Taraxerol acetate
(Synonyms: 醋酸蒲公英霜) 目录号 : GC39040
Taraxerol acetate 是 COX-1 和 COX-2 抑制剂， IC50 值分别为 116.3 μM 和 94.7μM。Taraxerol acetate 具有抗癌作用并诱导细胞凋亡(apoptosis)。
Cas No.:2189-80-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Taraxerol acetate is a COX-1 and COX-2 inhibitor with IC50 values of 116.3 μM and 94.7 μM, respectively. Taraxerol acetate the has the anticancer potential and induces cell apoptosis[1].
[1]. Ubaid Ur Rehman1 A, et al. Molecular docking of taraxerol acetate as a new COX inhibitor. Journal of the Bangladesh Pharmacological Society [2]. Hong JF, et al. Anticancer activity of taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration.Mol Med Rep. 2016 Jun;13(6):4541-8.
| Cas No. | 2189-80-2 | SDF | |
| 别名 | 醋酸蒲公英霜 | ||
| Canonical SMILES | C[C@]12C3=CC[C@@](C)(CCC(C)(C)C4)[C@]4([H])[C@@]3(CC[C@]1([H])[C@@]5([C@@](C(C)([C@@H](OC(C)=O)CC5)C)([H])CC2)C)C | ||
| 分子式 | C32H52O2 | 分子量 | 468.75 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1333 mL | 10.6667 mL | 21.3333 mL |
| 5 mM | 0.4267 mL | 2.1333 mL | 4.2667 mL |
| 10 mM | 0.2133 mL | 1.0667 mL | 2.1333 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
[Retracted] Anticancer activity of Taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration
Mol Med Rep 2021 Jun;23(6):461.PMID:33876628DOI:10.3892/mmr.2021.12100.
Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 3, 4, 7 and 10) contained apparent anomalies, including repeated patternings of data within the same figure panels. Furthermore, Fig. 3 contained data that bore striking similarities to data published in Fig. 6 in another paper published in Molecular Medicine Reports, which has now been retracted [Zhu Y‑Y, Huang H‑Y and Wu Y‑L: Anticancer and apoptotic activities of oleanolic acid are mediated through cell cycle arrest and disruption of mitochondrial membrane potential in HepG2 human hepatocellular carcinoma cells. Mol Med Rep 12: 5012‑5018, 2015]. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Molecular Medicine Reports 13: 4541‑4548, 2016; DOI: 10.3892/mmr.2016.5105].
Anticancer activity of Taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration
Mol Med Rep 2016 Jun;13(6):4541-8.PMID:27081915DOI:10.3892/mmr.2016.5105.
The aim of the present study was to investigate the in vitro and in vivo anticancer and apoptotic effects of Taraxerol acetate in U87 human glioblastoma cells. The effects on cell cycle phase distribution, cell cycle-associated proteins, autophagy, DNA fragmentation and cell migration were assessed. Cell viability was determined using the MTT assay, and phase contrast and fluorescence microscopy was utilized to determine the viability and apoptotic morphological features of the U87 cells. Flow cytometry using propidium iodide and Annexin V-fluorescein isothiocyanate demonstrated the effect of Taraxerol acetate on the cell cycle phase distribution and apoptosis induction. Western blot analysis was performed to investigate the effect of the Taraxerol acetate on cell cycle‑associated proteins and autophagy‑linked LC3B‑II proteins. The results demonstrated that Taraxerol acetate induced dose‑ and time‑dependent cytotoxic effects in the U87 cells. Apoptotic induction following Taraxerol acetate treatment was observed and the percentage of apoptotic cells increased from 7.3% in the control cells, to 16.1, 44.1 and 76.7% in the 10, 50 and 150 µM Taraxerol acetate‑treated cells, respectively. Furthermore, Taraxerol acetate treatment led to sub‑G1 cell cycle arrest with a corresponding decrease in the number of S‑phase cells. DNA fragments were observed as a result of the gel electrophoresis experiment following Taraxerol acetate treatment. To investigate the inhibitory effects of Taraxerol acetate on the migration of U87 cell, a wound healing assay was conducted. The number of cells that migrated to the scratched area decreased significantly following treatment with Taraxerol acetate. In addition, Taraxerol acetate inhibited tumor growth in a mouse xenograft model. Administration of 0.25 and 0.75 µg/g Taraxerol acetate reduced the tumor weight from 1.2 g in the phosphate‑buffered saline (PBS)‑treated group (control) to 0.81 and 0.42 g, respectively. Similarly, 0.25 and 0.75 µg/g Taraxerol acetate injection reduced the tumor volume from 1.3 cm3 in the PBS-treated group (control) to 0.67 and 0.25 cm3, respectively.
Taraxerol acetate at 100 K
Acta Crystallogr C 1999 Dec 15;55 ( Pt 12):2129-31.PMID:10641284DOI:10.1107/s0108270199011403.
The title triterpene, D-friedoolean-14-en-3 beta-yl acetate, C32H52O2, was isolated from dichloromethane extracts of the roots of common ragweed Ambrosia artemisiifolia. The skeleton contains five fused six-membered rings with an average Csp3-Csp3 bond distance of 1.549 (6) A and one double bond of length 1.348 (6) A. The D and E rings are cis-fused. The compound also contains a beta-oriented acetate group with a C-O distance 1.461 (5) A.
[Effects of taraxerol and Taraxerol acetate on cell cycle and apoptosis of human gastric epithelial cell line AGS]
Zhong Xi Yi Jie He Xue Bao 2011 Jun;9(6):638-42.PMID:21669168DOI:10.3736/jcim20110610.
Objective: To investigate the effects of taraxerol and Taraxerol acetate on cell cycle and apoptosis of human gastric epithelial cell line AGS cells. Methods: The inhibitory effects of taraxerol and Taraxerol acetate at different concentrations on AGS cell growth were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) method and the concentrations of taraxerol and Taraxerol acetate to be used in following experiments were decided. Then, cell cycle analysis was performed by FACScan flow cytometry after culture with taraxerol or Taraxerol acetate. Annexin V-fluorescein isothiocyanate/propidium iodide staining was used to measure cell apoptosis. Results: Taraxerol significantly inhibited AGS cell proliferation in a dose- and time-dependent manner. Taraxerol arrested the AGS cells at G(2)/M stage. 110 μmol/L taraxerol elevated the population of AGS cells arrested in G(2)/M phase compared with solvent (P<0.05). Taraxerol also promoted early cell apoptosis in AGS cells. 110 μmol/L taraxerol increased the early cell apoptosis rate from 4.45% to 10.29%, which was 1.31 times higher than that of the untreated cells. However, Taraxerol acetate had a lower inhibitory effect than taraxerol, and it showed a tendency of G(2)/M arrest and apoptosis promotion but with no statistical significance (P>0.05). Conclusion: Taraxerol has inhibitory effects on AGS cell growth through inducing G(2)/M arrest and promotion of cell apoptosis. Taraxerol acetate has less effect on cell cycle arrest and apoptosis of AGS cells than taraxerol.
Taraxerol Induces Cell Apoptosis through A Mitochondria-Mediated Pathway in HeLa Cells
Cell J 2017 Oct;19(3):512-519.PMID:28836414DOI:10.22074/cellj.2017.4543.
Objectives: Taraxerol acetate has potent anti-cancer effects via the induction of apoptosis, autophagy, cell cycle arrest, and inhibition of cell migration. However, whether taraxerol induced apoptosis and its underlying mechanisms of action is not clear. In the present study, we assess the effects of taraxerol on the mitochondrial apoptotic pathway and determine the release of cytochrome c to the cytosol and activation of caspases. Materials and methods: In this experimental study, we mainly investigated the effect of taraxerol on HeLa cells. We tested cell viability by the MTT assay and morphologic changes, analyzed apoptosis by DAPI staining and flow cytometry. We also determined reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) using a Microplate Reader. In addition, the apoptotic proteins were tested by Western blot. Results: Taraxerol enhanced ROS levels and attenuated the MMP (Δψm) in HeLa cells. Taraxerol induced apoptosis mainly via the mitochondrial pathway including the release of cytochrome c to the cytosol and activation of caspases 9 and 3, and anti-poly (ADPribose) polymerase (PARP). Taraxerol could induce the down-regulation of the anti-apoptotic protein Bcl-2 and up-regulation of pro-apoptotic protein Bax. It suppressed the PI3K/ Akt signaling pathway. Conclusions: These results demonstrated that taraxerol induced cell apoptosis through a mitochondria-mediated pathway in HeLa cells. Thus, taraxerol might be a potential anticervical cancer candidate.