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    CAS No. 69618-96-8 Price $463 / 5mg
    Catalog No.CFN92154Purity>=98%
    Molecular Weight542.5Type of CompoundFlavonoids
    FormulaC30H22O10Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Chamaejasmine could be a candidate drug for osteosarcoma and breast cancer chemoprevention, induces apoptosis in MG63 and HEp-2 cells by Akt inactivation and dephosphorylation of BAD. It inhibits Bcl-2 expression and induces Bax expression to desintegrate the outer mitochondrial membrane and causes cytochrome c release.
    Targets: Bcl-2/Bax | Caspase | p53 | p21 | NF-kB | IkB | CDK | Akt | GSK-3 | PARP | ROS | P450 (e.g. CYP17) | IKK
    In vitro:
    Tumour Biol. 2015 Jul;36(7):5433-9.
    Apoptosis induced by chamaejasmine in human osteosarcoma cells through p53 pathway.[Pubmed: 25677904 ]
    Osteosarcoma cancer is one of the most lethal malignancies, and there is no effective preventive measure to date. Chamaejasmine is the major ingredient in Stellera chamaejasme L. Except its potent pain-relieving efficacy as reported, Chamaejasmine also exerted its anti-tumor activity in several tumor models.
    Here, we reported that Chamaejasmine had a profound anti-proliferative effect on human osteosarcoma cells in a concentration-dependent and time-dependent manner, which was associated with an increase of p21 and bax and a decrease of bcl-2 and consequently increased caspase-3 activity. The main mechanism of anti-tumor potency was mainly attributed to the induction of p53. Chamaejasmine hugely elevated the expression of p53. The results of p53 shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to Chamaejasmine, implicating the important role of p53 played in Chamaejasmine's anti-tumor activity.
    In conclusion, results showed Chamaejasmine induced apoptosis in MG63 cells and could be a candidate drug for osteosarcoma cancer chemoprevention.
    Molecules. 2013 Jan 11;18(1):845-58.
    Chamaejasmine arrests cell cycle, induces apoptosis and inhibits nuclear NF-κB translocation in the human breast cancer cell line MDA-MB-231.[Pubmed: 23344197]
    In this study, the anticancer activity of Chamaejasmine was characterized in the human breast cancer cell line, MDA-MB-231.
    Cell viability and cell cycle distribution were determined by MTT assay and flow cytometry, respectively. Western blotting was performed to determine changes in levels of various proteins. Results showed that treatment with Chamaejasmine (4-16 μM) inhibited cell proliferation, which correlated with G2/M phase arrest and apoptosis in MDA-MB-231 cells. Chamaejasmine treatment of MDA-MB-231 cells resulted in induction of WAF1/p21 and KIP1/p27, decrease in cyclins A and cyclins B1. Cyclin-dependent kinase (cdk) 2 and cdc2 was also decreased after Chamaejasmine treatment. Moreover, inhibition of nuclear translocation, phosphorylation of NF-κB, activation of IKKα and IKKβ, inhibition of phosphorylation and degradation of IκBα were also detected in this work.
    Our findings suggested that Chamaejasmine could be explored as a preventive and perhaps as a chemotherapeutic agent in the management of breast cancer.
    Chamaejasmine Description
    Source: The roots of Stellera chamaejasme Linn.
    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

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.8433 mL 9.2166 mL 18.4332 mL 36.8664 mL 46.0829 mL
    5 mM 0.3687 mL 1.8433 mL 3.6866 mL 7.3733 mL 9.2166 mL
    10 mM 0.1843 mL 0.9217 mL 1.8433 mL 3.6866 mL 4.6083 mL
    50 mM 0.0369 mL 0.1843 mL 0.3687 mL 0.7373 mL 0.9217 mL
    100 mM 0.0184 mL 0.0922 mL 0.1843 mL 0.3687 mL 0.4608 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:
    Molecules. 2011 Sep 27;16(10):8152-64.
    Chamaejasmine inactivates Akt to trigger apoptosis in human HEp-2 larynx carcinoma cells.[Pubmed: 21952497]
    In the present study, we investigated the mechanisms of Chamaejasmine action on human HEp-2 larynx carcinoma cells, which possess constitutively active Akt.
    Results indicated that Chamaejasmine showed more notable anticancer activity than apigenin against HEp-2, PC-3, NCI-H1975, HT-29 and SKOV-3. Moreover, Chamaejasmine presented most significantly inhibition towards HEp-2, with IC₅₀ values of 1.92 µM. Treatment of HEp-2 cells with Chamaejasmine (1-4 μM) resulted in significant dose-dependent decrease in Akt phosphorylation at Serine473. Chamaejasmine-mediated dephosphorylation of Akt resulted in inhibition of its kinase activity, which was confirmed by reduced phosphorylation of proapoptotic proteins BAD and glycogen synthase kinase-3, essential downstream targets of Akt. Inactivation of Akt seems to be associated with downregulation of insulin-like growth factor receptor 1 protein level and inhibition of its autophosphorylation upon Chamaejasmine treatment. Exposure to Chamaejasmine significantly induced caspase-9 and caspase-3 activity. In vivo, Chamaejasmine intake through gavage resulted in inactivation of Akt and induction of apoptosis in HEp-2 tumors.
    These results suggest that Akt inactivation and dephosphorylation of BAD is a critical event, at least in part, in Chamaejasmine-induced HEp-2 cells apoptosis.
    Molecules. 2011 Sep 27;16(10):8165-80.
    Chamaejasmine induces apoptosis in human lung adenocarcinoma A549 cells through a Ros-mediated mitochondrial pathway.[Pubmed: 21952498 ]
    In the present study, the anticancer activity of Chamaejasmine towards A549 human lung adenocarcinoma cells was investigated.
    In order to explore the underlying mechanism of cell growth inhibition of Chamaejasmine, cell cycle distribution, ROS generation, mitochondrial membrane potential (Δψ(m)) disruption, and expression of cytochrome c, Bax, Bcl-2, caspase-3, caspase-9 and PARP were measured in A549 cells. Chamaejasmine inhibited the growth of A549 cells in a time and dose-dependent manner. The IC₅₀ value was 7.72 µM after 72 h treatment. Chamaejasmine arrested the cell cycle in the G2/M phase and induced apoptosis via a ROS-mediated mitochondria-dependent pathway. Western blot analysis showed that Chamaejasmine inhibited Bcl-2 expression and induced Bax expression to desintegrate the outer mitochondrial membrane and causing cytochrome c release. Mitochondrial cytochrome c release was associated with the activation of caspase-9 and caspase-3 cascade, and active-caspase-3 was involved in PARP cleavage.
    All of these signal transduction pathways are involved in initiating apoptosis. To the best of our knowledge, this is the first report demonstrating the cytotoxic activity of Chamaejasmine towards A549 in vitro.