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    CAS No. 28957-04-2 Price $40 / 20mg
    Catalog No.CFN99164Purity>=98%
    Molecular Weight364.43Type of CompoundDiterpenoids
    FormulaC20H28O6Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Our products had been exported to the following research institutions and universities, And still growing.
  • Nicolaus Copernicus Uniwersity (Poland)
  • Universiti Sains Malaysia (Malaysia)
  • John Innes Centre (United Kingdom)
  • University of Pretoria (South Africa)
  • Auburn University (USA)
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  • Regional Crop Research Institute (Korea)
  • Sanford Burnham Medical Research... (USA)
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    Biological Activity
    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.
    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.
    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.
    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.
    Oridonin can induce apoptosis of PANC-1 cells through JNK and p38 MAPK pathway proteins.
    Oridonin Description
    Source: The herbs of Rabdosia rubescens (Hamst.) C.Y.Wu et Hsuan.
    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.
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    Calculate Dilution Ratios(Only for Reference)
    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.
    Kinase Assay:
    Cell Mol Biol (Noisy-le-grand). 2014 Dec 30;60(6):29-36.
    Oridonin inhibits tumor growth in glioma by inducing cell cycle arrest and apoptosis.[Pubmed: 25553351]
    Glioma is the most common malignant intracranial tumors. Despite newly developed therapies, these treatments mainly target oncogenic signals, and unfortunately, fail to provide enough survival benefit in both human patients and mouse xenograft models, especially the first-generation therapies. Oridonin is purified from the Chinese herb Rabdosia rubescens and considered to exert extensive anti-cancer effects on human tumorigenesis.
    In this study, we systemically investigated the role of Oridonin in tumor growth and the underlying mechanisms in human glioma. We found that Oridonin inhibited cell proliferations in a dose- and time-dependent manner in both glioma U87 and U251 cells. Moreover, these anti-cancer effects were also confirmed in a mouse model bearing glioma. Furthermore, cell cycle arrest in S phase was observed in Oridonin-mediated growth inhibition by flow cytometry. Cell cycle arrest in S phase led to eventual cell apoptosis, as revealed by Hoechst 33342 staining and annexin V/PI double-staining. The cell apoptosis might be accomplished through a mitochondrial manner.
    In all, we were the first to our knowledge to report that Oridonin could exert anti-cancer effects on tumor growth in human glioma by inducing cell cycle arrest and eventual cell apoptosis. The identification of Oridonin as a critical mediator of glioma growth may potentiate Oridonin as a novel therapeutic strategies in glioma treatments.
    Cell Research:
    Acta Biochim Biophys Sin (Shanghai). 2015 Mar;47(3):164-73.
    Oridonin inhibits BxPC-3 cell growth through cell apoptosis.[Pubmed: 25651847]
    Oridonin, an ent-kaurene diterpenoid extracted from the traditional Chinese herb Rabdosia rubescens, has multiple biological and pharmaceutical functions and has been used clinically for many years. While the antitumor function of Oridonin has been corroborated by numerous lines of evidence, its anticancer mechanism has not been well documented.
    In this study, the pancreatic cancer cell line BxPC-3 was used as a model to investigate a possible anticancer mechanism of Oridonin through examining its effects on cell viability. The results showed that Oridonin affected cell viability in a time- and dose-dependent manner. After exposure to different Oridonin concentrations, growth rates and cell cycle arrest of BxPC-3 cells were significantly reduced compared with untreated cells, suggesting its effects on proliferation inhibition. Detailed signaling pathway analysis by western blot analysis revealed that low-dose Oridonin treatment inhibited BxPC-3 cell proliferation by up-regulating p53 and down-regulating cyclin-dependent kinase 1 (CDK1), which led to cell cycle arrest in the G2/M phase. A high-dose Oridonin not only arrested BxPC-3 cells in the G2/M phase but also induced cell accumulation in the S phase, presumably through γH2AX up-regulation and DNA damage.
    In addition, our results showed that a cell subpopulation was stained with propidium iodide after Oridonin treatment. Protein quantification showed that cleaved poly(ADP-ribose) polymerase (PARP) expression was increased after a high-dose Oridonin treatment, especially after long-term exposure. Accompanied by the increased level of deactivated PARP in BxPC-3 cells, the apoptosis initiators caspase-3 and caspase-7 expressions were also significantly increased, suggesting that caspase-mediated apoptosis contributed to cell death.