiinflammatory activity.
    Planta Med . 2017 Jul;83(11):901-911.
    Correlating In Vitro Target-Oriented Screening and Docking: Inhibition of Matrix Metalloproteinases Activities by Flavonoids[Pubmed: 28288492]
    Abstract Metalloproteases are a family of zinc-containing endopeptidases involved in a variety of pathological disorders. The use of flavonoid derivatives as potential metalloprotease inhibitors has recently increased.Particular plants growing in Sicily are an excellent yielder of the flavonoids luteolin, apigenin, and their respective glycoside derivatives (7-O-rutinoside, 7-O-glucoside, and 7-O-glucuronide).The inhibitory activity of luteolin, apigenin, and their respective glycoside derivatives on the metalloproteases MMP-1, MMP-3, MMP-13, MMP-8, and MMP-9 was assessed and rationalized correlating in vitro target-oriented screening and in silico docking.The flavones apigenin, luteolin, and their respective glucosides have good ability to interact with metalloproteases and can also be lead compounds for further development. Glycones are more active on MMP-1, -3, -8, and -13 than MMP-9. Collagenases MMP-1, MMP-8, and MMP-13 are inhibited by compounds having rutinoside glycones. Apigenin and luteolin are inactive on MMP-1, -3, and -8, which can be interpreted as a better selectivity for both -9 and -13 peptidases. The more active compounds are apigenin-7-O-rutinoside on MMP-1 and luteolin-7-O-rutinoside on MMP-3. The lowest IC50 values were also found for apigenin-7-O-glucuronide, apigenin-7-O-rutinoside, and luteolin-7-O-glucuronide. The glycoside moiety might allow for a better anchoring to the active site of MMP-1, -3, -8, -9, and -13. Overall, the in silico data are substantially in agreement with the in vitro ones (fluorimetric assay). Georg Thieme Verlag KG Stuttgart · New York.
    Biomed Pharmacother . 2018 Nov;107:1505-1513.
    Scutellarin inhibits human renal cancer cell proliferation and migration via upregulation of PTEN[Pubmed: 30257368]
    Abstract Background: Scutellarin is a naturally flavone glycoside that has been shown to exhibit anti-proliferative and anti-apoptotic activities among various human malignancies. However, the anti-cancer effect of Scutellarin in Renal cell carcinoma (RCC) and the underlying mechanism remains unclear. Methods and materials: RCC cell lines ACHN and 786-O were treated with different concentrations (0-210 μM) of Scutellarin in vitro. Cell viability and proliferation were investigated by MTT and colony formation assays. Cell invasion and migration were detected by Transwell assays. Cell apoptosis and cell cycle distribution was measured by flow cytometry. Western blot was used to investigate the expression levels of crucial proteins. Xenograft tumor model was established to evaluate tumor growth in vivo. Results: Scutellarin significantly inhibited RCC cell proliferation in a dose- and time- dependent manner. Treatment of RCC cells with Scutellarin (30, 60, and 90 μM) markedly induced apoptosis and cell cycle arrested at G0/G1 phase in a concentration-dependent characteristic. Cell invasion and migration capacities of RCC cells were also dose-dependently suppressed by Scutellarin treatment. Western blot assays revealed that the crucial proteins including cyclin D1, CDK2, Bcl2, MMP-2, and MMP-9 were significantly reduced while Bax, cleaved caspase 3 and p21 were increased by Scutellarin in RCC cells. In vivo assay indicated that Scutellarin possessed anti-cancer effect on xenograft without triggering toxic effect. Mechanically, Scutellarin dramatically increased the protein level of phosphatase and tensin homologue (PTEN) and inhibited the activity of P13K/AKT/mTOR signaling. Ectopic expression of PTEN enhanced the inhibitory effect of Scutellarin on RCC proliferation while knockdown of PTEN abrogated it through regulating its downstream P13K/AKT/mTOR signaling pathway. Conclusion: Scutellarin inhibited RCC cell proliferation and invasion partially by enhancing the expression of PTEN through inhibition of P13K/AKT/mTOR pathway, suggesting that Scutellarin might serve as a potential therapeutic agent in RCC treatment. Keywords: P13K/AKT/mTOR; PTEN; Proliferation; Renal cancer; Scutellarin.
    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.
    METHODS AND RESULTS:
    In this study, we investigated the involvement of STAT3 signalling in the antimelanoma action of AT-II. Daily administration of AT-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, AT-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 AT-II. These data suggest that inhibition of STAT3 signalling contributes to the antimelanoma action of AT-II.
    CONCLUSIONS:
    Our findings shed new light on the mechanism of action underlying the antimelanoma effects of AT-II and provide further pharmacological basis for developing AT-II as a novel melanoma chemopreventive/chemotherapeutic agent.
    J Ethnopharmacol. 2011 Jun 14;136(1):279-82.
    Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells.[Pubmed: 21524699]
    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.
    METHODS AND RESULTS:
    Cell viability was examined by MTT assay. Cell cycle distribution and apoptosis were determined by flow cytometry. Protein expression was determined by Western blotting. 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.
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