Atractylenolide IICAS# 73069-14-4 |
Quality Control & MSDS
3D structure
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Number of papers citing our products
| Cas No. | 73069-14-4 | SDF | Download SDF |
| PubChem ID | 14448070 | Appearance | White powder |
| Formula | C15H20O2 | M.Wt | 232.32 |
| Type of Compound | Sesquiterpenoids | Storage | Desiccate at -20°C |
| Synonyms | Asterolide | ||
| Solubility | Soluble in chloroform | ||
| Chemical Name | (4aS,8aR,9aS)-3,8a-dimethyl-5-methylidene-4a,6,7,8,9,9a-hexahydro-4H-benzo[f][1]benzofuran-2-one | ||
| SMILES | CC1=C2CC3C(=C)CCCC3(CC2OC1=O)C | ||
| Standard InChIKey | OQYBLUDOOFOBPO-KCQAQPDRSA-N | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | 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. |
| Targets | STAT | Src | CDK | Akt | ERK | Bcl-2/Bax | p38MAPK | Caspase | p53 | p21 |
| In vitro | GW26-e1245 Atractylenolide II and Atractylenolide III Inhibit Platelets Activities and Thrombus Formation[Reference: WebLink]J. Am. Coll. Cardiol., 2015, 66(16):C44-C44.Atractylenolide II and Atractylenolide III Inhibit Platelets Activities and Thrombus Formation. Determination of atractylenolide II in rat plasma by reversed-phase high-performance liquid chromatography.[Pubmed: 17236249]Biomed Chromatogr. 2007 Mar;21(3):299-303.
Antiinflammatory Principles of Atractylodes Rhizomes.[Reference: WebLink]Phytotherapy Research, 2007, 21(4):347-353.The crude drug"jutsu"prepared from Atractylodes rhizomes has been used for antiinflammatory purposes in Oriental medicine. |
| In vivo | Inhibition of STAT3 signalling contributes to the antimelanoma action of atractylenolide II.[Pubmed: 25073716]Exp Dermatol. 2014 Nov;23(11):855-7.Our previous studies showed that Atractylenolide II (AT-II) has antimelanoma effects in B16 melanoma cells. |
| Cell Research | Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells.[Pubmed: 21524699]J Ethnopharmacol. 2011 Jun 14;136(1):279-82.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. |
Atractylenolide II Dilution Calculator
Atractylenolide II Molarity Calculator
| 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 necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Atractylenolide II is a sesquiterpene compound isolated from the dried rhizome of Atractylodes macrocephala (Baizhu in Chinese); anti-proliferative activity. IC50 value: 82.3 μM(B16 melanoma cell, 48 h) [1] Target: anticancer natural compound in vitro: AT-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 AT-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 AT-II-mediated growth inhibition and apoptosis [1]. 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 [2]. in vivo: 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 [2].
References:
[1]. Ye Y, et al. Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells. J Ethnopharmacol. 2011 Jun 14;136(1):279-82.
[2]. Fu XQ, et al. Inhibition of STAT3 signalling contributes to the antimelanoma action of atractylenolide II. Exp Dermatol. 2014 Nov;23(11):855-7.
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Determination of atractylenolide II in rat plasma by reversed-phase high-performance liquid chromatography.[Pubmed:17236249]
Biomed Chromatogr. 2007 Mar;21(3):299-303.
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).
Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells.[Pubmed:21524699]
J Ethnopharmacol. 2011 Jun 14;136(1):279-82.
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 AT-II can inhibit B16 cells proliferation. Here we investigate the mechanistic basis for the anti-proliferative activity of AT-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: AT-II treatment for 48 h dose-dependently inhibited cell proliferation with an IC(50) of 82.3 muM, and induced G1 phase cell cycle arrest. Moreover, treatment with 75 muM AT-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, PFTalpha, significantly decreased AT-II-mediated growth inhibition and apoptosis. CONCLUSIONS: We demonstrated that the G1-arresting and apoptotic effects of AT-II in B16 cells involve p38 activation as well as ERK and Akt inactivation, and the cytotoxic/apoptotic effects of AT-II are potentially p53 dependent. These findings provided chemical and pharmacological basis for the traditional application of Baizhu in melanoma treatment.
