Cinobufotalin

CAS# 1108-68-5

Cinobufotalin

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Quality Control of Cinobufotalin

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Chemical structure

Cinobufotalin

3D structure

Chemical Properties of Cinobufotalin

Cas No. 1108-68-5 SDF Download SDF
PubChem ID 259776 Appearance Powder
Formula C26H34O7 M.Wt 458.54
Type of Compound Steroids Storage Desiccate at -20°C
Solubility DMSO : ≥ 35 mg/mL (76.33 mM)
*"≥" means soluble, but saturation unknown.
SMILES CC(=O)OC1C(C2(CCC3C(C24C1O4)CCC5(C3(CCC(C5)O)C)O)C)C6=COC(=O)C=C6
Standard InChIKey KBKUJJFDSHBPPA-ZNCGZLKOSA-N
Standard InChI InChI=1S/C26H34O7/c1-14(27)32-21-20(15-4-5-19(29)31-13-15)24(3)10-7-17-18(26(24)22(21)33-26)8-11-25(30)12-16(28)6-9-23(17,25)2/h4-5,13,16-18,20-22,28,30H,6-12H2,1-3H3/t16-,17-,18+,20-,21+,22+,23+,24+,25-,26+/m0/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 Cinobufotalin

The glandular body of Bufo bufo gargarizans Cantor

Biological Activity of Cinobufotalin

DescriptionCinobufotalin is a main cardiac toxin in toad, it is a novel anti-HCC agent, it induces growth inhibition and apoptosis in cultured HCC cells through ceramide production. Cinobufotalin is also an effective reversal agent for the multidrug resistance of tumors, it can reverse the adriamycin-resistance in Raji/ADR cells and the expression of P-gp and MRP-1 proteins. Cinobufotalin can promote the dendritic cells(DCs) derived from peripheral blood of patients with chronic hepatitis B to mature and effectively enhance its(the DCs') capabilities, therefore the treatment of cinobufotalin may potentiate the antiviral immunity of the patients with chronic hepatitis B(CHB).
TargetsAkt | P-gp | IL Receptor | MRP-1
In vitro

Ceramide production mediates cinobufotalin-induced growth inhibition and apoptosis in cultured hepatocellular carcinoma cells.[Pubmed: 25724183]

Tumour Biol. 2015 Feb 28.

Hepatocellular carcinoma (HCC) is a highly aggressive and lethal neoplasm with poor prognosis. The aim of this study is to investigate the anticancer activity of Cinobufotalin, a bufadienolide isolated from toad venom, in cultured HCC cells, and to study the underlying mechanisms.
METHODS AND RESULTS:
We found that Cinobufotalin (at nmol/L) significantly inhibited HCC cell growth and survival while inducing considerable cell apoptosis. Further, Cinobufotalin inhibited sphingosine kinase 1 (SphK1) activity and induced pro-apoptotic ceramide production. Ceramide synthase-1 small hairpin RNA (shRNA)-depletion inhibited Cinobufotalin-induced ceramide production and HCC cell apoptosis. On the other hand, the glucosylceramide synthase (GCS) inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) facilitated Cinobufotalin-induced ceramide production and cell apoptosis. SphK1 inhibitor II (SKI-II), similar to Cinobufotalin, increased cellular ceramide level and promoted HCC cell apoptosis. Finally, we observed that Cinobufotalin inactivated Akt-S6K1 signaling in HepG2 cells, which was again inhibited by ceramide synthase-1 shRNA-depletion.
CONCLUSIONS:
In conclusion, the results of this study suggest that Cinobufotalin induces growth inhibition and apoptosis in cultured HCC cells through ceramide production. Cinobufotalin may be investigated as a novel anti-HCC agent.

[Reversal effect of cinobufacini on multidrug resistance of Raji/ADR cells and its mechanisms].[Pubmed: 25338578]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014 Oct;22(5):1306-10.

The aim of this study was to explore the reversing effect of cinobufacini on multidrug resistance of Raji/ADR cells and its mechanisms.
METHODS AND RESULTS:
The growth inhibitory rate, half inhibitory concentration (IC50), reversing multiples to adriamycin- resistance were detected by MTT, and the curve of growth inhibitory rate was drawn; the MDR-1 and MRP-1 gene transcription was determined by RT-PCR; the expressions of P-gp and MRP-1 proteins were assayed by Western blot and flow cytometry. The results showed that the inhibitory rates of cinobufacini on Raji and Raji/ADR cells at 72 h were 75.6% and 69.3% respectively, the IC50 were 3.9 mmol/L and 4.6 mmol/L without significant difference (P > 0.05). The reversing multiples to adriamycin-resistance were 255.7 multiples, the transcription of mdr-1 and mrp-1 genes and the expression of P-gp and MRP-1 proteins significantly decreased (P < 0.05) in Raji/ADR cells after the treatment with Cinobufotalin.
CONCLUSIONS:
It is concluded that Cinobufotalin can reverse the adriamycin-resistance in Raji/ADR cells and the expression of P-gp and MRP-1 proteins were down-regulated through the transcriptional pathway. The Cinobufotalin is an effective reversal agent for the multidrug resistance of tumors.

In vivo

Neutralization of cardiac toxins oleandrin, oleandrigenin, bufalin, and cinobufotalin by digibind: monitoring the effect by measuring free digitoxin concentrations.[Pubmed: 9740315]

Life Sci. 1998;63(9):781-8.

Oleandrin plant poisoning is common in children and the plant extract is used in Chinese medicines. The toxicity is due to oleandrin and the deglycosylated metabolite oleandrigenin. Bufalin and Cinobufotalin (toad cardiac toxins) are also widely used in Chinese medicines like Chan SU, and Lu-Shen -WU. Severe toxicity from bufalin after consumption of toad soup has been reported.
METHODS AND RESULTS:
Taking advantage of structural similarities of these toxins with digitoxin, we demonstrated that these compounds can be rapidly detected in blood by the fluorescence polarization immunoassay for digitoxin. The cross reactivities of these compounds with digoxin assay were much lower. For example, when a drug free serum was supplemented with 10 microg/ml of oleandrin, we observed 127.7 ng/ml of digitoxin equivalent but only 2.4 ng/ml of digoxin equivalent concentration. Digibind neutralized all cardiac toxins studied as evidenced by significant fall of free concentrations. When aliquots of serum pool containing 50.0 microg/ml of oleandrin were supplemented with 0, 10.0, 25.0, 50.0, 100, and 200 microg/ml of digibind, the mean free concentrations were 30.6, 23.3, 16.0, 10.7, 7.8 and 5.5 microg/ml respectively. Similarly, with 50.0 microg/ml of oleandrigenin (total concentration: 36.2 ng/ml), the free concentration was 14.5 ng/ml digitoxin equivalent in the absence of digibind and 5.4 ng/ml in the presence of 200 microg/ml of digibind. In another specimen containing 500 ng/ml bufalin (total concentration: 156.9 ng/ml), the free concentration was 8.6 ng/ml in the absence of digibind and none detected in the presence of 100.0 microg/ml digibind.
CONCLUSIONS:
Because such neutralization may also occur in vivo, digibind may be useful in treating patients exposed to these toxins.

Protocol of Cinobufotalin

Cell Research

Effect of cinobufotalin on the dendritic cells derived from peripheral blood of patients with chronic hepatitis B[Reference: WebLink]

Pharmacology & Clinics of Chinese Materia Medica, 2007, 23(4):54-6.

To study the effect of Cinobufotalin on the morphous,phenotype and function of dendritic cells derived from peripheral blood of patients with chronic hepatitis B(CHB).
METHODS AND RESULTS:
All investigated people were divided into three group: normal control group, CHB group and CHB+Cinobufotalin (CHB+Cino) group. Mononuclear cells from the peripheral blood of patients with CHB and healthy adults were isolated and were cultured in the medium contained GM-CSF(100ng/ml) and IL-4(500u/ml) to induce DCs. After cultured 48 h, Cinobufotalin were added into the culture media of DCs of CHB+Cino grou. On culture day 7, the morphous of DCs was observed and taken pictures; the expression of CD40, HLA-DR, CD80 and CD86 molecules on DCs were detected by flow cytometer; the DCs' capacities of stimulating allogeneic lymphocyte proliferation was assayed with cell count kit 8(CCK8); the concentration of IL-12 in the supernatants of DCs' cultures was detected by ELISA.Compared with healthy controls, the DCs derived from peripheral blood of the patients of CHB group displayed immature cell morphous and had lower expression of surface molecules and lower capacities of stimulating allogeneic lymphocyte proliferation and secreting IL-12. But compared with the CHB group, the DCs incubated with Cinobufotalin( CHB+Cino group) displayed mature cell appearance like normal people's DCs and had higher expression of surface molecules including CD40, CD80 and CD86, and the abilities of stimulating allogeneic lymphocyte proliferation and secreting IL-12 of the DCs of CHB+Cino group were obviously higher.
CONCLUSIONS:
Cinobufotalin can promote the DCs derived from peripheral blood of patients with chronic hepatitis B to mature and effectively enhance its(the DCs') capabilities, therefore the treatment of Cinobufotalin may potentiate the antiviral immunity of the patients with CHB.

Cinobufotalin Dilution Calculator

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Preparing Stock Solutions of Cinobufotalin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.1808 mL 10.9042 mL 21.8083 mL 43.6167 mL 54.5209 mL
5 mM 0.4362 mL 2.1808 mL 4.3617 mL 8.7233 mL 10.9042 mL
10 mM 0.2181 mL 1.0904 mL 2.1808 mL 4.3617 mL 5.4521 mL
50 mM 0.0436 mL 0.2181 mL 0.4362 mL 0.8723 mL 1.0904 mL
100 mM 0.0218 mL 0.109 mL 0.2181 mL 0.4362 mL 0.5452 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 Cinobufotalin

Cinobufotalin is one of the bufadienolides prepared from toad venom; has anticancer activity. IC50 value: Target: in vitro: Cinobufotalin(CB) caused significant DNA fragmentation, decrease of MMP, and an increase in the intracellular Ca(2+) ion and ROS production. In addition, CB induced upregulation of Fas protein, proteolytic activation of cytochrome c, caspase-2, -3, -8 and -9 together with the activation of Bid and Bax [1]. cinobufotalin displayed considerable cytotoxicity against lung cancer cells (A549, H460 and HTB-58 lines) without inducing significant cell apoptosis. cinobufotalin mainly induces Cyp-D-dependent non-apoptotic death in cultured lung cancer cells [2]. cinobufotalin (at nmol/L) significantly inhibited HCC cell growth and survival while inducing considerable cell apoptosis. Further, cinobufotalin inhibited sphingosine kinase 1 (SphK1) activity and induced pro-apoptotic ceramide production. cinobufotalin inactivated Akt-S6K1 signaling in HepG2 cells, which was again inhibited by ceramide synthase-1 shRNA-depletion [3]. in vivo: Using a mice xenograft model, we found that cinobufotalin inhibited A549 lung cancer cell growth in vivo [2].

References:
[1]. Kai S, et al. Pre-clinical evaluation of cinobufotalin as a potential anti-lung cancer agent. Biochem Biophys Res Commun. 2014 Sep 26;452(3):768-74. [2]. Cheng L, et al. Ceramide production mediates cinobufotalin-induced growth inhibition and apoptosis in cultured hepatocellular carcinoma cells. Tumour Biol. 2015 Feb 28. [3]. Emam H, et al. Apoptotic cell death by the novel natural compound, cinobufotalin. Chem Biol Interact. 2012 Sep 30;199(3):154-60.

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References on Cinobufotalin

Ceramide production mediates cinobufotalin-induced growth inhibition and apoptosis in cultured hepatocellular carcinoma cells.[Pubmed:25724183]

Tumour Biol. 2015 Aug;36(8):5763-71.

Hepatocellular carcinoma (HCC) is a highly aggressive and lethal neoplasm with poor prognosis. The aim of this study is to investigate the anticancer activity of Cinobufotalin, a bufadienolide isolated from toad venom, in cultured HCC cells, and to study the underlying mechanisms. We found that Cinobufotalin (at nmol/L) significantly inhibited HCC cell growth and survival while inducing considerable cell apoptosis. Further, Cinobufotalin inhibited sphingosine kinase 1 (SphK1) activity and induced pro-apoptotic ceramide production. Ceramide synthase-1 small hairpin RNA (shRNA)-depletion inhibited Cinobufotalin-induced ceramide production and HCC cell apoptosis. On the other hand, the glucosylceramide synthase (GCS) inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) facilitated Cinobufotalin-induced ceramide production and cell apoptosis. SphK1 inhibitor II (SKI-II), similar to Cinobufotalin, increased cellular ceramide level and promoted HCC cell apoptosis. Finally, we observed that Cinobufotalin inactivated Akt-S6K1 signaling in HepG2 cells, which was again inhibited by ceramide synthase-1 shRNA-depletion. In conclusion, the results of this study suggest that Cinobufotalin induces growth inhibition and apoptosis in cultured HCC cells through ceramide production. Cinobufotalin may be investigated as a novel anti-HCC agent.

Neutralization of cardiac toxins oleandrin, oleandrigenin, bufalin, and cinobufotalin by digibind: monitoring the effect by measuring free digitoxin concentrations.[Pubmed:9740315]

Life Sci. 1998;63(9):781-8.

Oleandrin plant poisoning is common in children and the plant extract is used in Chinese medicines. The toxicity is due to oleandrin and the deglycosylated metabolite oleandrigenin. Bufalin and Cinobufotalin (toad cardiac toxins) are also widely used in Chinese medicines like Chan SU, and Lu-Shen -WU. Severe toxicity from bufalin after consumption of toad soup has been reported. Taking advantage of structural similarities of these toxins with digitoxin, we demonstrated that these compounds can be rapidly detected in blood by the fluorescence polarization immunoassay for digitoxin. The cross reactivities of these compounds with digoxin assay were much lower. For example, when a drug free serum was supplemented with 10 microg/ml of oleandrin, we observed 127.7 ng/ml of digitoxin equivalent but only 2.4 ng/ml of digoxin equivalent concentration. Digibind neutralized all cardiac toxins studied as evidenced by significant fall of free concentrations. When aliquots of serum pool containing 50.0 microg/ml of oleandrin were supplemented with 0, 10.0, 25.0, 50.0, 100, and 200 microg/ml of digibind, the mean free concentrations were 30.6, 23.3, 16.0, 10.7, 7.8 and 5.5 microg/ml respectively. Similarly, with 50.0 microg/ml of oleandrigenin (total concentration: 36.2 ng/ml), the free concentration was 14.5 ng/ml digitoxin equivalent in the absence of digibind and 5.4 ng/ml in the presence of 200 microg/ml of digibind. In another specimen containing 500 ng/ml bufalin (total concentration: 156.9 ng/ml), the free concentration was 8.6 ng/ml in the absence of digibind and none detected in the presence of 100.0 microg/ml digibind. Because such neutralization may also occur in vivo, digibind may be useful in treating patients exposed to these toxins.

[Reversal effect of cinobufacini on multidrug resistance of Raji/ADR cells and its mechanisms].[Pubmed:25338578]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014 Oct;22(5):1306-10.

The aim of this study was to explore the reversing effect of cinobufacini on multidrug resistance of Raji/ADR cells and its mechanisms. The growth inhibitory rate, half inhibitory concentration (IC50), reversing multiples to adriamycin- resistance were detected by MTT, and the curve of growth inhibitory rate was drawn; the MDR-1 and MRP-1 gene transcription was determined by RT-PCR; the expressions of P-gp and MRP-1 proteins were assayed by Western blot and flow cytometry. The results showed that the inhibitory rates of cinobufacini on Raji and Raji/ADR cells at 72 h were 75.6% and 69.3% respectively, the IC50 were 3.9 mmol/L and 4.6 mmol/L without significant difference (P > 0.05). The reversing multiples to adriamycin-resistance were 255.7 multiples, the transcription of mdr-1 and mrp-1 genes and the expression of P-gp and MRP-1 proteins significantly decreased (P < 0.05) in Raji/ADR cells after the treatment with Cinobufotalin. It is concluded that Cinobufotalin can reverse the adriamycin-resistance in Raji/ADR cells and the expression of P-gp and MRP-1 proteins were down-regulated through the transcriptional pathway. The Cinobufotalin is an effective reversal agent for the multidrug resistance of tumors.

Description

Cinobufotalin is a cardiotonic steroids or bufadienolides, is extracted from the skin secretions of the giant toads. Cinobufotalin has been used as a cardiotonic, diuretic and a hemostatic agent, Cinobufotalin is also a potential anti-lung cancer agent.

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