Cantharidin

Protein phosphatase 1 and 2A inhibitor CAS# 56-25-7

Cantharidin

Catalog No. BCN1280----Order now to get a substantial discount!

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Quality Control of Cantharidin

Number of papers citing our products

Chemical structure

Cantharidin

3D structure

Chemical Properties of Cantharidin

Cas No. 56-25-7 SDF Download SDF
PubChem ID 5944 Appearance White powder
Formula C10H12O4 M.Wt 196.20
Type of Compound Monoterpenoids Storage Desiccate at -20°C
Synonyms Cantharone
Solubility DMSO : 20 mg/mL (101.94 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
SMILES CC12C3CCC(C1(C(=O)OC2=O)C)O3
Standard InChIKey DHZBEENLJMYSHQ-XCVPVQRUSA-N
Standard InChI InChI=1S/C10H12O4/c1-9-5-3-4-6(13-5)10(9,2)8(12)14-7(9)11/h5-6H,3-4H2,1-2H3/t5-,6+,9+,10-
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 Cantharidin

1 Mylabris sp.

Biological Activity of Cantharidin

DescriptionCantharidin, a natural toxicant of blister beetles, is a strong inhibitor of protein phosphatases types 1 (PP1) and 2A (PP2A), and is a novel and potent multidrug resistance (MDR) reversal agent. Cantharidin has anti-tumor activity, it causes oxidative stress that provokes DNA damage and p53-dependent apoptosis, it impairs cell migration and invasion by suppressing MMP-2 and -9 through PI3K/NF-κB signaling pathways.
Targetsp53 | MMP(e.g.TIMP) | ERK | PI3K | FAK | MMP(e.g.TIMP) | COX | NF-kB | p65 | Rho | ROCK | p38MAPK | JNK | PKC | P-gp
In vitro

Cantharidin induces DNA damage and inhibits DNA repair-associated protein expressions in TSGH8301 human bladder cancer cell.[Pubmed: 25667459]

Anticancer Res. 2015 Feb;35(2):795-804.

Cantharidin is an active component of mylabris, which has been used as a traditional Chinese medicine. Cantharidin has been shown to have antitumor activity against several types of human cancers in vitro and in animal models in vivo.
METHODS AND RESULTS:
We investigated whether Cantharidin induces DNA damage and affects DNA damage repair-associated protein levels in TSGH8301 human bladder cancer cells. Using flow cytometry to measure viable cells, Cantharidin was found to reduce the number of viable cells in a dose-dependent manner. Comet assay, 4',6-diamidino-2-phenylindole (DAPI) staining and DNA gel electrophoresis were used to measure DNA damage and condensation; the results indicated that Cantharidin induced DNA damage (comet tail), DNA condensation (white DAPI staining) and DNA damage (DNA smear). Results from western blotting showed that Cantharidin inhibited the expression of DNA-dependent serine/threonine protein kinase, poly-ADP ribose polymerase, phosphate-ataxia-telangiectasia and RAD3-related, O-6-methylguanine-DNA methyltransferase, breast cancer susceptibility protein 1, mediator of DNA damage checkpoint protein 1, phospho-histone H2A.X, but increased that of phosphorylated p53 following 6 and 24 h treatment. Confocal laser microscopy was used to examine the protein translocation; Cantharidin suppressed the levels of p-H2A.X and MDC1 but increased the levels of p-p53 in TSGH8301 cells.
CONCLUSIONS:
In conclusion, we found that Cantharidin-induced cell death may occur through the induction of DNA damage and suppression of DNA repair-associated protein expression in TSGH8301 cells.

Cantharidin reverses multidrug resistance of human hepatoma HepG2/ADM cells via down-regulation of P-glycoprotein expression.[Pubmed: 18703276 ]

Cancer Lett. 2008 Dec 8;272(1):102-9.

Multidrug resistance (MDR) is a serious obstacle encountered in cancer treatment.
METHODS AND RESULTS:
In this study, we established an in vitro multiple drug resistant HepG2 cell line (HepG2/ADM), and characterized its MDR. This model was used to screen potential candidate chemosensitisers from over 200 purified naturally occurring compounds extracted from plants and animals. Cantharidin was found to have a significant reversal on MDR in our model. Further, our results showed that Cantharidin could significantly inhibit P-gp (P-glycoprotein) expression, mRNA transcription, as well as MDR1 promoter activity.
CONCLUSIONS:
These results suggest that Cantharidin is a novel and potent MDR reversal agent and may be a potential adjunctive agent for tumor chemotherapy.

Cantharidin, another natural toxin that inhibits the activity of serine/threonine protein phosphatases types 1 and 2A.[Pubmed: 8397101]

FEBS Lett. 1993 Sep 20;330(3):283-6.

Cantharidin, a natural toxicant of blister beetles, is a strong inhibitor of protein phosphatases types 1 (PP1) and 2A (PP2A).
METHODS AND RESULTS:
Like okadaic acid, Cantharidin inhibits the activity of the purified catalytic subunit of PP2A (IC50 = 0.16 microM) at a lower concentration than that of PP1 (IC50 = 1.7 microM) and only inhibits the activity of protein phosphatase type 2B (PP2B) at high concentrations. Dose-inhibition studies conducted with whole cell homogenates indicate that Cantharidin also inhibits the native forms of these enzymes.
CONCLUSIONS:
Thus, Cantharidin, which is economical and readily available, may be useful as an additional probe for studying the functions of serine/threonine protein phosphatases.

Protocol of Cantharidin

Kinase Assay

cDNA microarray analysis of the effect of cantharidin on DNA damage, cell cycle and apoptosis-associated gene expression in NCI-H460 human lung cancer cells in vitro.[Pubmed: 25815777]

Mol Med Rep. 2015 Jul;12(1):1030-42.

Cantharidin (CTD) induces cytotoxic effects in different types of human cancer cell; however, to date, there have been no studies on the effects of CTD on gene expression in human lung cancer cells and the potential associated signaling pathways.
METHODS AND RESULTS:
Therefore, the present study aimed to investigate how CTD affects the expression of key genes and functional pathways of human H460 lung cancer cells using complementary DNA microarray analysis. Human H460 lung cancer cells were cultured for 24 h in the presence or absence of 10 μM CTD; gene expression was then examined using microarray analysis. The results indicated that 8 genes were upregulated > 4-fold, 29 genes were upregulated >3-4-fold and 156 genes were upregulated >2-3-fold. In addition, 1 gene was downregulated >4 fold, 14 genes were downregulated >3-4-fold and 150 genes were downregulated >2-3 fold in H460 cells following exposure to CTD. It was found that CTD affected DNA damage genes, including DNIT3 and GADD45A, which were upregulated 2.26- and 2.60-fold, respectively, as well as DdiT4, which was downregulated 3.14-fold. In addition, the expression of genes associated with the cell cycle progression were altered, including CCND2, CDKL3 and RASA4, which were upregulated 2.72-, 2.19- and 2.72-fold, respectively; however, CDC42EP3 was downregulated 2.16-fold. Furthermore, apoptosis-associated genes were differentially expressed, including CARD6, which was upregulated 3.54-fold.
CONCLUSIONS:
In conclusion, the present study demonstrated that CTD affected the expression of genes associated with DNA damage, cell cycle progression and apoptotic cell death in human lung cancer H460 cells.

Cell Research

Cantharidin impairs cell migration and invasion of A375.S2 human melanoma cells by suppressing MMP-2 and -9 through PI3K/NF-κB signaling pathways.[Pubmed: 25667452]

Anticancer Res. 2015 Feb;35(2):729-38.

Cancer metastasis is the major cause of cancer patient death. Melanoma is a highly important metastasis in human cancer. Cantharidin (CTD), identified as an active component of natural mylabris (Mylabris phalerata Pallas), induces apoptosis in many human cancer cells.
METHODS AND RESULTS:
In the present study, we investigated the anti-metastasis effects of CTD in human melanoma cancer A375.S2 cells. Flow cytometry was used to measure CTD-induced cytotoxic effects in A375.S2 cells. Wound healing assay indicated that CTD suppressed the migration of A375.S2 cells in a dose-dependent manner. The Matrigel Transwell Assay was used for cell migration and invasion examination and the results showed that CTD inhibited both. Gelatin zymography was used to investigate the activities of MMP-2/9 and the results indicated that CTD inhibited the enzymatic activities of MMP-2/9 in A375.S2 cells. The protein expression of A375.S2 cells following incubation with CTD was examined by western blotting and the results showed that CTD decreased the expression of ERK1/2, PI3K, FAK, MMP-2, -9, COX-2, NF-κB p65, TIMP 1, TIMP 2, VEFG, uPA, Rho A, GRB2, ROCK-1 and Ras, but increased the expressions of p38, JNK, p-c-jun and PKC.
CONCLUSIONS:
Based on those observations, we suggest that CTD may be used as a novel anti-cancer metastasis agent of human melanoma cancer in the future.

Cantharidin Dilution Calculator

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Preparing Stock Solutions of Cantharidin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.0968 mL 25.4842 mL 50.9684 mL 101.9368 mL 127.421 mL
5 mM 1.0194 mL 5.0968 mL 10.1937 mL 20.3874 mL 25.4842 mL
10 mM 0.5097 mL 2.5484 mL 5.0968 mL 10.1937 mL 12.7421 mL
50 mM 0.1019 mL 0.5097 mL 1.0194 mL 2.0387 mL 2.5484 mL
100 mM 0.051 mL 0.2548 mL 0.5097 mL 1.0194 mL 1.2742 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 Cantharidin

Cantharidin, a natural toxin isolated from beetles in the families Meloidae and Oedemeridae, has been reported to be toxic to some pests, including the diamondback moth. IC50 value: Target: In vitro: A 48 h treatment of human erythrocytes with cantharidin significantly increased the percentage of annexin-V-binding cells (≥10 μg/mL), significantly decreased forward scatter (≥25 μg/mL), significantly increased [Ca2+]i (≥25 μg/mL), but did not significantly modify ceramide abundance or ROS [1]. In vivo:

References:
[1]. Alzoubi K, et al. Induction of Suicidal Erythrocyte Death by Cantharidin. Toxins (Basel). 2015 Jul 28;7(8):2822-34. [2]. Huang Z, et al. Lethal and Sublethal Effects of Cantharidin on Development and Reproduction of Plutella xylostella (Lepidoptera: Plutellidae). J Econ Entomol. 2015 Jun;108(3):1054-64. [3]. Shen M, et al. Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mRNA. Sci Rep. 2015 Jul 2;5:11836. [4]. Hsieh FS, et al. Inhibition of protein phosphatase 5 suppresses non-small cell lung cancer through AMP-activated kinase activation. Lung Cancer. 2017 Oct;112:81-89.

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References on Cantharidin

Cantharidin, another natural toxin that inhibits the activity of serine/threonine protein phosphatases types 1 and 2A.[Pubmed:8397101]

FEBS Lett. 1993 Sep 20;330(3):283-6.

Cantharidin, a natural toxicant of blister beetles, is a strong inhibitor of protein phosphatases types 1 (PP1) and 2A (PP2A). Like okadaic acid, Cantharidin inhibits the activity of the purified catalytic subunit of PP2A (IC50 = 0.16 microM) at a lower concentration than that of PP1 (IC50 = 1.7 microM) and only inhibits the activity of protein phosphatase type 2B (PP2B) at high concentrations. Dose-inhibition studies conducted with whole cell homogenates indicate that Cantharidin also inhibits the native forms of these enzymes. Thus, Cantharidin, which is economical and readily available, may be useful as an additional probe for studying the functions of serine/threonine protein phosphatases.

Molecular modes of action of cantharidin in tumor cells.[Pubmed:15710358]

Biochem Pharmacol. 2005 Mar 1;69(5):811-8.

Cancer chemotherapy is often limited by patient's toxicity and tumor drug resistance indicating that new drug development and modification of existing drugs is critical for improving the therapeutic response. Traditional Chinese medicine is a rich source of potential anticancer agents. In particular, Cantharidin (CAN), the active principle ingredient from the blister beetle, Mylabris, has anti-tumor activity, but the cytotoxic mechanism is unknown. In leukemia cells, Cantharidin induces apoptosis by a p53-dependent mechanism. Cantharidin causes both DNA single- and double-strand breaks. Colony-forming assays with knockout and transfectant cells lines showed that DNA polymerase beta, but not ERCC1, conferred increased cell survival after Cantharidin treatment, indicating that base excision repair (BER), rather than nucleotide excision repair (NER), is important for CAN-induced DNA lesions. Oxidative stress-resistant thymic lymphoma-derived WEHI7.2 variants are also more resistant to Cantharidin. These data suggest that Cantharidin treatment causes oxidative stress that provokes DNA damage and p53-dependent apoptosis.

Cantharidin reverses multidrug resistance of human hepatoma HepG2/ADM cells via down-regulation of P-glycoprotein expression.[Pubmed:18703276]

Cancer Lett. 2008 Dec 8;272(1):102-9.

Multidrug resistance (MDR) is a serious obstacle encountered in cancer treatment. In this study, we established an in vitro multiple drug resistant HepG2 cell line (HepG2/ADM), and characterized its MDR. This model was used to screen potential candidate chemosensitisers from over 200 purified naturally occurring compounds extracted from plants and animals. Cantharidin was found to have a significant reversal on MDR in our model. Further, our results showed that Cantharidin could significantly inhibit P-gp (P-glycoprotein) expression, mRNA transcription, as well as MDR1 promoter activity. These results suggest that Cantharidin is a novel and potent MDR reversal agent and may be a potential adjunctive agent for tumor chemotherapy.

cDNA microarray analysis of the effect of cantharidin on DNA damage, cell cycle and apoptosis-associated gene expression in NCI-H460 human lung cancer cells in vitro.[Pubmed:25815777]

Mol Med Rep. 2015 Jul;12(1):1030-42.

Cantharidin (CTD) induces cytotoxic effects in different types of human cancer cell; however, to date, there have been no studies on the effects of CTD on gene expression in human lung cancer cells and the potential associated signaling pathways. Therefore, the present study aimed to investigate how CTD affects the expression of key genes and functional pathways of human H460 lung cancer cells using complementary DNA microarray analysis. Human H460 lung cancer cells were cultured for 24 h in the presence or absence of 10 microM CTD; gene expression was then examined using microarray analysis. The results indicated that 8 genes were upregulated > 4-fold, 29 genes were upregulated >3-4-fold and 156 genes were upregulated >2-3-fold. In addition, 1 gene was downregulated >4 fold, 14 genes were downregulated >3-4-fold and 150 genes were downregulated >2-3 fold in H460 cells following exposure to CTD. It was found that CTD affected DNA damage genes, including DNIT3 and GADD45A, which were upregulated 2.26- and 2.60-fold, respectively, as well as DdiT4, which was downregulated 3.14-fold. In addition, the expression of genes associated with the cell cycle progression were altered, including CCND2, CDKL3 and RASA4, which were upregulated 2.72-, 2.19- and 2.72-fold, respectively; however, CDC42EP3 was downregulated 2.16-fold. Furthermore, apoptosis-associated genes were differentially expressed, including CARD6, which was upregulated 3.54-fold. In conclusion, the present study demonstrated that CTD affected the expression of genes associated with DNA damage, cell cycle progression and apoptotic cell death in human lung cancer H460 cells.

Cantharidin impairs cell migration and invasion of A375.S2 human melanoma cells by suppressing MMP-2 and -9 through PI3K/NF-kappaB signaling pathways.[Pubmed:25667452]

Anticancer Res. 2015 Feb;35(2):729-38.

Cancer metastasis is the major cause of cancer patient death. Melanoma is a highly important metastasis in human cancer. Cantharidin (CTD), identified as an active component of natural mylabris (Mylabris phalerata Pallas), induces apoptosis in many human cancer cells. In the present study, we investigated the anti-metastasis effects of CTD in human melanoma cancer A375.S2 cells. Flow cytometry was used to measure CTD-induced cytotoxic effects in A375.S2 cells. Wound healing assay indicated that CTD suppressed the migration of A375.S2 cells in a dose-dependent manner. The Matrigel Transwell Assay was used for cell migration and invasion examination and the results showed that CTD inhibited both. Gelatin zymography was used to investigate the activities of MMP-2/9 and the results indicated that CTD inhibited the enzymatic activities of MMP-2/9 in A375.S2 cells. The protein expression of A375.S2 cells following incubation with CTD was examined by western blotting and the results showed that CTD decreased the expression of ERK1/2, PI3K, FAK, MMP-2, -9, COX-2, NF-kappaB p65, TIMP 1, TIMP 2, VEFG, uPA, Rho A, GRB2, ROCK-1 and Ras, but increased the expressions of p38, JNK, p-c-jun and PKC. Based on those observations, we suggest that CTD may be used as a novel anti-cancer metastasis agent of human melanoma cancer in the future.

Cantharidin induces DNA damage and inhibits DNA repair-associated protein expressions in TSGH8301 human bladder cancer cell.[Pubmed:25667459]

Anticancer Res. 2015 Feb;35(2):795-804.

Cantharidin is an active component of mylabris, which has been used as a traditional Chinese medicine. Cantharidin has been shown to have antitumor activity against several types of human cancers in vitro and in animal models in vivo. We investigated whether Cantharidin induces DNA damage and affects DNA damage repair-associated protein levels in TSGH8301 human bladder cancer cells. Using flow cytometry to measure viable cells, Cantharidin was found to reduce the number of viable cells in a dose-dependent manner. Comet assay, 4',6-diamidino-2-phenylindole (DAPI) staining and DNA gel electrophoresis were used to measure DNA damage and condensation; the results indicated that Cantharidin induced DNA damage (comet tail), DNA condensation (white DAPI staining) and DNA damage (DNA smear). Results from western blotting showed that Cantharidin inhibited the expression of DNA-dependent serine/threonine protein kinase, poly-ADP ribose polymerase, phosphate-ataxia-telangiectasia and RAD3-related, O-6-methylguanine-DNA methyltransferase, breast cancer susceptibility protein 1, mediator of DNA damage checkpoint protein 1, phospho-histone H2A.X, but increased that of phosphorylated p53 following 6 and 24 h treatment. Confocal laser microscopy was used to examine the protein translocation; Cantharidin suppressed the levels of p-H2A.X and MDC1 but increased the levels of p-p53 in TSGH8301 cells. In conclusion, we found that Cantharidin-induced cell death may occur through the induction of DNA damage and suppression of DNA repair-associated protein expression in TSGH8301 cells.

The protein phosphatase inhibitor cantharidin alters vascular endothelial cell permeability.[Pubmed:10336542]

J Pharmacol Exp Ther. 1999 Jun;289(3):1480-6.

In this study, we characterized the effects of the protein phosphatases type 1 (PP 1) and type 2A (PP 2A) inhibitor Cantharidin in endothelial cells. We identified catalytic subunits of PP 1alpha, PP 2Aalpha, and PP 2Abeta immunologically in bovine aortic endothelial cells. Moreover, we detected mRNAs coding for catalytic subunits of PP 1alpha, PP 1beta, and PP 2Aalpha by hybridization with specific DNA probes in total RNA from these cells. Okadaic acid and Cantharidin inhibited the activities of catalytic subunits of PP 1 (okadaic acid, 0.01-1 microM; Cantharidin, 1-100 microM) and PP 2A (okadaic acid, 0.1 nM to 1 microM; Cantharidin, 0.1-100 microM) separated by column chromatography in a concentration-dependent manner. Moreover, Cantharidin (1 microM to 1 mM) increased the phosphorylation state of endothelial proteins including the regulatory light chains of myosin without affecting cytosolic calcium concentrations. Cantharidin (5-100 microM) increased the permeability of cultured endothelial cells in a time- and concentration-dependent manner. We suggest that inhibition of PP 1 and PP 2A activities by Cantharidin increases endothelial permeability by enhancing the phosphorylation state of endothelial regulatory proteins. Thus, Cantharidin might be a useful tool to study the function of protein phosphatases in endothelial barrier function.

Cantharidin effects on protein phosphatases and the phosphorylation state of phosphoproteins in mice.[Pubmed:7839375]

Toxicol Appl Pharmacol. 1995 Jan;130(1):95-100.

Our earlier studies indicated that the action of Cantharidin (CA) in mice is associated with binding to protein phosphatase 2A in liver cytosol and inhibition of its phosphorylase a phosphatase activity. In this investigation, we find that CA totally inhibits the phosphorylase a phosphatase activity in mouse liver, muscle, and skin cytosol at 5000 nM, with IC50s of 110-250 nM. About 50% of the phosphorylase a phosphatase activity of brain cytosol is sensitive to CA with an IC50 of approximately 80 nM and the remaining half is not inhibited even at 5000 nM. Intraperitoneal treatment of mice with CA leads to a dose-dependent decrease in phosphorylase a phosphatase activity with the aforementioned tissues displaying differential CA sensitivity. At 60 min after a 10 mg/kg CA dose, there is 90-95% inhibition of phosphorylase a phosphatase activity in liver and skin cytosol, 50% in muscle cytosol, and almost no inhibition in brain cytosol. The phosphorylation state of several phosphoproteins examined with tissue cytosol and [gamma-32P]ATP is increased by CA, in a concentration-dependent manner, as follows: endogenous glycogen phosphorylase a in muscle both in vitro and in vivo, and unidentified phosphoproteins in brain (approximately 34 and approximately 75 kDa) and skin (approximately 34 kDa) in vitro. These findings confirm the importance of protein phosphatases as primary targets of CA action in a variety of mouse tissues and, more generally, the possible use of CA and its analogs to investigate and potentially control some processes modulated by the reversible phosphorylation of proteins.

Description

Cantharidin, a natural toxin isolated from beetles in the families Meloidae and Oedemeridae, has been reported to be toxic to some pests, including the diamondback moth.

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