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  • 冬凌草甲素

    Oridonin

    冬凌草甲素
    产品编号 CFN99164
    CAS编号 28957-04-2
    分子式 = 分子量 C20H28O6 = 364.43
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Diterpenoids
    植物来源 The herbs of Rabdosia rubescens (Hamst.) C.Y.Wu et Hsuan.
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    冬凌草甲素 CFN99164 28957-04-2 10mg QQ客服:1413575084
    冬凌草甲素 CFN99164 28957-04-2 20mg QQ客服:1413575084
    冬凌草甲素 CFN99164 28957-04-2 50mg QQ客服:1413575084
    冬凌草甲素 CFN99164 28957-04-2 100mg QQ客服:1413575084
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • University of South Australia (Australia)
  • University of Malaya (Malaysia)
  • China Medical University (Taiwan)
  • Kyushu University (Japan)
  • Tohoku University (Japan)
  • Washington State University (USA)
  • University of Wuerzburg (Germany)
  • Subang Jaya Medical Centre (Malaysia)
  • University of Vigo (Spain)
  • Sanford Burnham Prebys Medical Discovery Institute (USA)
  • Amity University (India)
  • University of Toronto (Canada)
  • Ain Shams University (Egypt)
  • Wageningen University (Netherlands)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • J. of Agricultural Science2015, 1916-9760
  • University of Limpopo2016, 1-237
  • British Jou. Med.&Med. Research2014, 1802-1811
  • Journal of Applied Pharmaceutical Science2022, 0(00), pp:001-007
  • Molecules.2015, 20(11):20014-30
  • Plant Growth Regulation2020, 90(2):383-392
  • J Sep Sci.2018, 41(7):1682-1690
  • Int Immunopharmacol. 2020, 83:106403.
  • The Malaysian journal of pathology2019, 41(3):243-251
  • Food Sci Biotechnol.2023, 32(7):997-1003.
  • Front Pharmacol.2021, 12:762829.
  • HIV Med.2021, 22(8):690-704.
  • Anesth Pain Med (Seoul).2020, 15(4):478-485.
  • Planta Med.2022, 88(9-10):794-804.
  • Indian J. of Experimental Bio.2020, 9(58).
  • Tumour Biol.2015, 36(12):9385-93
  • Toxicol Rep.2021, 8:1131-1142.
  • Exp Biol Med (Maywood).2019, 244(16):1463-1474
  • LWT2021, 147:111620.
  • Mol Cell.2017, 68(4):673-685
  • Planta Med.2018, 84(15):1101-1109
  • Exp Ther Med.2019, 18(6):4388-4396
  • Phytomedicine.2022, 100:154058.
  • ...
  • 生物活性
    Description: Oridonin has anticancer activity, might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.It inhibits tumor growth in glioma by inducing cell cycle arrest and apoptosis, inhibits BxPC-3 cell growth through cell apoptosis.
    Targets: CDK | PARP | Caspase | mTOR | RAF | ERK | STAT | Bcl-2/Bax | JNK | p38MAPK
    In vitro:
    Sichuan Da Xue Xue Bao Yi Xue Ban. 2014 Nov;45(6):903-7.
    Anti-leukemia effect of oridonin on T-cell acute lymphoblastic leukemia[Pubmed: 25571712]
    To investigate the antileukemia effect of oridonin on T-cell acute lymphoblastic leukemia cell line CEM.
    METHODS AND RESULTS:
    Human T-cell acute lymphoblastic leukemia cell line CEM was cultured in vitro. The 50% inhibition concentration (IC50) of oridonin against CEM cells was examined using modified MTT assay. The cellular morphologic changes were observed using a light microscope. The percent of apoptosis of CEM cells after drug treatment was evaluated by flow cytometric analysis. The active levels of AKT/mTOR, RAF/MEK/ ERK, STAT5 signaling pathways and the expression levels of Bcl-2 and BAX were examined by Western blot. Oridonin inhibited the growth of CEM cells in time- and dose dependent manner and the ICs0 of oridonin was (7. 37± 1. 99) μmol/L after 72 h treatment. The cellular membrane of CEM cells treated with oridonin became unsharp, some of them disintegrated. Oridonin induced apoptosis in CEM cells and the percent of apoptosis rate after 0, 5, 7.5, 10 μmol/L oridonin treatment for 24 h were (4. 8±2. 11)%, (19.03±12.54)% ,(40.27± 3.31) / and (57. 23 ± 6. 69)% respectively. Oridonin inhibited activation of mTOR, P70S6, 4EBP1, RAF. ERK and STAT5 signaling protein, which were constitutively activated in CEM cells, however, oridonin had no inhibitory effect on AKT kinase. Oridonin down-regulated the level of anti apoptotic protein Bcl-2 and up-regulated the expression of pro-apoptotic protein Bax.
    CONCLUSIONS:
    Oridonin exerted antileukemia effect in CEM cells by inhibiting the activation of mTOR/P70/4EBP1, RAF/ERK and STATS signaling pathways, down-regulating the expression of Bel-2 and up-regulating the expression of BAX.
    Zhong Yao Cai. 2014 Jul;37(7):1230-3.
    Experimental study on anti-pancreatic cancer effect of oridonin.[Pubmed: 25566662]
    To investigate the apoptotic effect of oridonin in human pancreatic cancer cells PANC-1, and to explore the underlying mechanism.
    METHODS AND RESULTS:
    MTT assay was used to measure the cell viability. Apoptosis was determined by confocal laser scanning microscope after Hoechst 33342 staining and flow cytometry analysis after PI staining. The regulation of JNK and p38 MAPK signaling pathway proteins was examined by Western blot analysis. Treatment with oridonin for 24 h resulted in a marked decrease in cell viability in a dose-dependent manner. The IC50 value was determined as 49.80 μmol/L for 24 h. After treatment with 50 micromol/L and 80 μmol/L oridonin for 24 h, typical apoptotic nucleus alterations were observed with confocal laser scanning microscope and apoptotic rates of PANC-1 cells increased by flow cytometry analysis. Treatment with 80 μmol/L oridonin down-regulated protein expression of JNK, p38 and increased the expression of p-JNK, p-p38. Furthermore, 80 μmol/L oridonin treatment decreased the expression of down-stream proteins Caspase-9, Caspase-3 and PARP in the apoptotic pathway as well as activated the cleavage of Caspase-9.
    CONCLUSIONS:
    Oridonin can induce apoptosis of PANC-1 cells through JNK and p38 MAPK pathway proteins.
    Mol Cancer Ther . 2018 Jul;17(7):1540-1553.
    Targeting AKT with Oridonin Inhibits Growth of Esophageal Squamous Cell Carcinoma In Vitro and Patient-Derived Xenografts In Vivo[Pubmed: 29695636]
    Abstract Overexpression or activation of AKT is very well known to control cell growth, survival, and gene expression in solid tumors. Oridonin, an inflammatory medical and diterpenoid compound isolated from Rabdosia rubescens, has exhibited various pharmacologic and physiologic properties, including antitumor, antibacterial, and anti-inflammatory effects. In this study, we demonstrated that oridonin is an inhibitor of AKT and suppresses proliferation of esophageal squamous cell carcinoma (ESCC) in vitro and in vivo The role of AKT in ESCC was studied using immuno-histochemical analysis of a tumor microarray, the effect of AKT knockdown on cell growth, and treatment of cells with MK-2206, an AKT inhibitor. Oridonin blocked AKT kinase activity and interacted with the ATP-binding pocket of AKT. It inhibited growth of KYSE70, KYSE410, and KYSE450 esophageal cancer cells in a time- and concentration-dependent manner. Oridonin induced arrest of cells in the G2-M cell-cycle phase, stimulated apoptosis, and increased expression of apoptotic biomarkers, including cleaved PARP, caspase-3, caspase-7, and Bims in ESCC cell lines. Mechanistically, we found that oridonin diminished the phosphorylation and activation of AKT signaling. Furthermore, a combination of oridonin and 5-fluorouracil or cisplatin (clinical chemotherapeutic agents) enhanced the inhibition of ESCC cell growth. The effects of oridonin were verified in patient-derived xenograft tumors expressing high levels of AKT. In summary, our results indicate that oridonin acts as an AKT inhibitor to suppress the growth of ESCC by attenuating AKT signaling. Mol Cancer Ther; 17(7); 1540-53. ©2018 AACR.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.744 mL 13.7201 mL 27.4401 mL 54.8802 mL 68.6003 mL
    5 mM 0.5488 mL 2.744 mL 5.488 mL 10.976 mL 13.7201 mL
    10 mM 0.2744 mL 1.372 mL 2.744 mL 5.488 mL 6.86 mL
    50 mM 0.0549 mL 0.2744 mL 0.5488 mL 1.0976 mL 1.372 mL
    100 mM 0.0274 mL 0.1372 mL 0.2744 mL 0.5488 mL 0.686 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.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    Trichokaurin; Trichokaurin CFN97984 23811-50-9 C24H34O7 = 434.5 5mg QQ客服:3257982914
    毛叶香茶菜素; Maoyerabdosin CFN96034 90468-72-7 C24H36O9 = 468.5 5mg QQ客服:215959384
    毛萼乙素; Eriocalyxin B CFN97402 84745-95-9 C20H24O5 = 344.4 5mg QQ客服:1413575084
    毛萼晶乙; Maoecrystal B CFN97546 96850-29-2 C22H28O6 = 388.5 5mg QQ客服:2056216494
    毛叶香茶菜丁素; Odonicin CFN98822 51419-51-3 C24H30O7 = 430.5 5mg QQ客服:1413575084
    Hebeirubescensin H; Hebeirubescensin H CFN96853 887333-30-4 C20H28O7 = 380.43 5mg QQ客服:2159513211
    牛尾草素 F; Rabdoternin F CFN96855 155977-87-0 C21H30O7 = 394.46 5mg QQ客服:2159513211
    冬凌草乙素; Ponicidin CFN92259 52617-37-5 C20H26O6 = 362.4 5mg QQ客服:2159513211
    Rabdoserrin A; Rabdoserrin A CFN91931 96685-01-7 C20H26O5 = 346.42 5mg QQ客服:2056216494
    尾叶香茶菜丙素; Kamebakaurin CFN91932 73981-34-7 C20H30O5 = 350.45 5mg QQ客服:215959384

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