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    Pristimerin
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    CAS No. 1258-84-0 Price $128 / 20mg
    Catalog No.CFN90169Purity>=98%
    Molecular Weight464.64Type of CompoundTriterpenoids
    FormulaC30H40O4Physical DescriptionProwder
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    Pristimerin

    Pristimerin
    Product Name Pristimerin
    CAS No.: 1258-84-0
    Catalog No.: CFN90169
    Molecular Formula: C30H40O4
    Molecular Weight: 464.64 g/mol
    Purity: >=98%
    Type of Compound: Triterpenoids
    Physical Desc.: Prowder
    Targets: TNF-伪 | IL Receptor | ROS | NF-kB | p65 | IkB | HIF | PARP | Akt | mTOR | COX | VEGFR | PKC | Bcl-2/Bax | DNA/RNA Synthesis | Bcr-Abl | Antifection | IKK
    Source: The herbs of Tripterygium wilfordii Hook.f.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $128 / 20mg
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    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: Pristimerin is a naturally occurring triterpenoid that has been shown to suppress the proliferation of various cancer cell lines at the concentration (IC50) range of 0.2-4 μM, including those of breast, glioma, prostate, pancreatic, ovarian, colon. Pristimerin exhibits inhibitory effects against diverse phytopathogenic fungi, it shows good preventive effect and curative effect against wheat powdery mildew in vivo. It has a wide spectrum of targets including ROS, IKK, NF-κB, Akt, mTOR, Bcr-Abl.
    Targets: TNF-α | IL Receptor | ROS | NF-kB | p65 | IkB | HIF | PARP | Akt | mTOR | COX | VEGFR | PKC | Bcl-2/Bax | DNA/RNA Synthesis | Bcr-Abl | Antifection | IKK
    In vitro:
    Int Immunopharmacol. 2014 Aug;21(2):501-8.
    Pristimerin, a natural anti-tumor triterpenoid, inhibits LPS-induced TNF-α and IL-8 production through down-regulation of ROS-related classical NF-κB pathway in THP-1 cells.[Pubmed: 24957686]
    Pristimerin, a naturally occurring quinonemethide triterpenoid compound, is known to exert a variety of pharmacological activities.
    METHODS AND RESULTS:
    In the present study, we investigated the molecular actions of Pristimerin against LPS-induced inflammatory responses in human monocytic THP-1 cells. The results showed that Pristimerin inhibited the production of TNF-α and IL-8 in a dose-dependent manner. To explore the possible mechanisms underlying these inhibitions by Pristimerin, we examined the intracellular ROS level and the NF-κB protein signaling pathway. Pristimerin clearly scavenged LPS-induced intracellular ROS production. In addition, Pristimerin prevented LPS-induced NF-κB activation through the inhibition of phosphorylation of IKKα/β, phosphorylation and degradation of IκBα, as well as phosphorylation and nuclear translocation of NF-κB p65.
    CONCLUSIONS:
    These findings suggest that Pristimerin down-regulates the expression of pro-inflammatory mediators through blocking of NF-κB activation by inhibiting interconnected ROS/IKK/NF-κB signaling pathways.
    Pest Manag Sci. 2005 Jan;61(1):85-90.
    Antifungal properties of pristimerin and celastrol isolated from Celastrus hypoleucus.[Pubmed: 15593077 ]
    Pristimerin and celastrol isolated from the roots of Celastrus hypoleucus (Oliv) Warb f argutior Loes exhibited inhibitory effects against diverse phytopathogenic fungi.
    METHODS AND RESULTS:
    Pristimerin and celastrol were found to inhibit the mycelial growth of Rhizoctonia solani Kuhn and Glomerella cingulata (Stonem) Spauld & Schrenk in vitro by 83.6 and 62.6%, respectively, at 10 microg ml(-1). Pristimerin showed good preventive effect (96.7% at 100 microg ml(-1)) and curative effect (66.5% at 100 microg ml(-1)) against wheat powdery mildew in vivo. For celastrol, the preventive and curative effects against wheat powdery mildew were 80.5 and 45.4%, respectively, at 100 microg ml(-1).
    In vivo:
    Clin Immunol. 2014 Dec;155(2):220-30.
    Pristimerin, a naturally occurring triterpenoid, protects against autoimmune arthritis by modulating the cellular and soluble immune mediators of inflammation and tissue damage.[Pubmed: 25308129]
    Rheumatoid arthritis (RA) is a chronic autoimmune disorder affecting the synovial joints. The currently available drugs for RA are effective only in a proportion of patients and their prolonged use is associated with severe adverse effects. Thus, new anti-arthritic agents are being sought.
    METHODS AND RESULTS:
    We tested Pristimerin, a naturally occurring triterpenoid, for its therapeutic activity against rat adjuvant arthritis. Pristimerin effectively inhibited both arthritic inflammation and cartilage and bone damage in the joints. Pristimerin-treated rats exhibited a reduction in the pro-inflammatory cytokines (IL-6, IL-17, IL-18, and IL-23) and the IL-6/IL-17-associated transcription factors (pSTAT3 and ROR-γt), coupled with an increase in the immunomodulatory cytokine IL-10. Also increased was IFN-γ, which can inhibit IL-17 response. In addition, the Th17/Treg ratio was altered in favor of immune suppression and the RANKL/OPG ratio was skewed towards anti-osteoclastogenesis.
    CONCLUSIONS:
    This is the first report on testing Pristimerin in arthritis. We suggest further evaluation of Pristimerin in RA patients.
    Pristimerin 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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1522 mL 10.761 mL 21.522 mL 43.0441 mL 53.8051 mL
    5 mM 0.4304 mL 2.1522 mL 4.3044 mL 8.6088 mL 10.761 mL
    10 mM 0.2152 mL 1.0761 mL 2.1522 mL 4.3044 mL 5.3805 mL
    50 mM 0.043 mL 0.2152 mL 0.4304 mL 0.8609 mL 1.0761 mL
    100 mM 0.0215 mL 0.1076 mL 0.2152 mL 0.4304 mL 0.5381 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:
    Oncol Rep. 2015 Mar;33(3):1388-94.
    Inhibitory action of pristimerin on hypoxia‑mediated metastasis involves stem cell characteristics and EMT in PC-3 prostate cancer cells.[Pubmed: 25571882]
    The aim of the present study was to investigate whether Pristimerin affects the bone metastasis, stem cell characteristics and epithelial-mesenchymal transition (EMT) of prostate cancer (PCa) PC-3 cells subjected to hypoxia.
    METHODS AND RESULTS:
    The PC-3 cells were cultured under hypoxia or normoxia for 48 h and were then treated with increasing concentrations of Pristimerin from 0 to 0.8 μmol/l, under normoxia. Hypoxia‑inducible factor-1α (HIF-1α) was detected by western blotting. Proliferation was assessed with the CCK-8 assay. Transwell invasion assay was used to analyze the potency of invasion. Stem cell characteristics were detected by sphere formation, colony formation assay and western blotting, including CD44, KLF4, OCT4 and AGO2, which are stem cell characteristic-related markers. EMT was confirmed by the expression changes of EMT-related markers, including N-cadherin, fibronectin, vimentin and ZEB1, which were evaluated by western blotting. The addition of Pristimerin to the medium reduced the hypoxia-induced PC-3 cell proliferation in a dose-dependent manner. Pristimerin effectively inhibited hypoxia‑induced invasion of the PCa cells in vitro. Moreover, the treatment of cells with Pristimerin induced the reversal of hypoxia-induced stem cell characteristics and EMT, which was confirmed by sphere formation, colony formation assay and the expression changes of CSC- and EMT-related markers. The reversal of hypoxia‑induced stem cell characteristics and EMT in the PCa cells by low-dose Pristimerin was dose‑dependent.
    CONCLUSIONS:
    These results showed that treatment with Pristimerin may be a potential strategy for the suppression of hypoxia-induced metastasis through the reversal of hypoxia-induced stem cell characteristics and EMT in cancer cells, which justifies the potential use of Pristimerin as a practical chemopreventive approach for patients with PCa.
    J Integr Med. 2014 Jan;12(1):20-34.
    Pristimerin enhances recombinant adeno-associated virus vector-mediated transgene expression in human cell lines in vitro and murine hepatocytes in vivo.[Pubmed: 24461592]
    In the present study, we systemically evaluated the ability of two bioactive compounds from traditional Chinese medicine, celastrol and Pristimerin, to enhance recombinant adeno-associated virus (rAAV) serotype vector-mediated transgene expression both in human cell lines in vitro, and in murine hepatocytes in vivo.
    METHODS AND RESULTS:
    Human cell lines were infected with rAAV vectors with either mock treatment or treatment with celastrol or Pristimerin. The transgene expression, percentage of nuclear translocated viral genomes and the ubiquitination of intracellular proteins were investigated post-treatment. In addition, nonobese diabetic/severe combined immunodeficient gamma (NSG) mice were tail vain-injected with rAAV vectors and co-administered with either dimethyl sulfoxide, celastrol, Pristimerin or a positive control, bortezomib. The transgene expression in liver was detected and compared over time. We observed that treatment with Pristimerin, at as low as 1 μmol/L concentration, significantly enhanced rAAV2 vector-mediated transgene expression in vitro, and intraperitoneal co-administration with Pristimerin at 4 mg/(kg·d) for 3 d dramatically facilitated viral transduction in murine hepatocytes in vivo. The transduction efficiency of the tyrosine-mutant rAAV2 vectors as well as that of rAAV8 vectors carrying oversized transgene cassette was also augmented significantly by Pristimerin. The underlying molecular mechanisms by which Pristimerin mediated the observed increase in the transduction efficiency of rAAV vectors include both inhibition of proteasomal degradation of the intracellular proteins and enhanced nuclear translocation of the vector genomes.
    CONCLUSIONS:
    These studies suggest the potential beneficial use of Pristimerin and Pristimerin-containing herb extract in future liver-targeted gene therapy with rAAV vectors.
    Int J Oncol. 2014 May;44(5):1707-15.
    Pristimerin, a quinonemethide triterpenoid, induces apoptosis in pancreatic cancer cells through the inhibition of pro-survival Akt/NF-κB/mTOR signaling proteins and anti-apoptotic Bcl-2.[Pubmed: 24603988]
    Lack of effective therapeutics for pancreatic cancer at the present time underscores the dire need for safe and effective agents for the treatment of this malignancy. In the present study, we have evaluated the anticancer activity and the mechanism of action of Pristimerin (PM), a quinonemethide triterpenoid, against MiaPaCa-2 and Panc-1 pancreatic ductal adenocarcinoma (PDA) cell lines.
    METHODS AND RESULTS:
    Treatment with Pristimerin inhibited the proliferation and induced apoptosis in both cell lines as characterized by the increased Annexin V-binding and cleavage of PARP-1 and procaspases -3, -8 and -9. Pristimerin also induced mitochondrial depolarization and the release of cytochrome c from the mitochondria. The induction of apoptosis by Pristimerin was associated with the inhibition of the pro-survival Akt, NF-κB and mTOR signaling proteins and their downstream intermediaries such as Foxo-3α and cyclin D1 (Akt); Cox-2 and VEGF (NF-κB); p-S6K1 and p-4E-BP1 (mTOR) as well as PKCε. Treatment with Pristimerin also inhibited the expression of anti-apoptotic Bcl-2 and survivin but not Bcl-xL. The downregulation of Bcl-2 by Pristimerin was not due to proteasomal or lysosomal proteolytic degradation of Bcl-2, since treatment with Pristimerin in the presence of proteasomal inhibitors MG132 or lactacystin (LAC) or calpain inhibitor MG101 failed to block the downregulation of Bcl-2 by Pristimerin. On the other hand, RT-PCR analysis showed the inhibition of Bcl-2 mRNA by Pristimerin in a dose-related manner, indicating that inhibition of Bcl-2 by Pristimerin is mediated through the suppression of Bcl-2 gene expression.
    CONCLUSIONS:
    Thus, the mechanistic understanding of the antitumor activity of Pristimerin could facilitate in vivo efficacy studies of Pristimerin for pancreatic cancer.
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