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GW1929 

Cat. No.: HY-15655 Purity: 99.77%
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GW1929 is a potent PPAR-γ agonist, with a pKi of 8.84 for human PPAR-γ, and pEC50s of 8.56 and 8.27 for human PPAR-γ and murine PPAR-γ, respectively.

For research use only. We do not sell to patients.

GW1929 Chemical Structure

GW1929 Chemical Structure

CAS No. : 196808-24-9

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Free Sample (0.5-1 mg)   Apply Now  
10 mM * 1 mL in DMSO USD 119 In-stock
Estimated Time of Arrival: December 31
5 mg USD 108 In-stock
Estimated Time of Arrival: December 31
10 mg USD 180 In-stock
Estimated Time of Arrival: December 31
25 mg USD 396 In-stock
Estimated Time of Arrival: December 31
50 mg USD 708 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 6 publication(s) in Google Scholar

Top Publications Citing Use of Products

    GW1929 purchased from MCE. Usage Cited in: Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3322-3338.

    LAZ3 knock-down decreases NRF2 expression and nuclear translocation, while only the PPARa agonist (GW7647) can prevent this inhibition. Both PPARγ agonist (GW1929) and PPARδ agonist (GW0742) can not reverse these inhibitions.

    GW1929 purchased from MCE. Usage Cited in: Ecotoxicol Environ Saf. 2020 Sep 15;201:110801.

    PPARγ agonist (GW 1929) effectively increased the PPARγ expression. Immunofluorescence staining analysis the expression levels of PPARγ in HK2 cells.

    GW1929 purchased from MCE. Usage Cited in: Ecotoxicol Environ Saf. 2020 Sep 15;201:110801.

    PPARγ agonist (GW 1929) effectively increased the PPARγ expression. Western blotting analysis the expression levels of PPARγ in HK2 cells.

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    • Biological Activity

    • Protocol

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    • References

    • Customer Review

    Description

    GW1929 is a potent PPAR-γ agonist, with a pKi of 8.84 for human PPAR-γ, and pEC50s of 8.56 and 8.27 for human PPAR-γ and murine PPAR-γ, respectively.

    IC50 & Target[1]

    PPAR-γ

    8.56 (pEC50, Human PPAR-γ)

    In Vitro

    GW1929 is a potent PPAR-γ activator, with pKis of 8.84, < 5.5, and < 6.5 for human PPAR-γ, PPAR-α, and PPAR-δ, and pEC50s of 8.56 and 8.27 for human PPAR-γ and murine PPAR-γ, respectively[1]. GW1929 (10 μM) inhibits TBBPA-induced caspase-3 increase and TBBPA-stimulated LDH release in neocortical cell cultures[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    GW1929 (0.5, 1, 5 mg/kg, p.o.) highly decreases nonfasted plasma glucose levels in Zucker diabetic fatty (ZDF) rats after treatment for 14 days, and possesses antilipolytic efficacy. GW1929 (1, 5 mg/kg, p.o.) increases glucose-stimulated insuline secretion of β-cell in ZDF rats[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight

    495.57

    Formula

    C₃₀H₂₉N₃O₄

    CAS No.

    196808-24-9

    SMILES

    O=C(O)[[email protected]](CC1=CC=C(C=C1)OCCN(C)C2=NC=CC=C2)NC3=CC=CC=C3C(C4=CC=CC=C4)=O

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 35 mg/mL (70.63 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.0179 mL 10.0894 mL 20.1788 mL
    5 mM 0.4036 mL 2.0179 mL 4.0358 mL
    10 mM 0.2018 mL 1.0089 mL 2.0179 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (5.04 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (5.04 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    References
    Kinase Assay
    [1]

    Ligand binding to bacterially expressed ligand binding domain (LBD) of hPPAR-γ is determined by scintillation proximity assay (SPA). The assay measures the ability of putative ligands to displace receptor bound [3H]BRL 49653. Assays are conducted in 96-well plates. Wells contained varying concentrations of GW1929 or troglitazone; streptavidin-modified SPA beads to which biotinylates PPAR-γ LBD is prebound; and 10 nM of the specific radioligand [3H]BRL 49653 in a volume of 100 μL. The amount of nonspecific binding, as assessed by control wells that contained 50 μM of the corresponding unlabeled ligand, is subtracted from each data point. For each compound tested, plots of ligand concentration versus counts/min of radioligand bound are constructed, and apparent Ki values are estimated from a nonlinear least squares fit of the data, assuming simple competitive binding. The results are expressed as pKi, where pKi = -log10(KI)[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay
    [2]

    For the experiments, the cells are plated in 96-well plates at a density 2 × 105 cells per cm2 and cultured in the presence of TBBPA, in a concentrations range from 1 nM to 100 μM TBBPA. TBBPA is dissolved in DMSO, resulting in a final vehicle concentration of 0.1 % (v/v). Control (no vehicle) and DMSO-treated wells are included in the experimental design to determine the effect of DMSO. To study whether PPAR-γ is involved in the neurotoxic effect of TBBPA, cells are co-treated with 10 μM TBBPA and 10 μM GW1929 or GW9662. After 6 or 24 h of culture, 100 μL medium is collected for the LDH analysis, and the cells are collected and frozen at −70°C for the caspase-3 activity measurements[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [1]

    Animals are housed at 72°F and 50% relative humidity with a 12-h light and dark cycle, and fed Formulab Diet 5008. Age- (60-day) and glucose-matched male Zucker diabetic fatty rats are gavaged twice daily for 14 days with vehicle (0.05 M N-methylglucamine), GW1929 (0.5, 1.0, or 5.0 mg/kg), or troglitazone (as the milled extrudate, in a suspension in methylcellulose, 50, 150, and 500 mg/kg). Another group of animals receives a mixture of Humulin N and Humulin R by subcutaneous injection twice daily. On days 7 and 14 of dosing, nonfasted measurements of glucose, lactate, insuline, total cholesterol, TGs, F FAs, and hematocrit are obtained. On day 14 of dosing, samples for serum drug levels (2-h postdose) and glycosylated hemoglobin measurements are also collected. In addition, once weekly, three animals from each group are placed in metabolic chambers for 48 h for quantitation of 24-h food and water consumption. Body weights are recorded throughout the study. At the conclusion of the study, perfused pancreas experiments are performed on 12 animals (n = 4 per group) that have received either GW1929 (1 and 5 mg/kg) or vehicle, to directly evaluate the effects of treatment on basal and glucose-stimulated insuline secretion. The remaining animals are killed, and their pancreases are processed for immunocytochemistry[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References

    Purity: 99.77%

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    Keywords:

    GW1929GW 1929GW-1929PPARPeroxisome proliferator-activated receptorsInhibitorinhibitorinhibit

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