• ChemFaces is a professional high-purity natural products manufacturer.
  • Product Intended Use
  • 1. Reference standards
  • 2. Pharmacological research
  • 3. Inhibitors
  • Home
  • Natural Products
  • Bioactive
  • Screening Libraries
  • Hot Products
  • Plant Catalog
  • Customer Support
  • Product Use Citation
  • About Us
  • Contact Us
  • Natural Products
    Methyl protodioscin
    Information
    CAS No. 54522-52-0 Price $138 / 20mg
    Catalog No.CFN99585Purity>=98%
    Molecular Weight1063.23Type of CompoundSteroids
    FormulaC52H86O22Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
    How to Order
    Orders via your E-mail:

    1. Product number / Name / CAS No.
    2. Delivery address
    3. Ordering/billing address
    4. Contact information
    Sent to Email: info@chemfaces.com
    Contact Us
    Order & Inquiry & Tech Support

    Tel: (0086)-27-84237683
    Fax: (0086)-27-84254680
    E-mail: manager@chemfaces.com
    Address: No. 83, CheCheng Rd., WETDZ, Wuhan, Hubei 430056, PRC
    Delivery time
    Delivery & Payment method

    1. Usually delivery time: Next day delivery by 9:00 a.m. Order now

    2. We accept: Wire transfer & Credit card & Paypal & Western Union
    * Packaging according to customer requirements(5mg, 10mg, 20mg and more). We shipped via FedEx, DHL, UPS, EMS and others courier.
    Our products had been exported to the following research institutions and universities, And still growing.
  • Copenhagen University (Denmark)
  • Medizinische Universit?t Wien (Austria)
  • The Vancouver Prostate Centre (V... (Canada)
  • John Innes Centre (United Kingdom)
  • University of Eastern Finland (Finland)
  • Charles University in Prague (Czech Republic)
  • FORTH-IMBB (Greece)
  • Universidade Federal de Santa Ca... (Brazil)
  • University of Zurich (Switzerland)
  • Aveiro University (Portugal)
  • Harvard University (USA)
  • More...
  • Package
    Featured Products
    3,6'-Disinapoyl sucrose

    Catalog No: CFN90578
    CAS No: 139891-98-8
    Price: $138/20mg
    Sibiricose A5

    Catalog No: CFN90645
    CAS No: 107912-97-0
    Price: $138/20mg
    Sibiricaxanthone B

    Catalog No: CFN90644
    CAS No: 241125-81-5
    Price: $288/20mg
    Moracin P

    Catalog No: CFN92324
    CAS No: 102841-46-3
    Price: $418/5mg
    Norwogonin

    Catalog No: CFN92218
    CAS No: 4443-09-8
    Price: $388/10mg
    Biological Activity
    Description: Methyl protodioscin has anti-thrombosis, antiosteoporotic, anti-myocardial infarction, and cytotoxic activities. Methyl protodioscin shows strong cytotoxicity against most cell lines from solid tumors with GI50 ≤10.0 microM, but moderate cytotoxicity is shown against leukemia cell lines with GI50 10-30 microM. It potentially increase HDL cholesterol while reducing LDL cholesterol and triglycerides, it also can treat diverse inflammatory pulmonary diseases.
    Targets: LDL | Caspase | Bcl-2/Bax
    In vitro:
    Pharmacogn Mag. 2014 Jul;10(39):318-24.
    Methyl protodioscin induces G2/M cell cycle arrest and apoptosis in A549 human lung cancer cells.[Pubmed: 25210320]
    Methyl protodioscin (MPD) is a furostanol bisglycoside with antitumor properties. It has been shown to reduce proliferation, cause cell cycle arrest. The present study elucidates the mechanism underlying MPD's apoptotic effects, using the A549 human lung cancer cell line.
    METHODS AND RESULTS:
    The human pulmonary adenocarcinoma cell line A549 was obtained from the Cell Bank of the Animal Experiment Center, North School Region, Sun Yat-Sen University. All of the cells were grown in RPMI 1640 supplemented with 10% fetal calf serum (Hyclone, Logan, UT, USA), penicillin (10,000 U/l), and streptomycin (100 mg/l) at 37°C in a 5% CO2 humidified atmosphere. The induction of apoptosis was observed in flow cytometry and fluorescent staining experiments. MPD showed growth inhibitory effects in A549 cells in a dose- and time-dependent manner. The significant G2/M cell cycle arrest and apoptotic effect were also seen in A549 cells treated with MPD. MPD-induced apoptosis was accompanied by a significant reduction of mitochondrial membrane potential, release of mitochondrial cytochrome c to cytosol, activation of caspase-3, downregulation of Bcl-2, p-Bad, and upregulation of Bax.
    CONCLUSIONS:
    Our results show that the induction of apoptosis by MPD involves multiple molecular pathways and strongly suggest that Bcl-2 family proteins signaling pathways. In addition, mitochondrial membrane potential, mitochondrial cytochrome c and caspase-3 were also closely associated with MPD-induced apoptotic process in human A549 cells.
    Cancer Invest. 2003 Jun;21(3):389-93.
    The cytotoxicity of methyl protodioscin against human cancer cell lines in vitro.[Pubmed: 12901285]
    Methyl protodioscin (NSC-698790) was a furostanol saponin isolated from the rhizome of Dioscorea collettii var. hypoglauca (Dioscoreaceae), a Chinese herbal remedy for the treatment of cervical carcinoma, carcinoma of the urinary bladder, and renal tumors for centuries.
    METHODS AND RESULTS:
    To systematically evaluate its potential anticancer activity, Methyl protodioscin was tested cytotoxicity in vitro against human cancer cell lines by the NCI's (National Cancer Institute) anticancer drug screen. As a result, Methyl protodioscin showed strong cytotoxicity against most cell lines from solid tumors with GI50 < or = 10.0 microM, especially selectively against one colon cancer line (HCT-15) and one breast cancer line (MDA-MB-435) with GI50 < 2.0 microM but moderate cytotoxicity was shown against leukemia cell lines with GI50 10-30 microM.
    CONCLUSIONS:
    The data are consistent with the fact that the rhizome of D. collettii var. hypoglauca has been employed for the treatment of solid tumors rather than leukemia in China for centuries. Based on an analysis using the COMPARE computer program with Methyl protodioscin as a seed compound, no compounds in the NCI's anticancer drug screen database have cytotoxicity patterns similar to those of Methyl protodioscin, indicating a potential novel mechanism of anticancer action.
    In vivo:
    Phytomedicine. 2015 May 15;22(5):568-72.
    Dioscin and methylprotodioscin isolated from the root of Asparagus cochinchinensis suppressed the gene expression and production of airway MUC5AC mucin induced by phorbol ester and growth factor.[Pubmed: 25981923 ]
    The root of Asparagus cochinchinensis (Lour.) Merr. has been utilized as mucoregulators and expectorants for controlling the airway inflammatory diseases in folk medicine. We investigated whether dioscin and Methyl protodioscin isolated from the root of Asparagus cochinchinensis (Lour.) Merr. suppress the gene expression and production of airway MUC5AC mucin induced by phorbol ester and growth factor.
    METHODS AND RESULTS:
    Confluent NCI-H292 cells were pretreated with dioscin or Methyl protodioscin for 30 min and then stimulated with EGF or PMA for 24 h. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. (1) Dioscin and Methyl protodioscin suppressed the expression of MUC5AC mucin gene induced by EGF or PMA; (2) dioscin suppressed the production of MUC5AC mucin induced by either EGF at 10(-5) M (p < 0.05) and 10(-6) M (p < 0.05) or PMA at 10(-4) M (p < 0.05), 10(-5) M (p < 0.05) and 10(-6) M (p < 0.05); (3) Methyl protodioscin also suppressed the production of MUC5AC mucin induced by either EGF at 10(-4) M (p < 0.05) or PMA at 10(-4) M (p < 0.05).
    CONCLUSIONS:
    These results suggest that dioscin and Methyl protodioscin isolated from the root of Asparagus cochinchinensis suppress the gene expression and production of MUC5AC mucin, by directly acting on airway epithelial cells, and the results are consistent with the traditional use of Asparagus cochinchinensis as remedy for diverse inflammatory pulmonary diseases.
    Methyl protodioscin Description
    Source: The roots of Dioscorea opposita Thunb.
    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.
    Recent ChemFaces New Products and Compounds
    Bisabolangelone

    Catalog No: CFN91876
    CAS No: 30557-81-4
    Price: $413/5mg
    Chebulagic acid

    Catalog No: CFN92295
    CAS No: 23094-71-5
    Price: $ / mg
    Vitexicarpin

    Catalog No: CFN98172
    CAS No: 479-91-4
    Price: $158/20mg
    Cryptochlorogenic acid

    Catalog No: CFN99117
    CAS No: 905-99-7
    Price: $128/20mg
    Epimedoside A

    Catalog No: CFN90762
    CAS No: 39012-04-9
    Price: $198/10mg
    Liquiritin apioside

    Catalog No: CFN90707
    CAS No: 199796-12-8
    Price: $288/20mg
    6''-O-acetylsaikosaponin A

    Catalog No: CFN95086
    CAS No: 64340-46-1
    Price: $268/10mg
    meso-Hannokinol

    Catalog No: CFN90864
    CAS No: N/A
    Price: $368/5mg
    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.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

    PMID: 29149595

    Scientific Reports 2017 Dec 11;7(1):17332.
    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

    Molecules. 2017 Oct 27;22(11). pii: E1829.
    doi: 10.3390/molecules22111829.

    PMID: 29077044

    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.
    doi: 10.1016/j.phymed.2017.12.030.

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 0.9405 mL 4.7027 mL 9.4053 mL 18.8106 mL 23.5133 mL
    5 mM 0.1881 mL 0.9405 mL 1.8811 mL 3.7621 mL 4.7027 mL
    10 mM 0.0941 mL 0.4703 mL 0.9405 mL 1.8811 mL 2.3513 mL
    50 mM 0.0188 mL 0.0941 mL 0.1881 mL 0.3762 mL 0.4703 mL
    100 mM 0.0094 mL 0.047 mL 0.0941 mL 0.1881 mL 0.2351 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
    Kinase Assay:
    Atherosclerosis. 2015 Apr;239(2):566-70.
    Methyl protodioscin increases ABCA1 expression and cholesterol efflux while inhibiting gene expressions for synthesis of cholesterol and triglycerides by suppressing SREBP transcription and microRNA 33a/b levels.[Pubmed: 25733328]
    Sterol regulatory element-binding proteins (SREBPs) regulate homeostasis of LDL, HDL and triglycerides. This study was aimed to determine if inhibition of SREBPs by Methyl protodioscin (MPD) regulates downstream gene and protein expressions of lipid metabolisms.
    METHODS AND RESULTS:
    In THP-1 macrophages, Methyl protodioscin increases levels of ABCA1 mRNA and protein in dose- and time-dependent manners, and apoA-1-mediated cholesterol efflux. The underlying mechanisms for the effects is that Methyl protodioscin inhibits the transcription of SREBP1c and SREBP2, and decreases levels of microRNA 33a/b hosted in the introns of SREBPs, which leads to reciprocally increase ABCA1 levels. In HepG2 cells, Methyl protodioscin shows the same effects as these observed in THP-1 macrophages.
    CONCLUSIONS:
    Methyl protodioscin also decreases the gene expressions of HMGCR, FAS and ACC for cholesterol and fatty acid synthesis. Methyl protodioscin further promotes LDL receptor through reducing the PCSK9 level. Collectively, the study demonstrates that Methyl protodioscin potentially increase HDL cholesterol while reducing LDL cholesterol and triglycerides.
    Cell Research:
    Planta Med. 2004 Mar;70(3):220-6.
    In vivo antiosteoporotic activity of a fraction of Dioscorea spongiosa and its constituent, 22-O-methylprotodioscin.[Pubmed: 15114498]
    Methyl protodioscin (NSC-698790) was a furostanol saponin isolated from the rhizome of Dioscorea collettii var. hypoglauca (Dioscoreaceae), a Chinese herbal remedy for the treatment of cervical carcinoma, carcinoma of the urinary bladder, and renal tumors for centuries.
    METHODS AND RESULTS:
    To systematically evaluate its potential anticancer activity, Methyl protodioscin was tested cytotoxicity in vitro against human cancer cell lines by the NCI's (National Cancer Institute) anticancer drug screen. As a result, Methyl protodioscin showed strong cytotoxicity against most cell lines from solid tumors with GI50 < or = 10.0 microM, especially selectively against one colon cancer line (HCT-15) and one breast cancer line (MDA-MB-435) with GI50 < 2.0 microM but moderate cytotoxicity was shown against leukemia cell lines with GI50 10-30 microM. The data are consistent with the fact that the rhizome of D. collettii var. hypoglauca has been employed for the treatment of solid tumors rather than leukemia in China for centuries.
    CONCLUSIONS:
    Based on an analysis using the COMPARE computer program with Methyl protodioscin as a seed compound, no compounds in the NCI's anticancer drug screen database have cytotoxicity patterns similar to those of Methyl protodioscin, indicating a potential novel mechanism of anticancer action.
    Animal Research:
    Traditional Chinese Drug Research & Clinical Pharmacology,2008, 19(1):3-5.
    Effects of Methyl Protodioscin on In-Vivo and In-Vitro Thrombosis and Blood Viscosity in Rats[Reference: WebLink]
    To investigate the effects of Methyl protodioscin (MPD ) on in-vitro and in-vivo thrombosis and blood viscosity in rats.
    METHODS AND RESULTS:
    The vitro thrombus was induced by Chandler method,and the length,wet and dry weight of the thrombus were measured. Thrombosis instrument was to observe the in-vivo occlusion time (OT). At the same time,determined the high-,middle-,low-shear blood viscosity as well as the plasma viscosity in rats was determined . Compared to normal group,middle-dose MPD group can delay the OT,and the high-dose group can decrease the length,wet and dry weight of in-vitro thrombus. The blood viscosity is reduced in all groups.
    CONCLUSIONS:
    MPD can inhibit the in-vitro thrombosis,decrease the dry and wet weight of thrombus and delay the OT. Moreover,MPD has the effects of lowering the whole blood viscosity and plasma viscosity.
    Traditional Chinese Drug Research & Clinical Pharmacology,2008, 19(1):1-3.
    Therapeutic Effects of Methyl Protodioscin for Myocardial Infarction in Rats[Reference: WebLink]
    To study the therapeutic effects of Methyl protodioscin (MPD ) on myocardial infarction in rats.
    METHODS AND RESULTS:
    Rat models of myocardial infarction were induced by ligation of coranary artery. Then myocardium infarction area and the vasoactive substance were measured to evaluate the therapeutic effect of MPD on acute myocardial infarction in rats. Compared with the control group,MPD lessened the myocardial infarction size dramatically,inhibited the increase of CK and LDH ,lowered the increased MDA content level and improved the activity of SOD and NO.
    CONCLUSIONS:
    MPD reduces the level of myocardium enzyme and the myocardial infarction size,and increases the capability of clearing oxygen free radical and function of the vascular endothelial cell. MPD by intravenous injection has a better effect than that by oral use.