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    Ergosterol peroxide
    CAS No. 2061-64-5 Price $238 / 5mg
    Catalog No.CFN98035Purity>=98%
    Molecular Weight428.7 Type of CompoundSteroids
    FormulaC28H44O3Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Ergosterol 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.
    Targets: TGF-β/Smad | ERK | p38MAPK | JNK | STAT | JAK | VEGFR | Akt | CDK | Wnt/β-catenin | Antifection
    In vitro:
    Phytother Res. 2012 Jun;26(6):938-43.
    Trypanocidal activity of ergosterol peroxide from Pleurotus ostreatus.[Pubmed: 22083593]
    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 (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.
    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.
    PLoS One. 2012;7(8):e44579.
    Ergosterol peroxide isolated from Ganoderma lucidum abolishes microRNA miR-378-mediated tumor cells on chemoresistance.[Pubmed: 22952996]
    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.
    Bmc Cancer, 2012, 12(1):1-11.
    Inhibition of STAT3 signaling and induction of SHP1 mediate antiangiogenic and antitumor activities of ergosterol peroxide in U266 multiple myeloma cells[Pubmed: 22260501]
    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.
    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.
    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.
    Pharmazie, 1989, 44(44):579-80.
    Antiviral activity of ergosterol peroxide.[Reference: WebLink]
    Antiviral activity of Ergosterol peroxide.
    Ergosterol peroxide Description
    Source: The herbs of Isodon eriocalyx
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Phytomedicine. 2014 Feb 15;21(3):372-8.
    Ergosterol peroxide from Cordyceps cicadae ameliorates TGF-β1-induced activation of kidney fibroblasts.[Pubmed: 24095053]
    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-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.
    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.
    Osteoclastogenesis inhibitory effect of ergosterol peroxide isolated from Pleurotus eryngii.[Pubmed: 23074896]
    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.
    J Ethnopharmacol. 2015 Sep 15;173:303-12.
    Ergosterol peroxide from Chaga mushroom (Inonotus obliquus) exhibits anti-cancer activity by down-regulation of the β-catenin pathway in colorectal cancer.[Pubmed: 26210065]
    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.
    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.
    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.
    Ergosterol peroxide activates Foxo3-mediated cell death signaling by inhibiting AKT and c-Myc in human hepatocellular carcinoma cells[Pubmed: 27058618]
    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.
    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.