Cucurbitacin D
Based on 1 publication(s) in Google Scholar
Cucurbitacin D is the active ingredient in Trichosanthes kirilowii and can disrupt the interaction between Hsp90 and two co-chaperones, Cdc37 and p23. Cucurbitacin D is an inflammasome activator. Cucurbitacin D induces cell cycle arrest and cell apoptosis, exhibiting anti-tumor and anti-inflammatory effects.
For research use only. We do not sell to patients.
- Purity : 99.93%
- CAS No.: 3877-86-9
- Formula: C30H44O7
- Molecular Weight:516.67
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Storage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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HY-N0417
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Publications Citing Use of MedChemExpress (MCE) Cucurbitacin D
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Biological Activity
Description
IC50 & Target
[1]|
HSP90 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Bel-7402 | IC50 |
1.41 μM
Compound: 143
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Cytotoxicity against human Bel7402 cells assessed as growth inhibition
Cytotoxicity against human Bel7402 cells assessed as growth inhibition
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[PMID: 25599949] |
| Cancer cell lines | IC50 |
<0.4 μM
Compound: Cucurbitacin D
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Growth inhibition of human breast cancer cells
Growth inhibition of human breast cancer cells
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[PMID: 15332833] |
| Cancer cell lines | IC50 |
<0.4 μM
Compound: Cucurbitacin D
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Growth inhibition of human CNS cancer cells
Growth inhibition of human CNS cancer cells
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[PMID: 15332833] |
| Cancer cell lines | IC50 |
<0.4 μM
Compound: Cucurbitacin D
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Growth inhibition of human colon cancer cells
Growth inhibition of human colon cancer cells
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[PMID: 15332833] |
| Cancer cell lines | IC50 |
<0.4 μM
Compound: Cucurbitacin D
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Growth inhibition of human lung cancer cells
Growth inhibition of human lung cancer cells
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[PMID: 15332833] |
| HeLa | IC50 |
0.7 μM
Compound: 3
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Cytotoxicity against human HeLa cells after 24 hrs by MTT assay
Cytotoxicity against human HeLa cells after 24 hrs by MTT assay
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[PMID: 21459003] |
| HepG2 | EC50 |
9 μM
Compound: 3
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Hepatoprotective activity in human HepG2 cells assessed as inhibition of CCl4-induced toxicity after 24 hrs by MTT assay
Hepatoprotective activity in human HepG2 cells assessed as inhibition of CCl4-induced toxicity after 24 hrs by MTT assay
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[PMID: 21459003] |
| HepG2 | IC50 |
77.33 μM
Compound: 3
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Cytotoxicity against human HepG2 cells after 24 hrs assessed as inhibition of cell viability by MTT assay
Cytotoxicity against human HepG2 cells after 24 hrs assessed as inhibition of cell viability by MTT assay
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[PMID: 21459003] |
| HSC-T6 | EC50 |
0.07 μM
Compound: 3
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Antiproliferative activity against serum-stimulated rat HSC-T6 cells after 24 hrs by MTT assay
Antiproliferative activity against serum-stimulated rat HSC-T6 cells after 24 hrs by MTT assay
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[PMID: 21459003] |
| HSC-T6 | IC50 |
26 μM
Compound: 3
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Cytotoxicity against rat HSC-T6 cell after 24 hrs by MTT assay
Cytotoxicity against rat HSC-T6 cell after 24 hrs by MTT assay
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[PMID: 21459003] |
| HT-29 | IC50 |
>10 μM
Compound: 9
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Cytotoxicity against human HT-29 cells after 3 days by mitochondrial transmembrane potential assay
Cytotoxicity against human HT-29 cells after 3 days by mitochondrial transmembrane potential assay
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[PMID: 22239601] |
| HT-29 | IC50 |
0.12 μM
Compound: 9
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Cytotoxicity against human HT-29 cells after 3 days by sulforhodamine B assay
Cytotoxicity against human HT-29 cells after 3 days by sulforhodamine B assay
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[PMID: 22239601] |
| JY | IC50 |
1.36 μM
Compound: 4
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Inhibition of LFA1 expressed in human JY cells interaction with ICAM1-IG expressed in human HeLa cell monolayer after 45 mins by cell adhesion assay
Inhibition of LFA1 expressed in human JY cells interaction with ICAM1-IG expressed in human HeLa cell monolayer after 45 mins by cell adhesion assay
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[PMID: 7852999] |
| MCF7 | GI50 |
0.02 μM
Compound: 2
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Cytotoxicity against human MCF7 cells
Cytotoxicity against human MCF7 cells
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[PMID: 14640532] |
| MCF7 | IC50 |
0.598 μM
Compound: 4
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Cytotoxicity against human MCF7 cells assessed as growth inhibition after 72 hrs by MTS/PMS assay
Cytotoxicity against human MCF7 cells assessed as growth inhibition after 72 hrs by MTS/PMS assay
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[PMID: 25756299] |
| NCI-H460 | GI50 |
0.013 μM
Compound: 2
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Cytotoxicity against human H460 cells
Cytotoxicity against human H460 cells
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[PMID: 14640532] |
| NCI-H460 | IC50 |
0.12 μg/mL
Compound: 5
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Antiproliferative activity against human NCI-H460 cells after 72 hrs
Antiproliferative activity against human NCI-H460 cells after 72 hrs
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[PMID: 17190463] |
| SF-268 | GI50 |
0.021 μM
Compound: 2
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Cytotoxicity against human SF268 cells
Cytotoxicity against human SF268 cells
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[PMID: 14640532] |
| SK-MEL-28 | IC50 |
1.22 μM
Compound: 143
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Cytotoxicity against human SK-MEL-28 cells assessed as growth inhibition
Cytotoxicity against human SK-MEL-28 cells assessed as growth inhibition
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[PMID: 25599949] |
In Vitro
Cucurbitacin D (0.5 μg/mL, 24 h) combined with doxorubicin can induce apoptosis in MCF7/ADR cells and cause G2/M cell cycle arrest[1].
Cucurbitacin D (0.125-16 μg/mL, 24-72 h) significantly inhibits the growth of MCF7 and MCF7/ADR cells in a dose- and time-dependent manner[1].
Cucurbitacin D (0.5-2 μg/mL, 24 h) inhibits STAT3 signaling in MCF7/ADR cells and suppresses the NF-κB signaling pathway[1].
Cucurbitacin D enhances the production of IL-1β in LPS (HY-D1056) induced THP-1, PECs, BMDMs, and RAW264 cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:MCF7/ADR induced by doxorubicin
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Concentration:0.5, 2 μg/mL
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Incubation Time:24 h
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Result:Reduced p-STAT3 levels, increased the expression of IκB and NF-κB in the cytoplasm, and reduced the expression of pNF-κB in the nucleus.
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Cell Line:MCF7, MCF7/ADR
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Concentration:0.125, 0.5, 2, 4, 8, 16 μg/mL
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Incubation Time:24, 48, 72 h
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Result:Inhibited cell proliferation.
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Cell Line:MCF7/ADR
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Concentration:0.5 μg/mL
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Incubation Time:24 h
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Result:Increased apoptosis by 114%.
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Cell Line:MCF7/ADR
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Concentration:0.5 μg/mL
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Incubation Time:24 h
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Result:Induced G2/M cell cycle arrest.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Xenograft cervical cancer cell model in nude mice[3]
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Dosage:1 mg/kg; three times a week; four weeks
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Administration:Intratumoral injection
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Result:Reduced tumor volume and weight, and the expression of pAKT and pSTAT3 proteins was significantly reduced.
Chemical Information
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CAS No. 3877-86-9
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Appearance Solid
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Molecular Weight 516.67
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Formula C30H44O7
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Color White to off-white
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SMILES
C[C@@]([C@@](CC=C(C(C)1C)[C@@]2([H])C[C@H](O)C1=O)([H])[C@@]2(C)C3=O)(C[C@@H](O)[C@]4([H])[C@@](C)(O)C(/C=C/C(C)(O)C)=O)[C@@]4(C3)C
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications (1)
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Journal Impact Factor
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Most Recent
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Biology (Basel)
Transcriptomic and Metabolomic Profiling Reveals the Antiproliferative Mechanism of Goose Serum and Plasma in SW1990 Cells. [Abstract]2026 May 15;15(10):788. PMID: 42187750
Solvent & Solubility
In Vitro:
DMSO : 110 mg/mL (212.90 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 2.75 mg/mL (5.32 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.75 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (27.5 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
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Data Sheet (282 KB)
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SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
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Handling Instructions (2659 KB)
References
[1]. Jin Mo Ku, et al. Cucurbitacin D induces cell cycle arrest and apoptosis by inhibiting STAT3 and NF-κB signaling in doxorubicin-resistant human breast carcinoma (MCF7/ADR) cells. Mol Cell Biochem. 2015 Nov;409(1-2):33-43. [Content Brief]
[2]. Yuan Song, et al. Cucurbitacin D is a new inflammasome activator in macrophages. Int Immunopharmacol. 2013 Dec;17(4):1044-50. [Content Brief]
[3]. Mohammed Sikander, et al. Cucurbitacin D exhibits potent anti-cancer activity in cervical cancer. Sci Rep. 2016 Nov 8:6:36594. [Content Brief]
[4]. Hall JA, et al. Cucurbitacin D Is a Disruptor of the HSP90 Chaperone Machinery. J Nat Prod. 2015 Apr 24;78(4):873-9. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.9355 mL | 9.6774 mL | 19.3547 mL | 48.3868 mL |
| 5 mM | 0.3871 mL | 1.9355 mL | 3.8709 mL | 9.6774 mL | |
| 10 mM | 0.1935 mL | 0.9677 mL | 1.9355 mL | 4.8387 mL | |
| 15 mM | 0.1290 mL | 0.6452 mL | 1.2903 mL | 3.2258 mL | |
| 20 mM | 0.0968 mL | 0.4839 mL | 0.9677 mL | 2.4193 mL | |
| 25 mM | 0.0774 mL | 0.3871 mL | 0.7742 mL | 1.9355 mL | |
| 30 mM | 0.0645 mL | 0.3226 mL | 0.6452 mL | 1.6129 mL | |
| 40 mM | 0.0484 mL | 0.2419 mL | 0.4839 mL | 1.2097 mL | |
| 50 mM | 0.0387 mL | 0.1935 mL | 0.3871 mL | 0.9677 mL | |
| 60 mM | 0.0323 mL | 0.1613 mL | 0.3226 mL | 0.8064 mL | |
| 80 mM | 0.0242 mL | 0.1210 mL | 0.2419 mL | 0.6048 mL | |
| 100 mM | 0.0194 mL | 0.0968 mL | 0.1935 mL | 0.4839 mL |
Cucurbitacin D Related Classifications
HY-N1986 Related Classifications
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