Home >> Research Area >>Natural Products>>Steroids>> Ergosterol peroxide

Ergosterol peroxide

CAS# 2061-64-5

Ergosterol peroxide

Catalog No. BCN4897----Order now to get a substantial discount!

Product Name & Size Price Stock
Ergosterol peroxide: 5mg $265 In Stock
Ergosterol peroxide: 10mg Please Inquire In Stock
Ergosterol peroxide: 20mg Please Inquire Please Inquire
Ergosterol peroxide: 50mg Please Inquire Please Inquire
Ergosterol peroxide: 100mg Please Inquire Please Inquire
Ergosterol peroxide: 200mg Please Inquire Please Inquire
Ergosterol peroxide: 500mg Please Inquire Please Inquire
Ergosterol peroxide: 1000mg Please Inquire Please Inquire

Quality Control of Ergosterol peroxide

Number of papers citing our products

Chemical structure

Ergosterol peroxide

3D structure

Chemical Properties of Ergosterol peroxide

Cas No. 2061-64-5 SDF Download SDF
PubChem ID 5351516 Appearance Powder
Formula C28H44O3 M.Wt 428.7
Type of Compound Steroids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
SMILES CC(C)C(C)C=CC(C)C1CCC2C1(CCC3C24C=CC5(C3(CCC(C5)O)C)OO4)C
Standard InChIKey VXOZCESVZIRHCJ-KGHQQZOUSA-N
Standard InChI InChI=1S/C28H44O3/c1-18(2)19(3)7-8-20(4)22-9-10-23-25(22,5)13-12-24-26(6)14-11-21(29)17-27(26)15-16-28(23,24)31-30-27/h7-8,15-16,18-24,29H,9-14,17H2,1-6H3/b8-7+/t19-,20+,21-,22+,23+,24+,25+,26+,27+,28-/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 Ergosterol peroxide

The herbs of Isodon eriocalyx

Biological Activity of Ergosterol peroxide

DescriptionErgosterol peroxide is an inhibitor of osteoclast differentiation, which has antiviral, trypanocidal, antitumor, and antiangiogenic actions, it can stimulate Foxo3a activity by inhibiting pAKT and c-Myc and activating pro-apoptotic protein Puma and Bax to induce cancer cell death.Ergosterol peroxide can ameliorate TGF-β1-induced activation of kidney fibroblasts, it has the potential to be developed as a therapeutic agent to prevent renal fibrosis.
TargetsTGF-β/Smad | ERK | p38MAPK | JNK | STAT | JAK | VEGFR | Akt | CDK | Wnt/β-catenin | Antifection
In vitro

Trypanocidal activity of ergosterol peroxide from Pleurotus ostreatus.[Pubmed: 22083593]

Phytother Res. 2012 Jun;26(6):938-43.

Chagas' disease, which is caused by the protozoan parasite Trypanosoma cruzi, is a public health problem in South America affecting millions of people, and more recently several thousands in countries where the disease is not endemic. Due to the magnitude of the problem, finding a cure for this disease remains a major challenge.
METHODS AND RESULTS:
The aim of this study is to evaluate the trypanocidal activity of Ergosterol peroxide (5α, 8α-epidioxy-22E-ergosta-6, 22-dien-3β-ol) isolated from Pleurotus ostreatus (Jacq.) P. Kumm. f. sp. Florida. The Ergosterol peroxide showed strong trypanocidal activity on the intracellular form of T. cruzi. Ergosterol peroxide had an inhibitory concentration (IC₅₀) of 6.74 µg/mL on T. cruzi, but showed no lytic action on erythrocytes and no cytotoxic effect on mammalian cells at concentrations higher than 1600 µg/mL. The interaction of Trypanosoma cruzi with Ergosterol peroxide in vitro resulted in a strong lytic activity possibly due to the disruption of the parasite membrane.
CONCLUSIONS:
This is the first report of trypanocidal activity, a new biological property of Ergosterol peroxide isolated from Pleurotus ostreatus (Jacq.) P. Kumm. f. sp. Florida.

Ergosterol peroxide isolated from Ganoderma lucidum abolishes microRNA miR-378-mediated tumor cells on chemoresistance.[Pubmed: 22952996]

PLoS One. 2012;7(8):e44579.

Due to an altered expression of oncogenic factors and tumor suppressors, aggressive cancer cells have an intrinsic or acquired resistance to chemotherapeutic agents. This typically contributes to cancer recurrence after chemotherapy. microRNAs are short non-coding RNAs that are involved in both cell self-renewal and cancer development.
METHODS AND RESULTS:
Here we report that tumor cells transfected with miR-378 acquired properties of aggressive cancer cells. Overexpression of miR-378 enhanced both cell survival and colony formation, and contributed to multiple drug resistance. Higher concentrations of chemotherapeutic drugs were needed to induce death of miR-378-transfected cells than to induce death of control cells. We found that the biologically active component isolated from Ganoderma lucidum could overcome the drug-resistance conferred by miR-378. We purified and identified the biologically active component of Ganoderma lucidum as Ergosterol peroxide.
CONCLUSIONS:
We demonstrated that Ergosterol peroxide produced greater activity in inducing death of miR-378 cells than the GFP cells. Lower concentrations of Ergosterol peroxide were needed to induce death of the miR-378-transfected cells than in the control cells. With further clinical development, Ergosterol peroxide represents a promising new reagent that can overcome the drug-resistance of tumor cells.

Inhibition of STAT3 signaling and induction of SHP1 mediate antiangiogenic and antitumor activities of ergosterol peroxide in U266 multiple myeloma cells[Pubmed: 22260501]

Bmc Cancer, 2012, 12(1):1-11.

Ergosterol peroxide (EP) derived from edible mushroom has been shown to exert anti-tumor activity in several cancer cells. In the present study, anti-angiogenic activity of EP was investigated with the underlying molecular mechanisms in human multiple myeloma U266 cells.
METHODS AND RESULTS:
Despite weak cytotoxicity against U266 cells, EP suppressed phosphorylation, DNA binding activity and nuclear translocalization of signal transducer and activator of transcription 3 (STAT3) in U266 cells at nontoxic concentrations. Also, EP inhibited phosphorylation of the upstream kinases Janus kinase 2 (JAK2) and Src in a time-dependent manner. Furthermore, EP increased the expression of protein tyrosine phosphatase SHP-1 at protein and mRNA levels, and conversely silencing of the SHP-1 gene clearly blocked EP-mediated STAT3 inactivation. In addition, EP significantly decreased vascular endothelial growth factor (VEGF), one of STAT3 target genes at cellular and protein levels as well as disrupted in vitro tube formation assay. Moreover, EP significantly suppressed the growth of U266 cells inoculated in female BALB/c athymic nude mice and immunohistochemistry revealed that EP effectively reduced the expression of STAT3 and CD34 in tumor sections compared to untreated control.
CONCLUSIONS:
These findings suggest that EP can exert antitumor activity in multiple myeloma U266 cells partly with antiangiogenic activity targeting JAK2/STAT3 signaling pathway as a potent cancer preventive agent for treatment of multiple myeloma cells.

Antiviral activity of ergosterol peroxide.[Reference: WebLink]

Pharmazie, 1989, 44(44):579-80.

Antiviral activity of Ergosterol peroxide.

Protocol of Ergosterol peroxide

Kinase Assay

Ergosterol peroxide activates Foxo3-mediated cell death signaling by inhibiting AKT and c-Myc in human hepatocellular carcinoma cells[Pubmed: 27058618]

Ergosterol peroxide from Chaga mushroom (Inonotus obliquus) exhibits anti-cancer activity by down-regulation of the β-catenin pathway in colorectal cancer.[Pubmed: 26210065]

Osteoclastogenesis inhibitory effect of ergosterol peroxide isolated from Pleurotus eryngii.[Pubmed: 23074896]

Ergosterol peroxide from Cordyceps cicadae ameliorates TGF-β1-induced activation of kidney fibroblasts.[Pubmed: 24095053]

Phytomedicine. 2014 Feb 15;21(3):372-8.

Chronic kidney disease is a growing public health problem with an urgent need for new pharmacological agents. Ergosterol peroxide (EP) is the major sterol produced by Cordyceps cicadae Shing (C. cicadae), a widely used traditional Chinese medicine. C. cicadae has been used to treat many kinds of diseases and has a potential benefit on renoprotection.
METHODS AND RESULTS:
This study aimed to investigate the anti-fibrotic effects of EP as well as the underlying mechanisms. A normal rat kidney fibroblast cell line (NRK-49F) was stimulated to undergo fibroblast activation by transforming growth factor-β1 (TGF-β1) and EP treatment was applied to explore its potential anti-fibrotic effects. Cell proliferation was investigated using MTT analysis. Fibrosis-associated protein expression was analyzed using immunohistochemistry and/or Western blotting. EP treatment attenuated TGF-β1-induced renal fibroblast proliferation, expression of cytoskeleton protein and CTGF, as well as ECM production. Additionally, EP blocked TGF-β1-stimulated phosphorylation of ERK1/2, p38 and JNK pathway. Moreover, the TGF-β1-induced expression of fibronectin was attenuated by either inhibition of MAPKs or by EP treatment.
CONCLUSIONS:
In conclusion, our findings demonstrate that EP is able to suppress TGF-β1-induced fibroblasts activation in NRK-49F. This new information provides a line of theoretical evidence supporting the use of C. cicadae in the intervention of kidney disease and suggests that EP has the potential to be developed as a therapeutic agent to prevent renal fibrosis.

Nat Prod Commun. 2012 Sep;7(9):1163-4.

Ergosterol peroxide was isolated from the ethanol extract of Pleurotus eryngii as an inhibitor of osteoclast differentiation.
METHODS AND RESULTS:
This compound showed an inhibitory effect in a dose-dependent manner and an inhibition rate of up to 62% with low cytotoxicity, even at a concentration as low as 1.0 microg/mL.

J Ethnopharmacol. 2015 Sep 15;173:303-12.

In this study, we examined the effect of different fractions and components of Chaga mushroom (Inonotus Obliquus) on viability and apoptosis of colon cancer cells. Among them, one component showed the most effective growth inhibition and was identified as Ergosterol peroxide by NMR analysis. We investigated the anti-proliferative and apoptosis mechanisms of Ergosterol peroxide associated with its anti-cancer activities in human colorectal cancer (CRC) cell lines and tested its anti-tumor effect on colitis-induced CRC developed by Azoxymethane (AOM)/Dextran sulfate sodium (DSS) in a mouse model.
METHODS AND RESULTS:
We used MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays, flow cytometry assays, Western blot analysis, colony formation assays, reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry (IHC), and AOM/DSS mouse models to study the molecular mechanism of metastatic activities in CRC cells. Ergosterol peroxide inhibited cell proliferation and also suppressed clonogenic colony formation in HCT116, HT-29, SW620 and DLD-1 CRC cell lines. The growth inhibition observed in these CRC cell lines was the result of apoptosis, which was confirmed by FACS analysis and Western blotting. Ergosterol peroxide inhibited the nuclear levels of β-catenin, which ultimately resulted in reduced transcription of c-Myc, cyclin D1, and CDK-8. Ergosterol peroxide administration showed a tendency to suppress tumor growth in the colon of AOM/DSS-treated mice, and quantification of the IHC staining showed a dramatic decrease in the Ki67-positive staining and an increase in the TUNEL staining of colonic epithelial cells in AOM/DSS-treated mice by Ergosterol peroxide for both prevention and therapy.
CONCLUSIONS:
Our data suggest that Ergosterol peroxide suppresses the proliferation of CRC cell lines and effectively inhibits colitis-associated colon cancer in AOM/DSS-treated mice. Ergosterol peroxide down-regulated β-catenin signaling, which exerted anti-proliferative and pro-apoptotic activities in CRC cells. These properties of Ergosterol peroxide advocate its use as a supplement in colon cancer chemoprevention.

Oncotarget. 2016 Jun 7; 7(23): 33948–33959.

Sterols are the important active ingredients of fungal secondary metabolites to induce death of tumor cells. In our previous study, we found that Ergosterol peroxide (5α, 8α-epidioxiergosta-6, 22-dien-3β-ol), purified from Ganoderma lucidum, induced human cancer cell death.
METHODS AND RESULTS:
Since the amount of purified Ergosterol peroxide is not sufficient to perform in vivo experiments or apply clinically, we developed an approach to synthesize Ergosterol peroxide chemically. After confirming the production of Ergosterol peroxide, we examined the biological functions of the synthetic Ergosterol peroxide. The results showed that Ergosterol peroxide induced cell death and inhibited cell migration, cell cycle progression, and colony growth of human hepatocellular carcinoma cells. We further examined the mechanism associated with this effect and found that treatment with Ergosterol peroxide increased the expression of Foxo3 mRNA and protein in HepG2 cells. The upstream signal proteins pAKT and c-Myc, which can inhibit Foxo3 functions, were clearly decreased in HepG2 cells treated with Ergosterol peroxide. The levels of Puma and Bax, pro-apoptotic proteins, were effectively enhanced.
CONCLUSIONS:
Our results suggest that Ergosterol peroxide stimulated Foxo3 activity by inhibiting pAKT and c-Myc and activating pro-apoptotic protein Puma and Bax to induce cancer cell death.

Ergosterol peroxide Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Ergosterol peroxide Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Ergosterol peroxide

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3326 mL 11.6632 mL 23.3263 mL 46.6527 mL 58.3158 mL
5 mM 0.4665 mL 2.3326 mL 4.6653 mL 9.3305 mL 11.6632 mL
10 mM 0.2333 mL 1.1663 mL 2.3326 mL 4.6653 mL 5.8316 mL
50 mM 0.0467 mL 0.2333 mL 0.4665 mL 0.9331 mL 1.1663 mL
100 mM 0.0233 mL 0.1166 mL 0.2333 mL 0.4665 mL 0.5832 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Ergosterol peroxide

Trypanocidal activity of ergosterol peroxide from Pleurotus ostreatus.[Pubmed:22083593]

Phytother Res. 2012 Jun;26(6):938-43.

Chagas' disease, which is caused by the protozoan parasite Trypanosoma cruzi, is a public health problem in South America affecting millions of people, and more recently several thousands in countries where the disease is not endemic. Due to the magnitude of the problem, finding a cure for this disease remains a major challenge. The aim of this study is to evaluate the trypanocidal activity of Ergosterol peroxide (5alpha, 8alpha-epidioxy-22E-ergosta-6, 22-dien-3beta-ol) isolated from Pleurotus ostreatus (Jacq.) P. Kumm. f. sp. Florida. The Ergosterol peroxide showed strong trypanocidal activity on the intracellular form of T. cruzi. Ergosterol peroxide had an inhibitory concentration (IC(5)(0)) of 6.74 microg/mL on T. cruzi, but showed no lytic action on erythrocytes and no cytotoxic effect on mammalian cells at concentrations higher than 1600 microg/mL. The interaction of Trypanosoma cruzi with Ergosterol peroxide in vitro resulted in a strong lytic activity possibly due to the disruption of the parasite membrane. This is the first report of trypanocidal activity, a new biological property of Ergosterol peroxide isolated from Pleurotus ostreatus (Jacq.) P. Kumm. f. sp. Florida.

Ergosterol peroxide from Cordyceps cicadae ameliorates TGF-beta1-induced activation of kidney fibroblasts.[Pubmed:24095053]

Phytomedicine. 2014 Feb 15;21(3):372-8.

Chronic kidney disease is a growing public health problem with an urgent need for new pharmacological agents. Ergosterol peroxide (EP) is the major sterol produced by Cordyceps cicadae Shing (C. cicadae), a widely used traditional Chinese medicine. C. cicadae has been used to treat many kinds of diseases and has a potential benefit on renoprotection. This study aimed to investigate the anti-fibrotic effects of EP as well as the underlying mechanisms. A normal rat kidney fibroblast cell line (NRK-49F) was stimulated to undergo fibroblast activation by transforming growth factor-beta1 (TGF-beta1) and EP treatment was applied to explore its potential anti-fibrotic effects. Cell proliferation was investigated using MTT analysis. Fibrosis-associated protein expression was analyzed using immunohistochemistry and/or Western blotting. EP treatment attenuated TGF-beta1-induced renal fibroblast proliferation, expression of cytoskeleton protein and CTGF, as well as ECM production. Additionally, EP blocked TGF-beta1-stimulated phosphorylation of ERK1/2, p38 and JNK pathway. Moreover, the TGF-beta1-induced expression of fibronectin was attenuated by either inhibition of MAPKs or by EP treatment. In conclusion, our findings demonstrate that EP is able to suppress TGF-beta1-induced fibroblasts activation in NRK-49F. This new information provides a line of theoretical evidence supporting the use of C. cicadae in the intervention of kidney disease and suggests that EP has the potential to be developed as a therapeutic agent to prevent renal fibrosis.

Inhibition of STAT3 signaling and induction of SHP1 mediate antiangiogenic and antitumor activities of ergosterol peroxide in U266 multiple myeloma cells.[Pubmed:22260501]

BMC Cancer. 2012 Jan 20;12:28.

BACKGROUND: Ergosterol peroxide (EP) derived from edible mushroom has been shown to exert anti-tumor activity in several cancer cells. In the present study, anti-angiogenic activity of EP was investigated with the underlying molecular mechanisms in human multiple myeloma U266 cells. RESULTS: Despite weak cytotoxicity against U266 cells, EP suppressed phosphorylation, DNA binding activity and nuclear translocalization of signal transducer and activator of transcription 3 (STAT3) in U266 cells at nontoxic concentrations. Also, EP inhibited phosphorylation of the upstream kinases Janus kinase 2 (JAK2) and Src in a time-dependent manner. Furthermore, EP increased the expression of protein tyrosine phosphatase SHP-1 at protein and mRNA levels, and conversely silencing of the SHP-1 gene clearly blocked EP-mediated STAT3 inactivation. In addition, EP significantly decreased vascular endothelial growth factor (VEGF), one of STAT3 target genes at cellular and protein levels as well as disrupted in vitro tube formation assay. Moreover, EP significantly suppressed the growth of U266 cells inoculated in female BALB/c athymic nude mice and immunohistochemistry revealed that EP effectively reduced the expression of STAT3 and CD34 in tumor sections compared to untreated control. CONCLUSION: These findings suggest that EP can exert antitumor activity in multiple myeloma U266 cells partly with antiangiogenic activity targeting JAK2/STAT3 signaling pathway as a potent cancer preventive agent for treatment of multiple myeloma cells.

Ergosterol peroxide activates Foxo3-mediated cell death signaling by inhibiting AKT and c-Myc in human hepatocellular carcinoma cells.[Pubmed:27058618]

Oncotarget. 2016 Jun 7;7(23):33948-59.

Sterols are the important active ingredients of fungal secondary metabolites to induce death of tumor cells. In our previous study, we found that Ergosterol peroxide (5alpha, 8alpha-epidioxiergosta-6, 22-dien-3beta-ol), purified from Ganoderma lucidum, induced human cancer cell death. Since the amount of purified Ergosterol peroxide is not sufficient to perform in vivo experiments or apply clinically, we developed an approach to synthesize Ergosterol peroxide chemically. After confirming the production of Ergosterol peroxide, we examined the biological functions of the synthetic Ergosterol peroxide. The results showed that Ergosterol peroxide induced cell death and inhibited cell migration, cell cycle progression, and colony growth of human hepatocellular carcinoma cells. We further examined the mechanism associated with this effect and found that treatment with Ergosterol peroxide increased the expression of Foxo3 mRNA and protein in HepG2 cells. The upstream signal proteins pAKT and c-Myc, which can inhibit Foxo3 functions, were clearly decreased in HepG2 cells treated with Ergosterol peroxide. The levels of Puma and Bax, pro-apoptotic proteins, were effectively enhanced. Our results suggest that Ergosterol peroxide stimulated Foxo3 activity by inhibiting pAKT and c-Myc and activating pro-apoptotic protein Puma and Bax to induce cancer cell death.

Ergosterol peroxide isolated from Ganoderma lucidum abolishes microRNA miR-378-mediated tumor cells on chemoresistance.[Pubmed:22952996]

PLoS One. 2012;7(8):e44579.

Due to an altered expression of oncogenic factors and tumor suppressors, aggressive cancer cells have an intrinsic or acquired resistance to chemotherapeutic agents. This typically contributes to cancer recurrence after chemotherapy. microRNAs are short non-coding RNAs that are involved in both cell self-renewal and cancer development. Here we report that tumor cells transfected with miR-378 acquired properties of aggressive cancer cells. Overexpression of miR-378 enhanced both cell survival and colony formation, and contributed to multiple drug resistance. Higher concentrations of chemotherapeutic drugs were needed to induce death of miR-378-transfected cells than to induce death of control cells. We found that the biologically active component isolated from Ganoderma lucidum could overcome the drug-resistance conferred by miR-378. We purified and identified the biologically active component of Ganoderma lucidum as Ergosterol peroxide. We demonstrated that Ergosterol peroxide produced greater activity in inducing death of miR-378 cells than the GFP cells. Lower concentrations of Ergosterol peroxide were needed to induce death of the miR-378-transfected cells than in the control cells. With further clinical development, Ergosterol peroxide represents a promising new reagent that can overcome the drug-resistance of tumor cells.

Ergosterol peroxide from Chaga mushroom (Inonotus obliquus) exhibits anti-cancer activity by down-regulation of the beta-catenin pathway in colorectal cancer.[Pubmed:26210065]

J Ethnopharmacol. 2015 Sep 15;173:303-12.

AIM OF THE STUDY: In this study, we examined the effect of different fractions and components of Chaga mushroom (Inonotus Obliquus) on viability and apoptosis of colon cancer cells. Among them, one component showed the most effective growth inhibition and was identified as Ergosterol peroxide by NMR analysis. We investigated the anti-proliferative and apoptosis mechanisms of Ergosterol peroxide associated with its anti-cancer activities in human colorectal cancer (CRC) cell lines and tested its anti-tumor effect on colitis-induced CRC developed by Azoxymethane (AOM)/Dextran sulfate sodium (DSS) in a mouse model. MATERIALS AND METHODS: We used MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays, flow cytometry assays, Western blot analysis, colony formation assays, reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry (IHC), and AOM/DSS mouse models to study the molecular mechanism of metastatic activities in CRC cells. RESULTS: Ergosterol peroxide inhibited cell proliferation and also suppressed clonogenic colony formation in HCT116, HT-29, SW620 and DLD-1 CRC cell lines. The growth inhibition observed in these CRC cell lines was the result of apoptosis, which was confirmed by FACS analysis and Western blotting. Ergosterol peroxide inhibited the nuclear levels of beta-catenin, which ultimately resulted in reduced transcription of c-Myc, cyclin D1, and CDK-8. Ergosterol peroxide administration showed a tendency to suppress tumor growth in the colon of AOM/DSS-treated mice, and quantification of the IHC staining showed a dramatic decrease in the Ki67-positive staining and an increase in the TUNEL staining of colonic epithelial cells in AOM/DSS-treated mice by Ergosterol peroxide for both prevention and therapy. CONCLUSION: Our data suggest that Ergosterol peroxide suppresses the proliferation of CRC cell lines and effectively inhibits colitis-associated colon cancer in AOM/DSS-treated mice. Ergosterol peroxide down-regulated beta-catenin signaling, which exerted anti-proliferative and pro-apoptotic activities in CRC cells. These properties of Ergosterol peroxide advocate its use as a supplement in colon cancer chemoprevention.

Osteoclastogenesis inhibitory effect of ergosterol peroxide isolated from Pleurotus eryngii.[Pubmed:23074896]

Nat Prod Commun. 2012 Sep;7(9):1163-4.

Ergosterol peroxide was isolated from the ethanol extract of Pleurotus eryngii as an inhibitor of osteoclast differentiation. This compound showed an inhibitory effect in a dose-dependent manner and an inhibition rate of up to 62% with low cytotoxicity, even at a concentration as low as 1.0 microg/mL.

Keywords:

Ergosterol peroxide,2061-64-5,Natural Products, buy Ergosterol peroxide , Ergosterol peroxide supplier , purchase Ergosterol peroxide , Ergosterol peroxide cost , Ergosterol peroxide manufacturer , order Ergosterol peroxide , high purity Ergosterol peroxide

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: