Cucurbitacin E

CAS# 18444-66-1

Cucurbitacin E

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Quality Control of Cucurbitacin E

Number of papers citing our products

Chemical structure

Cucurbitacin E

3D structure

Chemical Properties of Cucurbitacin E

Cas No. 18444-66-1 SDF Download SDF
PubChem ID 5281319 Appearance White powder
Formula C32H44O8 M.Wt 556.67
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms α-Elaterin; α-Elaterine
Solubility DMSO : 50 mg/mL (89.82 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name [(E,6R)-6-[(8S,9R,10R,13R,14S,16R,17R)-2,16-dihydroxy-4,4,9,13,14-pentamethyl-3,11-dioxo-8,10,12,15,16,17-hexahydro-7H-cyclopenta[a]phenanthren-17-yl]-6-hydroxy-2-methyl-5-oxohept-3-en-2-yl] acetate
SMILES CC(=O)OC(C)(C)C=CC(=O)C(C)(C1C(CC2(C1(CC(=O)C3(C2CC=C4C3C=C(C(=O)C4(C)C)O)C)C)C)O)O
Standard InChIKey NDYMQXYDSVBNLL-MUYMLXPFSA-N
Standard InChI InChI=1S/C32H44O8/c1-17(33)40-27(2,3)13-12-23(36)32(9,39)25-21(35)15-29(6)22-11-10-18-19(14-20(34)26(38)28(18,4)5)31(22,8)24(37)16-30(25,29)7/h10,12-14,19,21-22,25,34-35,39H,11,15-16H2,1-9H3/b13-12+/t19-,21-,22+,25+,29+,30-,31+,32+/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Cucurbitacin E

1 Citrullus sp. 2 Cucumis sp. 3 Cucurbita sp. 4 Gratiola sp. 5 Iberis sp.

Biological Activity of Cucurbitacin E

DescriptionCucurbitacin 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.
TargetsIL Receptor | VEGFR | JAK | STAT | ROS | NF-kB | p38MAPK | TNF-α | p65 | ERK | Caspase | p21
In vitro

Growth inhibitory effect of Cucurbitacin E on breast cancer cells.[Pubmed: 24040444]

nt J Clin Exp Pathol. 2013 Aug 15;6(9):1799-805.

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.

Cucurbitacin E and I in Iberis amara: Feeding inhibitors for Phyllotreta nemorum.[Reference: WebLink]

Phytochemistry, 1977, 16(10):1519-22.

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.

In vivo

Cucurbitacin E, a tetracyclic triterpenes compound from Chinese medicine, inhibits tumor angiogenesis through VEGFR2-mediated Jak2-STAT3 signaling pathway.[Pubmed: 20732905 ]

Carcinogenesis. 2010 Dec;31(12):2097-104.

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.

Anti-inflammatory and analgesic effects of cucurbitacins from Wilbrandia ebracteata.[Pubmed: 9434604 ]

Planta Med. 1997 Dec;63(6):525-8.

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.

Protocol of Cucurbitacin E

Kinase Assay

Cucurbitacin E suppresses cytokine expression in human Jurkat T cells through down-regulating the NF-κB signaling.[Pubmed: 25921411]

Cucurbitacin-E inhibits multiple cancer cells proliferation through attenuation of Wnt/β-catenin signaling.[Pubmed: 24885795]

Cancer Biother Radiopharm. 2014 Jun;29(5):210-4.

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 (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.

Structure Identification
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.

Cucurbitacin E Dilution Calculator

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Preparing Stock Solutions of Cucurbitacin E

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.7964 mL 8.982 mL 17.964 mL 35.9279 mL 44.9099 mL
5 mM 0.3593 mL 1.7964 mL 3.5928 mL 7.1856 mL 8.982 mL
10 mM 0.1796 mL 0.8982 mL 1.7964 mL 3.5928 mL 4.491 mL
50 mM 0.0359 mL 0.1796 mL 0.3593 mL 0.7186 mL 0.8982 mL
100 mM 0.018 mL 0.0898 mL 0.1796 mL 0.3593 mL 0.4491 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Cucurbitacin E

Cucurbitacin E is a natural compound which from the climbing stem of Cucumic melo L. Cucurbitacin E significantly suppresses the activity of the cyclin B1/CDC2 complex.

In Vitro:To explore the antitumor activity of Cucurbitacin E (CuE) against colorectal cancer (CRC) cells, an in vitro study is initiated in which each of the CRC cell lines is exposed to increasing doses of Cucurbitacin E (0, 2.5, 5, and 7.5 μM) over a period of 24 h. The proliferation of the Cucurbitacin E-treated cancer cells is then measured using the MTT method. Cucurbitacin E is shown to induce morphological changes in the primary colon cancer cells. Microscopic observation showed that following exposure to Cucurbitacin E (5 μM) between 6 and 24 h, the primary colon cancer cells underwent a remarkable change in morphology. Cucurbitacin E inhibits tumor growth by arresting the cell cycle in the G2/M phase via GADD45γ gene expression and the blockage of cyclin B1/CDC2 complex in primary CRC cells[1].

In Vivo:A high fat diet mice model of metabolic syndrome (HFD-MetS) is developed to assess the role of Cucurbitacin E (CuE) on body weight and fat tissue biology. Significant decrease in body weights of HFD-MetS mice treated with Cucurbitacin E (0.5mg/kg) are found as compared to HFD-MetS mice treated with vehicle alone. Cucurbitacin E treatment reduces all fat pads weights in HFD-MetS mice. 55% reduction is observed in total fat in mice, after treatment with Cucurbitacin E in comparison to HFD-MetS mice. Abdominal obesity is strongly associated with metabolic syndrome. Central obesity is reduced to 50% after Cucurbitacin E treatment as compared to HFD MetS mice, elucidating the effectiveness of Cucurbitacin E in targeting MetS[2].

References:
[1]. Hsu YC, et al. Therapeutic ROS targeting of GADD45γ in the induction of G2/M arrest in primary human colorectal cancer cell lines by cucurbitacin E. Cell Death Dis. 2014 Apr 24;5:e1198. [2]. Murtaza M, et al. Cucurbitacin E reduces obesity and related metabolic dysfunction in mice by targeting JAK-STAT5 signaling pathway. PLoS One. 2017 Jun 9;12(6):e0178910.

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References on Cucurbitacin E

Cucurbitacin E, a tetracyclic triterpenes compound from Chinese medicine, inhibits tumor angiogenesis through VEGFR2-mediated Jak2-STAT3 signaling pathway.[Pubmed:20732905]

Carcinogenesis. 2010 Dec;31(12):2097-104.

Cucurbitacin E (CuE, alpha-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. 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. 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.

Morphological and physicochemical characterization of liposomes loading cucurbitacin E, an anti-proliferative natural tetracyclic triterpene.[Pubmed:24291009]

Chem Phys Lipids. 2014 Jan;177:64-70.

Cucurbitacin E (Cuc E), an oxygenated triterpene molecule, has demonstrated anti-proliferative effect on various cancer cells. Here, we examined the effect of Cuc 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 Cuc E at molar ratios 100:12 and 100:20. The loading efficiency of Cuc E was found to be higher than 98% upon HPLC analysis. The thermodynamic parameters suggest that Cuc E does not penetrate into the bilayers and interacts with the polar/apolar interface of the lipid membranes. Blank and Cuc 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 Cuc E loaded liposomes. AFM images showed that the size and the height of Cuc E loaded liposomes were respectively smaller and higher than blank ones. Results suggest that Cuc E produces modifications in the lipid membrane structures.

Cucurbitacin-E inhibits multiple cancer cells proliferation through attenuation of Wnt/beta-catenin signaling.[Pubmed:24885795]

Cancer Biother Radiopharm. 2014 Jun;29(5):210-4.

Recent studies suggest that the use of cucurbitacins could inhibit cancer cell progression. 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/beta-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. Taken together, the results of this study provide a novel mechanism that may contribute to the antineoplastic effects of CuE in cancer cells.

Cucurbitacin E suppresses cytokine expression in human Jurkat T cells through down-regulating the NF-kappaB signaling.[Pubmed:25921411]

Acta Biochim Biophys Sin (Shanghai). 2015 Jun;47(6):459-65.

Cucurbitacin E (CucE), a triterpenoid isolated from Cucurbitaceae plants, has been shown to possess an anti-in fl ammatory or immunosuppressive activity in vitro and in vivo, yet the underlying mechanism has been incompletely understood. The aim of the present study was to explore its effect on cytokine expression and the underlying mechanism in human Jurkat T cells as a cellular model. The results showed that CucE significantly inhibited the production of interleukin-2, tumor necrosis factor-alpha, and interferon-gamma 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 CucE treatment, suggesting a potential modulatory effect on the critical signaling pathways for cytokine expression, including nuclear factor-kappaB (NF-kappaB) or mitogen-activated protein kinases (MAPKs). In support of its effect on the NF-kappaB signaling pathway, CucE decreased the phosphorylation levels of inhibitor of kappaB (IkappaB) and NF-kappaB/p65 in PDB + Ion-stimulated cells. Further supporting this, the nuclear translocation of NF-kappaB/p65 was significantly suppressed in response to PDB plus Ion stimulation in the presence of CucE. The phosphorylation of p38MAPK, c-Jun N-terminal kinase (JNK), and Erk1/2, however, was not decreased or slightly increased at some time points by CucE treatment. Collectively, these data suggest that CucE may exhibit immunosuppressive effect by attenuating critical cytokine expression through down-regulating the NF-kappaB signaling pathway.

Anti-inflammatory and analgesic effects of cucurbitacins from Wilbrandia ebracteata.[Pubmed:9434604]

Planta Med. 1997 Dec;63(6):525-8.

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. 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 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. These findings suggest that CH2Cl2 extract has potent anti-inflammatory and analgesic action and that F-III and cucurbitacin B and E may account for these actions.

Growth inhibitory effect of Cucurbitacin E on breast cancer cells.[Pubmed:24040444]

Int J Clin Exp Pathol. 2013 Aug 15;6(9):1799-805. eCollection 2013.

OBJECTIVE: 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: 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. RESULTS: 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.

Description

Cucurbitacin E is a natural compound which from the climbing stem of Cucumic melo L. Cucurbitacin E significantly suppresses the activity of the cyclin B1/CDC2 complex.

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