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    Cucurbitacin B
    CAS No. 6199-67-3 Price $100 / 20mg
    Catalog No.CFN99129Purity>=98%
    Molecular Weight558.70Type of CompoundTriterpenoids
    FormulaC32H46O8Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $46.8 / In-stock
    Other Packaging *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap
    Our products had been exported to the following research institutions and universities, And still growing.
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    Related Libraries
  • Anticancer Compound Library
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  • Biological Activity
    Description: Cucurbitacin B, an effective HIF-1 inhibitor, has antitumor activity, it inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells. It inhibited AKT signaling activation through up-regulation of PTEN.
    Targets: PKA | cAMP | HIF | mTOR | Akt | ERK | JAK | STAT | p53
    In vitro:
    Eur Rev Med Pharmacol Sci. 2014;18(21):3297-303.
    Cucurbitacin B inhibits neuroblastoma cell proliferation through up-regulation of PTEN.[Pubmed: 25487942]
    Cucurbitacins belong to a class of highly oxidized tetracyclic triterpenoids. Recent studies suggest that the use of Cucurbitacin could repress cancer cell progression. However, the biological effect of Cucurbitacin-B in neuroblastoma cells remains unexplored.
    MTT and BrdU (bromodeoxyuridine) incorporation assays were used to determine the anti-proliferation roles of Cucurbitacin-B. Real-time PCR and Western blot assays were used to detect the expression of cell cycle regulators. Small interfering RNAs (siRNAs) were used to silence the expression of PTEN (phosphatase and tensin homolog gene).We found that Cucurbitacin-B inhibited growth and modulated expression of cell-cycle regulators in SHSY5Y cells. At the molecular level, we found that Cucurbitacin-B inhibited AKT signaling activation through up-regulation of PTEN. Indeed, PTEN deficiency using siRNA oligos attenuated the anti-proliferative roles of Cucurbitacin-B.
    These results provide evidence for a mechanism that may contribute to the antineoplastic effects of Cucurbitacin-B in neuroblastoma.
    PLoS One. 2014 Apr 1;9(4):e93547.
    VASP activation via the Gα13/RhoA/PKA pathway mediates cucurbitacin-B-induced actin aggregation and cofilin-actin rod formation.[Pubmed: 24691407]
    Cucurbitacin B (CuB), a potent antineoplastic agent of cucurbitacin triterpenoids, induces rapid disruption of actin cytoskeleton and aberrant cell cycle inhibiting carcinogenesis. However, the underlying molecular mechanism of such anticancer effects remains incompletely understood.
    In this study, we showed that CuB treatment rapidly induced vasodilator-stimulated phosphoprotein (VASP) phosphorylation (i.e. activation) at the Ser157 residue and generated VASP clumps which were co-localized with amorphous actin aggregates prior to the formation of highly-ordered cofilin-actin rods in melanoma cells. Knockdown of VASP or inhibition of VASP activation using PKA-specific inhibitor H89 suppressed CuB-induced VASP activation, actin aggregation and cofilin-actin rod formation. The VASP activation was mediated by cAMP-independent PKA activation as CuB decreased the levels of cAMP while MDL12330A, an inhibitor of adenylyl cyclase, had weak effect on VASP activation. Knockdown of either Gα13 or RhoA not only suppressed VASP activation, but also ameliorated CuB-induced actin aggregation and abrogated cofilin-actin rod formation.
    Collectively, our studies highlighted that the CuB-induced actin aggregation and cofilin-actin rod formation was mediated via the Gα13/RhoA/PKA/VASP pathway.
    In vivo:
    Eur J Pharmacol. 2014 Jan 15;723:46-54.
    Cucurbitacin B inhibits the translational expression of hypoxia-inducible factor-1α.[Pubmed: 24333213]
    Cucurbitacin B is a triterpenoid compound isolated from Trichosanthes kirilowii Maximowicz, which has been used in oriental medicine for its antitumor activities. However, the mechanisms by which Cucurbitacin B inhibits tumor growth are not fully understood.
    We here demonstrated the effect of Cucurbitacin B on hypoxia-inducible factor-1 (HIF-1) activation. Cucurbitacin B showed the potent inhibitory activity against HIF-1 activation induced by hypoxia in various human cancer cell lines. This compound markedly decreased the hypoxia-induced accumulation of HIF-1α protein dose-dependently, whereas it did not affect the expressions of HIF-1β. Further analysis revealed that Cucurbitacin B inhibited HIF-1α protein synthesis, without affecting the expression level of HIF-1α mRNA or degradation of HIF-1α protein. Rather, we found that suppression of HIF-1α accumulation by Cucurbitacin B correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and extracellular signal-regulated kinase-1/2 (ERK1/2), a pathway known to regulate HIF-1α expression at the translational level. Cucurbitacin B also activated Akt, a mechanistic feature exhibited by established mTOR inhibitors in many tumor cells. Furthermore, Cucurbitacin B prevented hypoxia-induced expression of HIF-1 target genes and suppresses the invasiveness of tumor cells. In vivo studies further confirmed the inhibitory effect of Cucurbitacin B on the expression of HIF-1α proteins, leading to a decrease growth of HeLa cells in a xenograft tumor model.
    These results show that Cucurbitacin B is an effective inhibitor of HIF-1 and provide new perspectives into the mechanism of its anticancer activity.
    Cucurbitacin B Description
    Source: The rhizomes of Hemsleya amabilis Diels.
    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 1.7899 mL 8.9493 mL 17.8987 mL 35.7974 mL 44.7467 mL
    5 mM 0.358 mL 1.7899 mL 3.5797 mL 7.1595 mL 8.9493 mL
    10 mM 0.179 mL 0.8949 mL 1.7899 mL 3.5797 mL 4.4747 mL
    50 mM 0.0358 mL 0.179 mL 0.358 mL 0.7159 mL 0.8949 mL
    100 mM 0.0179 mL 0.0895 mL 0.179 mL 0.358 mL 0.4475 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:
    Cancer Biother Radiopharm. 2012 Oct;27(8):495-503.
    Cucurbitacin B regulates immature myeloid cell differentiation and enhances antitumor immunity in patients with lung cancer.[Pubmed: 22746287 ]
    The aberrant activation of the JAK2/STAT3 signaling in immature myeloid dendritic cells (DCs) is associated with immune tolerance and poor antitumor immunity.
    The objective of this study was to test the hypothesis that Cucurbitacin B (CuB), a selective inhibitor of JAK2/STAT3 signaling, could promote DC differentiation and improve antitumor immunity. Twelve patients with advanced lung cancers were treated orally with CuB daily for 7 consecutive days. The frequency of peripheral blood myeloid DCs and immature myeloid cells (imCs) in those patients and healthy controls was characterized longitudinally by flow cytometry. The effect of CuB on the differentiation of DCs and p53-specific T responses was evaluated in vitro. The percentages of Lin(-)DR(-)CD33(+) imCs and Lin(-)DR(+)CD33(+) DCs were significantly different between patients with lung cancers and healthy controls (1.55% vs. 0.82%, p=0.002; 0.60% vs. 1.90%, p=0.000). Treatment with CuB significantly increased the frequency of Lin(-)DR(+)CD33(+), but reduced the frequency of Lin(-)DR(-)CD33(+) in patients with lung cancers (p<0.05). Treatment with CuB induced the differentiation of DCs cocultured with tumor cells 16HBE/BPDE and enhanced the sensitivity of 16HBE/BPDE cells to p53-specific CTL by inhibiting the JAK2/STAT3 activation, but also enhancing the interferon-γ-related STAT1 activation in 16HBE/BPDE cells.
    CuB significantly reduced the frequency of imCs in patients with lung cancers and enhanced the effect of p53-specific CTL on tumor 16HBE/BPDE cells.
    Cell Research:
    Int J Cancer. 2008 Sep 15;123(6):1364-75.
    Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme.[Pubmed: 18561312]
    Cell lines:U87, T98G, U118, U343, and U373 cells
    Concentrations: 0~1 μM
    Incubation Time: 48 h
    For proliferation measurements, the cells are placed into 96 well plates, and cell growth is measured at various times by MTT assay according to the protocol.