Cucurbitacin DCAS# 3877-86-9 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 3877-86-9 | SDF | Download SDF |
PubChem ID | 5281318 | Appearance | White powder |
Formula | C30H44O7 | M.Wt | 516.67 |
Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
Synonyms | Elatericin A | ||
Solubility | Soluble in ethanol and methan | ||
Chemical Name | (2S,8S,9R,10R,13R,14S,16R,17R)-17-[(E,2R)-2,6-dihydroxy-6-methyl-3-oxohept-4-en-2-yl]-2,16-dihydroxy-4,4,9,13,14-pentamethyl-2,7,8,10,12,15,16,17-octahydro-1H-cyclopenta[a]phenanthrene-3,11-dione | ||
SMILES | CC1(C2=CCC3C4(CC(C(C4(CC(=O)C3(C2CC(C1=O)O)C)C)C(C)(C(=O)C=CC(C)(C)O)O)O)C)C | ||
Standard InChIKey | SRPHMISUTWFFKJ-QJNWWGCFSA-N | ||
Standard InChI | InChI=1S/C30H44O7/c1-25(2,36)12-11-21(33)30(8,37)23-19(32)14-27(5)20-10-9-16-17(13-18(31)24(35)26(16,3)4)29(20,7)22(34)15-28(23,27)6/h9,11-12,17-20,23,31-32,36-37H,10,13-15H2,1-8H3/b12-11+/t17-,18+,19-,20+,23+,27+,28-,29+,30+/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. |
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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. |
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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. |
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 | Cucurbitacin D is a new inflammasome activator in macrophages.[Pubmed: 24140411]Int Immunopharmacol. 2013 Dec;17(4):1044-50.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. Cucurbitacin-D-induced CDK1 mRNA up-regulation causes proliferation arrest of a non-small cell lung carcinoma cell line (NSCLC-N6).[Pubmed: 25202060]Anticancer Res. 2014 Sep;34(9):4797-806.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. Cucurbitacin D isolated from Trichosanthes kirilowii induces apoptosis in human hepatocellular carcinoma cells in vitro.[Pubmed: 19185617]Int Immunopharmacol. 2009 Apr;9(4):508-13.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.
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In vivo | 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]Blood Cells Mol Dis. 2010 Dec 15;45(4):269-75.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. |
Kinase Assay | 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 ]Cucurbitacin D induces growth inhibition, cell cycle arrest, and apoptosis in human endometrial and ovarian cancer cells.[Pubmed: 23150173]Tumour Biol. 2013 Feb;34(1):285-91.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. Mol Cell Biochem. 2015 Nov;409(1-2):33-43.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.
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Cucurbitacin D Dilution Calculator
Cucurbitacin D Molarity Calculator
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 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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Cucurbitacin-D-induced CDK1 mRNA up-regulation causes proliferation arrest of a non-small cell lung carcinoma cell line (NSCLC-N6).[Pubmed:25202060]
Anticancer Res. 2014 Sep;34(9):4797-806.
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. 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. CucD 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. 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.
Cucurbitacin D is a new inflammasome activator in macrophages.[Pubmed:24140411]
Int Immunopharmacol. 2013 Dec;17(4):1044-50.
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. In this study, immunomodulating activities of Cucurbitacin D were investigated in macrophages. Cucurbitacin D could increase LPS-induced interleukin (IL)-1beta 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-1beta 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. 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.
Cucurbitacin D induces growth inhibition, cell cycle arrest, and apoptosis in human endometrial and ovarian cancer cells.[Pubmed:23150173]
Tumour Biol. 2013 Feb;34(1):285-91.
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. 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. Our results suggest that Cucurbitacin D might be a new therapeutic option for the treatment of endometrial and ovarian cancers.
Cucurbitacin D isolated from Trichosanthes kirilowii induces apoptosis in human hepatocellular carcinoma cells in vitro.[Pubmed:19185617]
Int Immunopharmacol. 2009 Apr;9(4):508-13.
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. 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. These results suggest that Cucurbitacin D isolated from Trichosanthes kirilowii could be a valuable candidate for anti-tumor drug.
Cucurbitacin D induces cell cycle arrest and apoptosis by inhibiting STAT3 and NF-kappaB signaling in doxorubicin-resistant human breast carcinoma (MCF7/ADR) cells.[Pubmed:26169986]
Mol Cell Biochem. 2015 Nov;409(1-2):33-43.
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. 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-kappaB, IkappaB, and caspases were measured by Western blot analysis. Nuclear staining of Stat3 and NF-kappaB was measured by immunocytochemistry. STAT3 and NF-kappaB transcriptional activity was detected by STAT3 and NF-kappaB 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 IkappaBalpha level in the cytosol and a decrease in the p-NF-kappaB level in the nucleus. Finally, Cucurbitacin D inhibited translocation of Stat3 and NF-kappaB and decreased transcriptional activity in the nucleus. Cucurbitacin D decreases cell proliferation and induces apoptosis by inhibiting Stat3 and NF-kappaB signaling in doxorubicin-resistant breast cancer cells. Cucurbitacin D could be used as a useful compound to treat adriamycin-resistant patients.
Cucurbitacin D induces fetal hemoglobin synthesis in K562 cells and human hematopoietic progenitors through activation of p38 pathway and stabilization of the gamma-globin mRNA.[Pubmed:20926322]
Blood Cells Mol Dis. 2010 Dec 15;45(4):269-75.
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 beta-thalassemia. For the first time, we identified Cucurbitacin D (CuD), an oxygenated tetracyclic triterpenoid, as a molecular entity inducing gamma-globin gene expression and HbF synthesis in K562 cells and human hematopoietic progenitors from a beta-thalassemia patient. CuD demonstrated a higher potency in HbF induction when compared with hydroxyurea, which was revealed by the evidence that CuD results in a higher fetal cell percentage and greater HbF content in K562 cells, in addition, to being less cytotoxic. Moreover, CuD also promotes higher HbF expression in primary erythroid cells. In the study to elucidate the molecular mechanisms of CuD's action, our data indicated that CuD-stimulated HbF synthesis was mediated by p38 pathway activation. At the post-transcriptional level, CuD treatment led to a significant elongation of the gamma-globin mRNA half-life in K562 cells. Taken together, the results suggest that CuD may be a potential therapeutic agent for beta-hemoglobinopathies, including sickle cell anemia and beta-thalassemia.