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    Triptolide
    Information
    CAS No. 38748-32-2 Price $138 / 20mg
    Catalog No.CFN99196Purity>=98%
    Molecular Weight360.40Type of CompoundDiterpenoids
    FormulaC20H24O6Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Triptolide has immunosuppressive, anti-inflammatory, and anti-cancer activities, it induces apoptosis in tumor cells by blocking NF-KB activation and sensitizing tumor cells for TNF-a induced programmed cell death, it inhibits TGF-β1-induced cell proliferation and migration of rat airway smooth muscle cells, by suppressing Smad signaling and NF-κB ,respectively. Triptolide is an inhibitor of heat shock factor (HSF1), inhibits HSP90-CDC37 binding and induces acetylation of HSP90, and also inhibits MDM2 expression in a dose-dependent manner with IC50 values range from 47 to 73 nM.
    Targets: NF-kB | IkB | p65 | TGF-β/Smad | ERK | IKK | HSF-1 | HSP90 | MDM2
    In vitro:
    Biochem Biophys Res Commun. 2015 Jan 16;456(3):815-20.
    Triptolide inhibits proliferation of Epstein-Barr virus-positive B lymphocytes by down-regulating expression of a viral protein LMP1.[Pubmed: 25511707]
    Epstein-Barr virus (EBV) infects various types of cells and mainly establishes latent infection in B lymphocytes. The viral latent membrane protein 1 (LMP1) plays important roles in transformation and proliferation of B lymphocytes infected with EBV. Triptolide is a compound of Tripterygium extracts, showing anti-inflammatory, immunosuppressive, and anti-cancer activities.
    METHODS AND RESULTS:
    In this study, it is determined whether Triptolide inhibits proliferation of Epstein-Barr virus-positive B lymphocytes. The CCK-8 assays were performed to examine cell viabilities of EBV-positive B95-8 and P3HR-1 cells treated by Triptolide. The mRNA and protein levels of LMP1 were examined by real time-PCR and Western blotting, respectively. The activities of two LMP1 promoters (ED-L1 and TR-L1) were determined by Dual luciferase reportor assay. The results showed that Triptolide inhibited the cell viability of EBV-positive B lymphocytes, and the over-expression of LMP1 attenuated this inhibitory effect. Triptolide decreased the LMP1 expression and transcriptional levels in EBV-positive B cells. The activity of LMP1 promoter ED-L1 in type III latent infection was strongly suppressed by Triptolide treatment. In addition, Triptolide strongly reduced growth of B95-8 induced B lymphoma in BALB/c nude mice.
    CONCLUSIONS:
    These results suggest that Triptolide decreases proliferation of EBV-induced B lymphocytes possibly by a mechanism related to down-regulation of the LMP1 expression.
    In vivo:
    Mol Cell Endocrinol. 2015 Jan 5;399:346-53.
    Triptolide inhibits osteoclast formation, bone resorption, RANKL-mediated NF-қB activation and titanium particle-induced osteolysis in a mouse model.[Pubmed: 25448849]
    The RANKL-induced NF-κB signaling pathway is required for osteoclast formation and function.
    METHODS AND RESULTS:
    By screening for compounds that inhibit RANKL-induced NF-κB activation using a luciferase reporter gene assay in RAW264.7 cells, we identified Triptolide (PG490), as a candidate compound targeting osteoclast differentiation and osteoclast-mediated osteolysis. Triptolide (PG490) is an active compound of the medicinal herb Tripterygium wilfordii Hook F (TWHF) or Lei Gong Teng with known anti-inflammatory properties. We found that Triptolide inhibited osteoclastogenesis and bone resorption, as well as RANKL-induced NF-қB activities as monitored by luciferase reporter gene assays and the nuclear translocation of p65. In vivo studies showed that Triptolide attenuates titanium-induced osteolysis and osteoclast formation in a mouse calvarial model.
    CONCLUSIONS:
    Considering that drugs which protect against localized bone loss are critically needed for the effective treatment of particle-induced osteolysis, our data suggest that Triptolide might have therapeutic potential for the treatment of bone lytic diseases caused by prosthetic wear particles.
    Triptolide Description
    Source: The herbs of Tripterygium wilfordii Hook.f.
    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 2.7747 mL 13.8735 mL 27.7469 mL 55.4939 mL 69.3674 mL
    5 mM 0.5549 mL 2.7747 mL 5.5494 mL 11.0988 mL 13.8735 mL
    10 mM 0.2775 mL 1.3873 mL 2.7747 mL 5.5494 mL 6.9367 mL
    50 mM 0.0555 mL 0.2775 mL 0.5549 mL 1.1099 mL 1.3873 mL
    100 mM 0.0277 mL 0.1387 mL 0.2775 mL 0.5549 mL 0.6937 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:
    Exp Cell Res. 2015 Feb 15;331(2):362-8.
    Triptolide inhibits TGF-β1-induced cell proliferation in rat airway smooth muscle cells by suppressing Smad signaling.[Pubmed: 25447441]
    We have reported that Triptolide can inhibit airway remodeling in a murine model of asthma via TGF-β1/Smad signaling. In the present study, we aimed to investigate the effect of Triptolide on airway smooth muscle cells (ASMCs) proliferation and the possible mechanism.
    METHODS AND RESULTS:
    Rat airway smooth muscle cells were cultured and made synchronized, then pretreated with different concentration of Triptolide before stimulated by TGF-β1. Cell proliferation was evaluated by MTT assay. Flow cytometry was used to study the influence of Triptolide on cell cycle and apoptosis. Signal proteins (Smad2, Smad3 and Smad7) were detected by western blotting analysis. Triptolide significantly inhibited TGF-β1-induced ASMC proliferation (P<0.05). The cell cycle was blocked at G1/S-interphase by Triptolide dose dependently. No pro-apoptotic effects were detected under the concentration of Triptolide we used. Western blotting analysis showed TGF-β1 induced Smad2 and Smad3 phosphorylation was inhibited by Triptolide pretreatment, and the level of Smad7 was increased by Triptolide pretreatment.
    CONCLUSIONS:
    Triptolide may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation via negative regulation of Smad signaling pathway.
    Mol Med Rep. 2015 Feb;11(2):791-6.
    Triptolide inhibits cell proliferation and tumorigenicity of human neuroblastoma cells.[Pubmed: 25354591]
    Triptolide is a diterpene triepoxide, extracted from the Chinese herb Tripterygium wilfordii Hook F, which has been shown to have antitumor activity in a number of cancers. Neuroblastoma is an aggressive extracranial pediatric solid tumor, with significant chemotherapeutic resistance.
    METHODS AND RESULTS:
    In this study, Triptolide was hypothesized to be a potential therapeutic agent for neuroblastoma. The effects of Triptolide on neuroblastoma cell growth and tumor development were investigated. Cell growth and proliferation were evaluated using a cell counting kit‑8 assay and a 5-bromo-2-deoxyuridine staining assay. Cell cycle and apoptosis were detected by flow cytometry. Reverse transcription‑quantitative polymerase chain reaction was conducted to detect the expression levels of the apoptosis‑associated proteins, caspase‑3 and caspase‑9. The tumorigenicity of neuroblastoma cells was assessed by a soft agar clonogenic assay and an in vivo tumorigenic assay. The results demonstrated that exposure of BE(2)‑C human neuroblastoma cells to Triptolide resulted in a reduction in cell growth and proliferation, and the induction of cell death and apoptosis, together with cell cycle arrest in the S phase. A soft agar assay indicated that Triptolide inhibited the colony‑forming ability of BE(2)‑C neuroblastoma cells. The xenograft experiment showed that Triptolide significantly reduced tumor growth and development in vivo.
    CONCLUSIONS:
    The data suggested that this Chinese herb may be a potential novel chemotherapeutic agent for neuroblastoma.
    Animal Research:
    Immunology. 2014 Sep 29.
    Triptolide inhibits TGF-β1 induced proliferation and migration of rat airway smooth muscle cells by suppressing NF-κB but not ERK1/2.[Pubmed: 25267491]
    Airway remodeling contributes to increased mortality in asthma. We have reported that Triptolide can inhibit airway remodeling in a mouse asthma model. In this study, we aimed to investigate the effect of Triptolide on airway smooth muscle cells (ASMCs) proliferation, migration and the possible mechanism.
    METHODS AND RESULTS:
    Rat airway smooth muscle cells were cultured and made synchronized, then pretreated with different concentrations of Triptolide before stimulated by TGF-β1. Cell proliferation was evaluated by cell counting and MTT assay. Flow cytometry was used to study the influence of Triptolide on cell cycle. Migration was measured by Transwell analysis. Signal proteins (NF-κB p65 and ERK1/2) were detected by western blotting analysis. LDH releasing test and flow cytometry analysis of apoptosis were also performed to explore the potential cytotoxic or pro-apoptotic effects of Triptolide. Triptolide significantly inhibited TGF-β1 induced ASMC proliferation and migration (p<0.05). The cell cycle was blocked at G1/S-interphase by Triptolide dose dependently. Western blotting analysis showed TGF-β1 induced NF-κB p65 phosphorylation was inhibited by Triptolide pretreatment, but ERK1/2 was not affected. No cytotoxic or pro-apoptotic effects were detected under the concentration of Triptolide we used.
    CONCLUSIONS:
    Triptolide may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation and migration through inactivation of NF-κB pathway.