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Cucurbitacin D
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Product Name Cucurbitacin D
Price: $238 / 10mg
CAS No.: 3877-86-9
Catalog No.: CFN90209
Molecular Formula: C30H44O7
Molecular Weight: 516.67 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The rhizomes of Hemsleya amabilis Diels.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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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 / $142.6 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Cucurbitacin D has anticancer effects, it induces apoptosis through caspase-3 and phosphorylation of JNK in hepatocellular carcinoma cells. Cucurbitacin D may be a potential therapeutic agent for β-hemoglobinopathies, including sickle cell anemia and β-thalassemia. Cucurbitacin D is a new inflammasome activator in macrophages, it can initiate immunomodulating activity in macrophages to lead to inflammasome activation as well as enhancement of LPS signaling.
Targets: IL Receptor | JNK | STAT | NF-kB | Caspase | ERK | CDK | p38MAPK
In vitro:
Int Immunopharmacol. 2013 Dec;17(4):1044-50.
Cucurbitacin D is a new inflammasome activator in macrophages.[Pubmed: 24140411]
We previously reported that Cucurbitacin D isolated from Trichosanthes kirilowii has anti-tumor roles to leukemia cells. However, the effect of Cucurbitacin D on immune cells is not fully understood although there is no toxic activity to normal cells.
METHODS AND RESULTS:
In this study, immunomodulating activities of Cucurbitacin D were investigated in macrophages. Cucurbitacin D could increase LPS-induced interleukin (IL)-1β production in culture supernatant of THP-1 cells, peritoneal exudate cells (PECs), bone marrow derived macrophages (BMDMs), and RAW264 cells. At the transcriptional level, Cucurbitacin D enhanced LPS-induced IL-1β mRNA expression through activation of ERK1/2 mitogen-activated protein kinases (MAPKs). At the posttranscriptional level, the activation of caspase-1 induced by Cucurbitacin D has also been demonstrated following treatment with a caspase-1 inhibitor and siRNA. Importantly, Cucurbitacin D has further been shown to induce inflammasome activation independent of ERK1/2 activation. Western blotting showed interaction of NOD-like receptor family, pyrin domain containing 3 (NALP3) and apoptosis-associated speck-like protein containing a caspase-activating and recruitment domain (ASC), suggesting activation of the inflammasome and a possible reason for activation of caspase-1.
CONCLUSIONS:
Taken together, these results suggest that Cucurbitacin D could initiate immunomodulating activity in macrophages to lead to inflammasome activation as well as enhancement of LPS signaling.
Anticancer Res. 2014 Sep;34(9):4797-806.
Cucurbitacin-D-induced CDK1 mRNA up-regulation causes proliferation arrest of a non-small cell lung carcinoma cell line (NSCLC-N6).[Pubmed: 25202060]
Despite progress in chemotherapeutic agents, non-small cell lung cancers (NSCLC) still have a poor survival rate. Thus, development of new therapeutic strategies, specifically against cancer cells is still required.
METHODS AND RESULTS:
For this purpose, we treated the non-small cell lung cancer cell line NSCLC-N6 with the natural product Cucurbitacin D (CucD) - extracted from the plant Ecballium elaterium in order first to assess its in vitro cytotoxicity, but also to study the genetic changes that it could bring out. Cucurbitacin D has shown a blocking in the G1 phase of the cell cycle in NSCLC-N6 cells prior to apoptotic cell death. The reverse transcriptase-polymerase chain reaction-differential display (RT-PCR-DD) technique was also applied on treated cells to elucidate the genetic mechanisms involved. We revealed an overexpression of Cyclin-dependent kinase 1 (CDK1) mRNA after treatment and, with the use of antisense oligonucleotides, an effective role in the proliferation arrest of NSCLC-N6 cells.
CONCLUSIONS:
The present study provides new insights about the mechanisms of proliferation arrest in tumor cells and open new ways of treatment to target tumor growth.
Int Immunopharmacol. 2009 Apr;9(4):508-13.
Cucurbitacin D isolated from Trichosanthes kirilowii induces apoptosis in human hepatocellular carcinoma cells in vitro.[Pubmed: 19185617]
The aim of the present study is to examine the effects of the anti-tumor component isolated from Trichosanthes kirilowii on human hepatocellular carcinoma cells.
METHODS AND RESULTS:
Using Sephadex G-25 column chromatography, Sep-Pak Plus C18 cartridge and high-performance liquid chromatography (HPLC), we isolated the active component from trichosanthes extract. By fast atom bombardment mass spectrometric analysis, the molecular mass of the active fraction was determined, the active components identified, and their mechanisms of action were analyzed by cell growth assay, cell cycle analysis, TUNEL staining and Western blot analysis. We found that the anti-tumor components isolated from the extract of trichosanthes (EOT) are Cucurbitacin D and dihydroCucurbitacin D, and suggest that Cucurbitacin D induces apoptosis through caspase-3 and phosphorylation of JNK in hepatocellular carcinoma cells.
CONCLUSIONS:
These results suggest that Cucurbitacin D isolated from Trichosanthes kirilowii could be a valuable candidate for anti-tumor drug.
In vivo:
Blood Cells Mol Dis. 2010 Dec 15;45(4):269-75.
Cucurbitacin D induces fetal hemoglobin synthesis in K562 cells and human hematopoietic progenitors through activation of p38 pathway and stabilization of the γ-globin mRNA.Cucurbitacin D induces fetal hemoglobin synthesis in K562 cells and human hematop[Pubmed: 20926322]
The search for novel therapeutic candidates targeting fetal hemoglobin (HbF) activation to reduce the imbalance of globin genes is regarded as a promising approach for the clinical management of sickle cell disease and β-thalassemia.
METHODS AND RESULTS:
For the first time, we identified Cucurbitacin D (CuD), an oxygenated tetracyclic triterpenoid, as a molecular entity inducing γ-globin gene expression and HbF synthesis in K562 cells and human hematopoietic progenitors from a β-thalassemia patient. Cucurbitacin D demonstrated a higher potency in HbF induction when compared with hydroxyurea, which was revealed by the evidence that Cucurbitacin D results in a higher fetal cell percentage and greater HbF content in K562 cells, in addition, to being less cytotoxic. Moreover, Cucurbitacin D also promotes higher HbF expression in primary erythroid cells. In the study to elucidate the molecular mechanisms of Cucurbitacin D's action, our data indicated that Cucurbitacin D-stimulated HbF synthesis was mediated by p38 pathway activation. At the post-transcriptional level, Cucurbitacin D treatment led to a significant elongation of the γ-globin mRNA half-life in K562 cells.
CONCLUSIONS:
Taken together, the results suggest that Cucurbitacin D may be a potential therapeutic agent for β-hemoglobinopathies, including sickle cell anemia and β-thalassemia.
Cucurbitacin D 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 1.9355 mL 9.6774 mL 19.3547 mL 38.7094 mL 48.3868 mL
5 mM 0.3871 mL 1.9355 mL 3.8709 mL 7.7419 mL 9.6774 mL
10 mM 0.1935 mL 0.9677 mL 1.9355 mL 3.8709 mL 4.8387 mL
50 mM 0.0387 mL 0.1935 mL 0.3871 mL 0.7742 mL 0.9677 mL
100 mM 0.0194 mL 0.0968 mL 0.1935 mL 0.3871 mL 0.4839 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
Kinase Assay:
Tumour Biol. 2013 Feb;34(1):285-91.
Cucurbitacin D induces growth inhibition, cell cycle arrest, and apoptosis in human endometrial and ovarian cancer cells.[Pubmed: 23150173]
Cucurbitacin D, a newly isolated triterpenoid cucurbitacin, has been found to possess anticancer effects. The purpose of this study was to elucidate the effects of Cucurbitacin D on human endometrial and ovarian cancer cells.
METHODS AND RESULTS:
Human endometrial and ovarian cancer cells were treated with various concentrations of Cucurbitacin D, and its effects on cell growth, the cell cycle, apoptosis, and their related measurements were investigated in vitro. All endometrial and ovarian cancer cell lines were sensitive to the growth-inhibitory effect of Cucurbitacin D. Cell cycle analysis indicated that their exposure to Cucurbitacin D increased the proportion in the sub-G0/G1 phases and G2/M phases of the cell cycle. Induction of apoptosis was confirmed by annexin V staining of externalized phosphatidylserine and loss of the transmembrane potential of mitochondria. This induction occurred in concert with altered expression of genes related to cell growth, malignant phenotype, and apoptosis.
CONCLUSIONS:
Our results suggest that Cucurbitacin D might be a new therapeutic option for the treatment of endometrial and ovarian cancers.
Mol Cell Biochem. 2015 Nov;409(1-2):33-43.
Cucurbitacin D induces cell cycle arrest and apoptosis by inhibiting STAT3 and NF-κB signaling in doxorubicin-resistant human breast carcinoma (MCF7/ADR) cells.[Pubmed: 26169986 ]
Breast cancer is the most common cancer for women and is a major cause of mortality in women. Doxorubicin is a generally used chemotherapy drug for breast cancer. However, multidrug resistance of breast cancer interferes with the chemotherapy.
METHODS AND RESULTS:
We examined whether Cucurbitacin D affects doxorubicin resistance of MCF7/ADR breast cancer cells. Cell viability was measured by MTT assay. Levels of p-STAT3, p-NF-κB, IκB, and caspases were measured by Western blot analysis. Nuclear staining of Stat3 and NF-κB was measured by immunocytochemistry. STAT3 and NF-κB transcriptional activity was detected by STAT3 and NF-κB luciferase reporter gene assays. Analysis of cell cycle arrest was performed by flow cytometry. Induction of apoptosis by Cucurbitacin D was measured by Annexin V-FITC/propidium iodide assay. More than 90% of MCF7/ADR cells lived upon treatment with doxorubicin for 24 h. However, upon treatment with Cucurbitacin D, cell death was more than 60%. Co-administration of Cucurbitacin D and doxorubicin induced apoptosis, and G2/M cell cycle arrest, and inhibited upregulated Stat3 by doxorubicin on MCF7/ADR cells. Additionally, Cucurbitacin D led to an increase in the IκBα level in the cytosol and a decrease in the p-NF-κB level in the nucleus. Finally, Cucurbitacin D inhibited translocation of Stat3 and NF-κB and decreased transcriptional activity in the nucleus.
CONCLUSIONS:
Cucurbitacin D decreases cell proliferation and induces apoptosis by inhibiting Stat3 and NF-κB signaling in doxorubicin-resistant breast cancer cells. Cucurbitacin D could be used as a useful compound to treat adriamycin-resistant patients.
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