Cucurbitacin D

CAS# 3877-86-9

Cucurbitacin D

Catalog No. BCN2355----Order now to get a substantial discount!

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Quality Control of Cucurbitacin D

Number of papers citing our products

Chemical structure

Cucurbitacin D

3D structure

Chemical Properties of Cucurbitacin D

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.
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 D

1 Begonia sp. 2 Bryonia sp. 3 Coccinia sp. 4 Colocynthis sp. 5 Cucurbita sp. 6 Ecballium sp. 7 Luffa sp.

Biological Activity of Cucurbitacin D

DescriptionCucurbitacin 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.
TargetsIL 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.
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.

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.
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.

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.
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

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.
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.

Protocol of Cucurbitacin D

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.
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.

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.

Cucurbitacin D Dilution Calculator

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Preparing Stock Solutions of Cucurbitacin D

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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Background on Cucurbitacin D

Cucurbitacin D is a cucurbitacin in which a lanostane skeleton is multi-substituted with hydroxy, methyl and oxo substituents, with unsaturation at positions 5 and 23. It is a cucurbitacin, a secondary alpha-hydroxy ketone and a tertiary alpha-hydroxy ketone. It derives from a hydride of a lanostane.
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References on Cucurbitacin D

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.

Description

Cucurbitacin D is an active component in Cucurbita texana, disrupts interactions between Hsp90 and two co-chaperones, Cdc37 and p23. Cucurbitacin D prevents Hsp90 client (Her2, Raf, Cdk6, pAkt) maturation without induction of the heat shock response. Anti-cancer activity.

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