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    Tetrandrine
    Information
    CAS No. 518-34-3 Price $30 / 20mg
    Catalog No.CFN99166Purity>=98%
    Molecular Weight622.76Type of CompoundAlkaloids
    FormulaC38H42N2O6Physical DescriptionCryst.
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Tetrandrine is a calcium channel blocker, which shows antitumor, antifibrotic, anti-oxidant, anti-inflammatory and immunosuppressive activity. It suppressed Wnt/β-catenin signaling transduction, the migration of DU145 and PC-3 cells, EOMA cell growth through the ROS/Akt pathway and inhibited inward rectifying potassium current in cultured bovine aortic endothelial cells.
    Targets: Caspase | Akt | Bcl-2/Bax | PI3K | TNF-α | TGF-β/Smad | ROS | CDK | p53 | p21
    In vitro:
    Asian J Androl. 2015 Feb 6.
    Tetrandrine suppresses proliferation, induces apoptosis, and inhibits migration and invasion in human prostate cancer cells.[Pubmed: 25677131]
    Tetrandrine (TET), a traditional Chinese medicine, exerts remarkable anticancer activity on various cancer cells. However, little is known about the effect of TET on human prostate cancer cells, and the mechanism of function of TET on prostate cancer has not yet been elucidated.
    METHODS AND RESULTS:
    To investigate the effects of TET on the suppression of proliferation, induction of apoptosis, and inhibition of migration and invasion in human prostate cancer cell lines, DU145 and PC-3. Inhibition of growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and clone formation assay, and flow cytometry analysis was performed to detect the induction of apoptosis. Activation of poly (ADP-ribose) polymerase, caspase-3, Akt, phospho-Akt, Bcl-2, and Bax was analyzed by Western blotting. Wound healing assay and transwell migration assay were used to evaluate the effect of TET on migration and invasion of cancer cells. TET inhibited the growth of DU145 and PC-3 cells in a dose- and time-dependent manner. Cell cloning was inhibited in the presence of TET in DU145 and PC-3 cells. TET suppressed the migration of DU145 and PC-3 cells. Transwell invasion assay showed that TET significantly weakened invasion capacity of DU145 and PC-3 cells. TET exhibited strong inhibitory effect on proliferation, migration, and invasion of prostate cancer cells. In addition, TET induced apoptosis in a dose-dependent manner by activating the caspase cascade and inhibiting phosphoinositide 3-kinase-Akt signal pathway.
    CONCLUSIONS:
    The accumulating evidence suggests that TET could be a potential therapeutic candidate against prostate cancer in a clinical setting.
    Acta Pharmacol Sin. 2000 Dec;21(12):1115-8.
    Tetrandrine inhibits inward rectifying potassium current in cultured bovine aortic endothelial cells.[Pubmed: 11603285]
    To study the effect of Tetrandrine (Tet) on inward rectifying potassium current in cultured bovine aortic endothelial cells.
    METHODS AND RESULTS:
    Inward rectifying potassium current (IRK) was observed by the whole cell patch-clamp technique. IRK was inhibited by Tet in a concentration-dependent manner and recovered to normal after wash with drug-free external solution. IRK was reduced from (582 +/- 48) pA to (221 +/- 40) pA at a holding potential of -70 mV by Tet 30 mumol/L. IC50 was 2.8 mumol/L.
    CONCLUSIONS:
    Tet inhibited inward rectifying potassium current in cultured bovine aortic endothelial cells.
    In vivo:
    J Gastroenterol Hepatol. 2007 Jan;22(1):99-111.
    Antifibrotic effects of tetrandrine on hepatic stellate cells and rats with liver fibrosis.[Pubmed: 17201889 ]
    Tetrandrine (TET), a traditional Chinese medicine, exerts remarkable anticancer activity on various cancer cells. However, little is known about the effect of TET on human prostate cancer cells, and the mechanism of function of TET on prostate cancer has not yet been elucidated.
    METHODS AND RESULTS:
    Anti-inflammation strategies are one of the proposed therapeutic approaches to hepatic fibrosis. Tetrandrine (C(38)H(42)O(8)N(2), molecular weight: 622; Tet), an alkaloid isolated from the Chinese medicinal herb Stephania tetrandra, has been shown to exert anti-inflammatory activity in pulmonary diseases. The purpose of the present study was to investigate the in vitro and in vivo effects of Tet on hepatic fibrosis.
    METHODS AND RESULTS:
    A cell line of rat hepatic stellate cells (HSC-T6) was stimulated with transforming growth factor-beta1 (TGF-beta1) or tumor necrosis factor-alpha (TNF-alpha). The inhibitory effects of Tet on the nuclear factor kappaB (NFkappaB) signaling cascade and molecular markers including intercellular adhesion molecule-1 (ICAM-1) and alpha-smooth muscle actin (alpha-SMA) secretion were assessed. Fibrosis was induced by dimethylnitrosamine (DMN) administration in rats for 4 weeks. Fibrotic rats were randomly assigned to one of the four groups: vehicle (0.7% carboxyl methyl cellulose, CMC), Tet (1 mg/kg), Tet (5 mg/kg), or silymarin (50 mg/kg), each given by gavage twice daily for 3 weeks starting after 1 week of DMN administration. At the end of the study, liver tissues were scored for fibrosis and analyzed for molecular markers of fibrosis. Tetrandrine (0.5-5.0 micromol/L) concentration-dependently inhibited NFkappaB transcriptional activity induced by TNF-alpha, including IkappaBalpha phosphorylation and mRNA expressions of ICAM-1 in HSC-T6 cells. In addition, Tet also inhibited TGF-beta1-induced alpha-SMA secretion and collagen deposition in HSC-T6 cells. Fibrosis scores of livers from DMN-treated rats with high-dose Tet (1.3 +/- 0.3) were significantly reduced in comparison with DMN-treated rats receiving saline (2.0 +/- 0.2). Hepatic collagen content of DMN rats was significantly reduced by either Tet or silymarin treatment.
    CONCLUSIONS:
    Double-staining results showed that alpha-SMA- and NFkappaB-positive cells were decreased in the fibrotic livers by Tet and silymarin treatment. In addition, mRNA expression of ICAM-1, alpha-SMA, and TGF-beta1 was attenuated by Tet treatment. Moreover, levels of plasma aspartate aminotransferase and alanine aminotransferase activities were reduced by Tet and silymarin treatment.
    Tetrandrine Description
    Source: The roots of Stephania tetrandra S. Moore.
    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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.6058 mL 8.0288 mL 16.0576 mL 32.1151 mL 40.1439 mL
    5 mM 0.3212 mL 1.6058 mL 3.2115 mL 6.423 mL 8.0288 mL
    10 mM 0.1606 mL 0.8029 mL 1.6058 mL 3.2115 mL 4.0144 mL
    50 mM 0.0321 mL 0.1606 mL 0.3212 mL 0.6423 mL 0.8029 mL
    100 mM 0.0161 mL 0.0803 mL 0.1606 mL 0.3212 mL 0.4014 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.
    Protocol
    Cell Research:
    Cancer Res. 2004 Dec 15;64(24):9086-92.
    Tetrandrine induces early G1 arrest in human colon carcinoma cells by down-regulating the activity and inducing the degradation of G1-S-specific cyclin-dependent kinases and by inducing p53 and p21Cip1.[Pubmed: 15604277]
    Tetrandrine is an antitumor alkaloid isolated from the root of Stephania tetrandra.
    METHODS AND RESULTS:
    We find that micromolar concentrations of Tetrandrine irreversibly inhibit the proliferation of human colon carcinoma cells in MTT and clonogenic assays by arresting cells in G(1). Tetrandrine induces G(1) arrest before the restriction point in nocodazole- and serum-starved synchronized HT29 cells, without affecting the G(1)-S transition in aphidicolin-synchronized cells. Tetrandrine-induced G(1) arrest is followed by apoptosis as shown by fluorescence-activated cell sorting, terminal deoxynucleotidyl transferase-mediated nick end labeling, and annexin V staining assays. Tetrandrine-induced early G(1) arrest is mediated by at least three different mechanisms. First, Tetrandrine inhibits purified cyclin-dependent kinase 2 (CDK2)/cyclin E and CDK4 without affecting significantly CDK2/cyclin A, CDK1/cyclin B, and CDK6. Second, Tetrandrine induces the proteasome-dependent degradation of CDK4, CDK6, cyclin D1, and E2F1. Third, Tetrandrine increases the expression of p53 and p21(Cip1) in wild-type p53 HCT116 cells.
    CONCLUSIONS:
    Collectively, these results show that Tetrandrine arrests cells in G(1) by convergent mechanisms, including down-regulation of E2F1 and up-regulation of p53/p21(Cip1).
    Animal Research:
    Int J Oncol. 2015 Jan;46(1):360-8.
    Tetrandrine induces G1/S cell cycle arrest through the ROS/Akt pathway in EOMA cells and inhibits angiogenesis in vivo.[Pubmed: 25355542]
    Tetrandrine, a bisbenzylisoquinoline alkaloid, is known to inhibit tumor cell proliferation and induce apoptosis in cancer models in vitro and in vivo.
    METHODS AND RESULTS:
    In the present study, Tetrandrine significantly inhibited the proliferation of mouse endothelial cells (EOMA cell) and induced G1/S arrest in EOMA cells, in which the expressions of cyclin D and cyclin E and CDKs were downregulated. Tetrandrine treatment also caused intracellular accumulation of reactive oxygen species (ROS). Pretreatment with NAC, which is a ROS inhibitor, blocked G1/S cell arrest and cyclin regulation induced by Tetrandrine, implying that ROS generation plays an important role in Tetrandrine-induced cell cycle arrest. Furthermore, a decreased phospho-Akt protein level after Tetrandrine treatment was reversible with the removal of the intracellular ROS by NAC. Notably, overexpression of Akt decreased Tetrandrine-induced G1/S arrest. Finally, we verified the antiangiogenic effects of Tetrandrine in vivo in a liver cancer xenograft model in nude mice.
    CONCLUSIONS:
    In conclusion, Tetrandrine inhibits EOMA cell growth through the ROS/Akt pathway, and it could be a promising compound for cancer therapy as an inhibitor of tumor vascular growth.
    Structure Identification:
    Int J Immunopharmacol. 1989;11(4):395-401.
    Anti-inflammatory and immunosuppressive properties of the bis-benzylisoquinolines: in vitro comparisons of tetrandrine and berbamine.[Pubmed: 2777433]
    Tetrandrine and berbamine are two naturally occurring analogues with a bis-benzylisoquinoline structure. Comparative in vitro studies show that Tetrandrine has significantly greater suppressive effects on adherence, locomotion and 3H-deoxyglucose uptake of neutrophils, as well as the mitogen-induced lymphocyte responses and mixed lymphocyte reactions. Also, Tetrandrine displayed anti-oxidant activity while berbamine did not. By contrast, berbamine demonstrated a significantly greater capacity for inhibition of NK cell cytotoxicity. These results show that Tetrandrine is superior to berbamine in most aspects of anti-inflammatory and immunosuppressive activity. Since these two alkaloids differ by only one substitution in the side chain of one of the benzene rings, these findings may provide further insight into structure-activity relationships and clues to the synthesis and development of active analogues of this promising class of drugs for the treatment of chronic inflammatory diseases.