Cucurbitacin E

Cucurbitacin E
Product Name Cucurbitacin E
CAS No.: 18444-66-1
Catalog No.: CFN90154
Molecular Formula: C32H44O8
Molecular Weight: 556.67 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: White powder
Targets: IL Receptor | VEGFR | JAK | STAT | ROS | NF-kB | p38MAPK | TNF-α | p65 | ERK | Caspase | p21
Source: The rhizomes of Hemsleya amabilis Diels.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $288/20mg
Cucurbitacin E has prevention of neurodegeneration, it has potent anti-proliferative, antineoplastic, anti-inflammatory and analgesic actions, it also exhibits immunosuppressive effect by attenuating critical cytokine expression through down-regulating the NF-κB signaling pathway.
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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

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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    nt J Clin Exp Pathol. 2013 Aug 15;6(9):1799-805.
    Growth inhibitory effect of Cucurbitacin E on breast cancer cells.[Pubmed: 24040444]
    Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.
    METHODS AND RESULTS:
    The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting. CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin.
    CONCLUSIONS:
    Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.
    Phytochemistry, 1977, 16(10):1519-22.
    Cucurbitacin E and I in Iberis amara: Feeding inhibitors for Phyllotreta nemorum.[Reference: WebLink]
    Cucurbitacin E and cucurbitacin I have been isolated from green parts of Iberis amara and identified by TLC, UV and MS.
    METHODS AND RESULTS:
    It is shown that cucurbitacins act as feeding inhibitors for the flea beetle Phyllotreta nemorum. The most potent feeding inhibitors in green parts of I. amara towards P. nemorum are Cucurbitacin E and I, and the concentrations of these compounds in the plant are found to be high enough to prevent feeding of the flea beetle.
    Carcinogenesis. 2010 Dec;31(12):2097-104.
    Cucurbitacin E, a tetracyclic triterpenes compound from Chinese medicine, inhibits tumor angiogenesis through VEGFR2-mediated Jak2-STAT3 signaling pathway.[Pubmed: 20732905 ]
    Cucurbitacin E (CuE, α-elaterin), a tetracyclic triterpenes compound from folk traditional Chinese medicine plants, has been shown to inhibit cancer cell growth, inflammatory response and bilirubin-albumin binding. However, the effects of CuE on tumor angiogenesis and its potential molecular mechanism are still unknown.
    METHODS AND RESULTS:
    Here, we demonstrated that CuE significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration and tubulogenesis in vitro and blocked angiogenesis in chick embryo chorioallantoic membrane assay and mouse corneal angiogenesis model in vivo. Furthermore, we found that CuE remarkably induced HUVEC apoptosis, inhibited tumor angiogenesis and suppressed human prostate tumor growth in xenograft tumor model. Finally, we showed that CuE blocked vascular endothelial growth factor receptor (VEGFR) 2-mediated Janus kinase (Jak) 2-signal transducer and activator of transcription (STAT) 3 signaling pathway in endothelial cells and suppressed the downstream protein kinases, such as extracellular signal-regulated kinase and p38 mitogen-activated protein kinases.
    CONCLUSIONS:
    Therefore, our studies provided the first evidence that CuE inhibited tumor angiogenesis by inhibiting VEGFR2-mediated Jak-STAT3 and mitogen-activated protein kinases signaling pathways and CuE is a potential candidate in angiogenesis-related disease therapy.
    Planta Med. 1997 Dec;63(6):525-8.
    Anti-inflammatory and analgesic effects of cucurbitacins from Wilbrandia ebracteata.[Pubmed: 9434604 ]
    The anti-inflammatory and antinociceptive actions of the CH2Cl2 extract and semipurified fraction (F-III) from roots of Wilbrandia ebracteata Cogn. have been investigated in rats and mice.
    METHODS AND RESULTS:
    The CH2Cl2 extract (1-10 mg/kg, i.p.; ID50 5 mg/kg) and (3-30 mg/kg, p.o.; ID50 15 mg/kg) inhibited, in a dose-related manner, carrageenan-induced paw edema in rats. The subfraction (F-III) from CH2Cl2 extract and compounds isolated as cucurbitacin B and Cucurbitacin E also inhibited carrageenan-induced edema. The CH2Cl2 extract and F-III also exhibited significant analgesic action in acetic acid-induced pain in mice. In the formalin test, the CH2Cl2 extract (0.3-10 mg/kg, i.p.) and (3-30 mg/kg, p.o.) caused inhibition of the neurogenic (first phase) and inflammatory phase (second phase) of formalin-induced pain. However, the CH2Cl2 extract was more effective in relation to the second phase than in inhibition of the formalin-induced edema.
    CONCLUSIONS:
    These findings suggest that CH2Cl2 extract has potent anti-inflammatory and analgesic action and that F-III and cucurbitacin B and Cucurbitacin E may account for these actions.
    Cancer Biother Radiopharm. 2014 Jun;29(5):210-4.
    Cucurbitacin-E inhibits multiple cancer cells proliferation through attenuation of Wnt/β-catenin signaling.[Pubmed: 24885795]
    Recent studies suggest that the use of cucurbitacins could inhibit cancer cell progression.
    METHODS AND RESULTS:
    In the current study, the authors analyzed the effect of Cucurbitacin E (CuE) in cancer cells using A549, Hep3B, and SW480 cells. The authors found that CuE inhibited cell proliferation and modulated the expression of cell cycle regulators in these cells. Moreover, the authors found that CuE inhibited Wnt/β-catenin signaling activation through upregulation of tumor suppressor Menin. Indeed, ablation of Menin using small interfering RNA (siRNA) oligos attenuated the antiproliferative roles of CuE.
    CONCLUSIONS:
    Taken together, the results of this study provide a novel mechanism that may contribute to the antineoplastic effects of CuE in cancer cells.
    Acta Biochim Biophys Sin (Shanghai). 2015 Jun;47(6):459-65.
    Cucurbitacin E suppresses cytokine expression in human Jurkat T cells through down-regulating the NF-κB signaling.[Pubmed: 25921411]
    Cucurbitacin E (CucE), a triterpenoid isolated from Cucurbitaceae plants, has been shown to possess an anti-inflammatory or immunosuppressive activity in vitro and in vivo, yet the underlying mechanism has been incompletely understood.
    METHODS AND RESULTS:
    The results showed that Cucurbitacin E significantly inhibited the production of interleukin-2, tumor necrosis factor-α, and interferon-γ in culture medium of cells treated with phorbol 12,13-dibutyrate (PDB) plus ionomycin (Ion). Furthermore, the mRNA levels of these cytokines in activated Jurkat T cells were also decreased upon Cucurbitacin E treatment, suggesting a potential modulatory effect on the critical signaling pathways for cytokine expression, including nuclear factor-κB (NF-κB) or mitogen-activated protein kinases (MAPKs). In support of its effect on the NF-κB signaling pathway, Cucurbitacin E decreased the phosphorylation levels of inhibitor of κB (IκB) and NF-κB/p65 in PDB + Ion-stimulated cells.However, was not decreased or slightly increased at some time points by Cucurbitacin E treatment.
    CONCLUSIONS:
    Collectively, these data suggest that Cucurbitacin E may exhibit immunosuppressive effect by attenuating critical cytokine expression through down-regulating the NF-κB signaling pathway.
    Chem Phys Lipids. 2014 Jan;177:64-70.
    Morphological and physicochemical characterization of liposomes loading cucurbitacin E, an anti-proliferative natural tetracyclic triterpene.[Pubmed: 24291009]
    Cucurbitacin E (Cuc E), an oxygenated triterpene molecule, has demonstrated anti-proliferative effect on various cancer cells.
    METHODS AND RESULTS:
    Here, we examined the effect of Cucurbitacin E on the membrane morphology and properties using differential scanning calorimetry, transmission electron microscopy and atomic force microscopy techniques. Dipalmitoylphosphatidylcholine vesicles were prepared by the thin film hydration method in the absence and presence of Cucurbitacin E at molar ratios 100:12 and 100:20. The loading efficiency of Cucurbitacin E was found to be higher than 98% upon HPLC analysis. The thermodynamic parameters suggest that Cucurbitacin E does not penetrate into the bilayers and interacts with the polar/apolar interface of the lipid membranes. Blank and Cucurbitacin E loaded liposomes prepared from a mixture of DPPC/DPPE/DPPG/Cho were imaged by TEM and AFM. Images obtained by TEM revealed unilamellar liposomes for blank and Cucurbitacin E loaded liposomes. AFM images showed that the size and the height of Cucurbitacin E loaded liposomes were respectively smaller and higher than blank ones.
    CONCLUSIONS:
    Results suggest that Cucurbitacin E produces modifications in the lipid membrane structures.
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