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    Daucosterol
    Information
    CAS No. 474-58-8 Price $118 / 20mg
    Catalog No.CFN98713Purity>=98%
    Molecular Weight576.9 Type of CompoundSteroids
    FormulaC35H60O6Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $55.2 / In-stock
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    10 mM * 1 mL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: Daucosterol has neuroprotective activity, it has proliferation-enhancing activity for neural stem cells (NSCs), may be involved in IGF1-AKT pathway, and it as an efficient and inexpensive growth factor alternative that could be potentially developed as a medicine for ischemic stroke treatment, can significantly reduce neuronal loss.Daucosterol exhibits moderate antibacterial activity against Bacillus subtilis and Staphylococcus aureus; it has anti-cancer and apoptotic effects in human colon cancer cell line HCT-116, at different doses induces cell cycle arrest at sub-G1 phase of the cell cycle.
    Targets: IGF-1R | Akt | Bcl-2/Bax | Caspase | GSK-3 | Antifection | IFN-γ | IL Receptor | ROS | gp120/CD4
    In vitro:
    J Steroid Biochem Mol Biol. 2014 Mar;140:90-9.
    Daucosterol promotes the proliferation of neural stem cells.[Pubmed: 24333794]
    Neural stem cells (NSCs) are self-regenerating cells, but their regenerative capacity is limited.
    METHODS AND RESULTS:
    The present study was conducted to investigate the effect of Daucosterol (a sterolin) on the promotion of NSC proliferation and determine the corresponding molecular mechanism. Results of cell counting kit-8 (CCK-8) assay showed that Daucosterol significantly increased the quantity of viable cells and the effectiveness of Daucosterol was similar to that of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). Flow cytometry detection of CFSE-labeled (CFSE, carboxyfluorescein diacetate succinimidyl ester) NSCs showed that Div Index (or the average number of cell divisions) and % Divided (or the percentage of cells that divided at least once) of the cells were increased, indicating that Daucosterol increased the percentage of NSCs re-entering the cell cycle. mRNA microarray analysis showed that 333 genes that are mostly involved in the mitotic cell cycle were up-regulated. By contrast, 627 genes that are mostly involved in differentiation were down-regulated. In particular, insulin-like growth factor I (IGF1) was considered as an important regulatory gene that functionally promoted NSC proliferation, and the increased expression of IGF1 protein was validated by ELISA. In addition, the phosphorylation of AKT was increased, indicating that the proliferation-enhancing activity of Daucosterol may be involved in IGF1-AKT pathway.
    CONCLUSIONS:
    Our study provided information about Daucosterol as an efficient and inexpensive growth factor alternative that could be used in clinical medicine and research applications.
    J Steroid Biochem Mol Biol. 2015 Apr 9;152:45-52.
    Daucosterol protects neurons against oxygen-glucose deprivation/reperfusion-mediated injury by activating IGF1 signaling pathway.[Pubmed: 25864625]
    We previously reported that Daucosterol (a sterolin) up-regulates the expression of insulin-like growth factor I (IGF1)(1) protein in neural stem cells.
    METHODS AND RESULTS:
    In this study, we investigated the effects of Daucosterol on the survival of cultured cortical neurons after neurons were subjected to oxygen and glucose deprivation and simulated reperfusion (OGD/R)(2), and determined the corresponding molecular mechanism. The results showed that post-treatment of Daucosterol significantly reduced neuronal loss, as well as apoptotic rate and caspase-3 activity, displaying the neuroprotective activity. We also found that Daucosterol increased the expression level of IGF1 protein, diminished the down-regulation of p-AKT(3) and p-GSK-3β(4), thus activating the AKT(5) signal pathway. Additionally, it diminished the down-regulation of the anti-apoptotic proteins Mcl-1(6) and Bcl-2(7), and decreased the expression level of the pro-apoptotic protein Bax(8), thus raising the ratio of Bcl-2/Bax. The neuroprotective effect of Daucosterol was inhibited in the presence of picropodophyllin (PPP)(9), the inhibitor of insulin-like growth factor I receptors (IGF1R)(10).
    CONCLUSIONS:
    Our study provided information about Daucosterol as an efficient and inexpensive neuroprotectants, to which the IGF1-like activity of Daucosterol contributes. Daucosterol could be potentially developed as a medicine for ischemic stroke treatment.
    Nat Prod Res. 2007 Aug;21(10):889-96.
    A novel daucosterol derivative and antibacterial activity of compounds from Arctotis arctotoides.[Pubmed: 17680499]
    Arctotis arctotoides is a perennial herb used medicinally for the treatment of various ailments in the Eastern Cape, South Africa. Different extracts of the plant were investigated for their antimicrobial constituents.
    METHODS AND RESULTS:
    This led to the isolation and identification of a new Daucosterol derivative 3-O-[beta-D-(6'-nonadeanoate)glucopyranosyl]-beta-sitosterol and seven known compounds namely: serratagenic acid, stigmasterol, Daucosterol, zaluzanin D, dehydrocostuslactone, nepetin, and pedalitin. The structures of the compounds were elucidated on the basis of spectral analysis, including homo and hetero nuclear correlation NMR experiments (COSY, NOESY, HMQC, HMBC) and mass spectra as well as by comparison with available data in the literature. The compounds exhibited antibacterial activity except stigmasterol, Daucosterol and dehydrocostuslactone.
    CONCLUSIONS:
    Nepetin was the most active against Bacillus subtilis and Staphylococcus aureus with the minimum inhibitory concentrations of 4 microg mL( - 1) and 31 microg mL( - 1), respectively, while others exhibited moderate activity.
    In vivo:
    Vaccine. 2007 May 10;25(19):3834-40.
    Immunoregulatory activity by daucosterol, a beta-sitosterol glycoside, induces protective Th1 immune response against disseminated Candidiasis in mice.[Pubmed: 17335944 ]

    METHODS AND RESULTS:
    In the present study, we investigated immunomodulatory effect of Daucosterol, a beta-sitosterol glycoside, against disseminated candidiasis caused by Candida albicans. Results showed that direct interaction of Daucosterol with C. albicans yeast cells resulted in no growth-inhibition by in vitro susceptibility analysis. In contrast, mice given Daucosterol (DS) intraperitoneally before intravenous challenge with live C. albicans yeast cells survived longer than DS-untreated control mice against disseminated candidiasis (P<0.05). By assessment of the fungal CFU in kidneys, DS-treated mice before the challenge developed about 81% fewer kidney CFU than untreated controls. This protection was removable by pretreatment of mice with anti-CD4+ antibody before the DS-treatment and challenge with the yeast. However, the protection was transferable by the CD4+ T cells from DS-treated mice not infected with the yeast. ELISA analysis revealed there were predominant production of IFNgamma and IL-2 cytokines as compared to IL-4, and IL-10 productions in DS-treated mice. By treatment of DS-given mice with anti-mouse IFNgamma, the protection was also abolished.
    CONCLUSIONS:
    Our studies show that DS protects mice against disseminated candidiasis by the CD4+ Th1 immune response.
    Daucosterol Description
    Source: The herbs of Dioscorea nipponica Makino
    Solvent: DMSO, Pyridine, Methanol, Ethanol, 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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    IF=36.216(2019)

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.7334 mL 8.667 mL 17.334 mL 34.6681 mL 43.3351 mL
    5 mM 0.3467 mL 1.7334 mL 3.4668 mL 6.9336 mL 8.667 mL
    10 mM 0.1733 mL 0.8667 mL 1.7334 mL 3.4668 mL 4.3335 mL
    50 mM 0.0347 mL 0.1733 mL 0.3467 mL 0.6934 mL 0.8667 mL
    100 mM 0.0173 mL 0.0867 mL 0.1733 mL 0.3467 mL 0.4334 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.
    Protocol
    Cell Research:
    Life Sci. 2015 Sep 15;137:37-43.
    Daucosterol inhibits cancer cell proliferation by inducing autophagy through reactive oxygen species-dependent manner.[Pubmed: 26209138]
    This study aims to evaluate the anti-cancer effect of Daucosterol and explore its possible mechanism.
    METHODS AND RESULTS:
    MTT and colony formation assay were performed to determine the effect of Daucosterol on cancer cell proliferation in vitro. H22 allograft model was used for the assessment of its anti-cancer activity in vivo. Intracellular generation of reactive oxygen species (ROS) was measured using DCFH-DA probe with flow cytometry system and a laser scanning confocal microscope. LC3 (microtubule-associated protein 1 light chain 3)-II conversion was monitored with immunofluorescence and immunoblotting to demonstrate Daucosterol-induced autophagy. We found that Daucosterol inhibits the proliferation of human breast cancer cell line MCF-7 and gastric cancer cell lines MGC803, BGC823 and AGS in a dose-dependent manner. Furthermore, Daucosterol inhibits murine hepatoma H22 cell growth in ICR mice. Daucosterol treatment induces intracellular ROS generation and autophagy, but not apoptotic cell death. Treatment with ROS scavenger GSH (reduced glutathione), NAC (N-acetyl-l-cysteine) or autophagy inhibitor 3-Methyladenine (3-MA) counteracted Daucosterol-induced autophagy and growth inhibition in BGC823 and MCF-7 cancer cells.
    CONCLUSIONS:
    Daucosterol inhibits cancer cell proliferation by inducing autophagy through ROS-dependent manner and could be potentially developed as an anti-cancer agent.
    Bangladesh Journal of Pharmacology, 2016, 11(2):395.
    Daucosterol inhibits colon cancer growth by inducing apoptosis, inhibiting cell migration and invasion and targeting caspase signalling pathway.[Reference: WebLink]
    The aim of the present investigation was to examine and demonstrate in detail the anti-cancer and apoptotic effects of Daucosterol in human colon cancer cell line HCT-116.
    METHODS AND RESULTS:
    The effects of this compound on cell migration, cell invasion, cell cycle analysis and caspase signalling pathway were also studied. Cell viability was evaluated by MTT assay using different doses of the drug. In vitro wound healing assay was used to study cell migration. Flow cytometry was involved to examine cell apoptosis as well as cell cycle phase distribution. Daucosterol induced significant, dose-dependent as well as time-dependent cytotoxic effects with IC50 values of 26.6 and 47.3 μM at 24 and 48 hours time intervals respectively. The percent of cells that migrated decreased from 99% in case of untreated control to 84.2, 45.2, 39.5 and 14.4% in groups treated with 0, 5, 50, 75 and 100 μM of Daucosterol respectively. Percentage of apoptotic cells increased from 2.5% in untreated control cells to 23.6, 46.9 and 74.2% in cells treated with 5, 50 and 100 μM dose of Daucosterol respectively.
    CONCLUSIONS:
    Daucosterol at different doses induced cell cycle arrest at sub-G1 phase of the cell cycle.