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Troglitazone

Troglitazone is a thiazolidinedione antidiabetic agent used to treat type 2 diabetes mellitus.
It acts as a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, enhancing insulin sensitivity and glucose homeostasis.
Troglitazone has been associated with rare but serious liver toxicity, leading to its withdrawal from the market in many countries.
Researchers studying troglitazone must carefully optimize their protocols to ensure reproducibility and accuracy, leveraging the power of AI-driven platforms like PubCompare.ai to identify the best published methods and products.
This MeSH term provides a concise overview of troglitazone's pharmacology and clinical use, as well as the importance of rigorous experimental design in this area of diabetes research.

Most cited protocols related to «Troglitazone»

The human urothelial cell line HBLAK, spontaneously outgrown from a standard lot of normal human uroepithelial cells, was kindly provided by CELLnTEC (Switzerland), from where the cell line is commercially available. This culture was established from morphologically inconspicuous primary urothelium taken from the urinary bladder of an 80 years old male patient who underwent surgery for a disease other than genitourinary cancer. The patient was not diagnosed for bladder cancer at the time of the surgery. Due to ethical guidelines no further follow-up data is available for the donor. HBLAK cells were cultured according to the manufacturer’s recommendation in serum-free CnT-Prime Epithelial Culture Medium (CELLnTEC) at 37°C and with 5%  CO2.
To study their differentiation capacity the cells were seeded subconfluently into 6-well plates and subsequently treated according to various published protocols [2, 3 (link)]. In one protocol, EGFR inhibition and PPARγ activation were achieved by treatment with 1 μM PD153035 (Merck, Germany) and 1 μM Troglitazone (Cayman, USA) in CnT-Prime Epithelial Culture Medium (ready to use and supplemented with EGF, CELLnTEC) or in KFSM medium without supplemented EGF (Life Technologies, Germany) for seven days, during which the medium was changed twice. For some experiments 5% FBS (Biochrom, Germany) was added to cells in CnT-Prime Medium. For a second, calcium-based protocol near-confluent cultures were maintained in CnT-Prime Medium supplemented with CaCl2 to a final concentration of 2 mM, with additional 5% FBS in some experiments, for a period of 10–14 days. The medium was changed every 3 days.
For comparison, primary cultures of normal urothelial cells (NHUC) were established from healthy ureters removed during tumor nephrectomy. These samples were collected with informed consent of the patients and their use was approved by the Ethics Committee of the Medical Faculty of the Heinrich-Heine-University, study number 1788. The cells were cultured as published previously [8 (link)] in KFSM medium supplemented with 5 ng/ml EGF and 50 μg/ml bovine pituitary extract (Life Technologies).
TERT-NHUC cells, kindly provided by Prof. M.A. Knowles, University of Leeds, UK, were cultured as previously described [9 (link)].
Publication 2016
Bos taurus Caimans Calcium Cancer of Bladder Cell Culture Techniques Cell Lines Cells EGFR protein, human Ethics Committees Faculty, Medical Genitourinary Cancer Homo sapiens Males Neoplasms Nephrectomy Operative Surgical Procedures Patients PD 153035 PPAR gamma Psychological Inhibition Serum TERT protein, human Tissue Donors Troglitazone Ureter Urinary Bladder Urothelium
HOF cells prepared as above were cultured in 100-mm or 150-mm dishes until reaching 90% to 100% confluence, washed with PBS twice, detached by 0.25% trypsin-EDTA, resuspended with a growth medium, and centrifuged at 300×g for 5 minutes. 3D organoid preparations were carried out on hanging drop culture plates (HDP1385; Sigma-Aldrich, St. Louis, MO, USA) as described recently.32 (link) Briefly, the cell pellet obtained as above was resuspended in a growth medium containing 0.25% METHOCEL (DuPont Nutrition & Biosciences, Copenhagen, Denmark) to stimulate morphological stability. Approximately 20,000 cells in a 28-µL drop were placed in each well of a hanging drop culture plate (day 0). Thereafter, 14 µL of the culture medium was removed and a fresh 14 µL of the culture medium was added to each well every day until day 12 for HOFs. During the course of the 3D culture, HOFs grew into a sphenoid-shaped organoid. Adipogenic differentiation of HOFs was induced by a cocktail containing 250-nM dexamethasone, 10-nM T3, 10 µg/ml insulin, and 10-mM troglitazone from day 1 through day 5. This was followed by the use of a cocktail containing 10 µg/ml insulin and 10-mM troglitazone from day 6 through day 11 for HOFs in the presence or absence of 100-µM BIM or 100-µM prostaglandin F2α (PGF2α). 3D cell organoids of HOFs at day 12 were collected for RNA preparation or immunostaining. As a control, 3D culture cells were treated as above in the growth medium containing 0.1% dimethyl sulfoxide without the adipogenic stimulation.
Publication 2020
Adipogenesis Cell Culture Techniques Cells Culture Media Dexamethasone Dinoprost Edetic Acid Hyperostosis, Diffuse Idiopathic Skeletal Insulin Methocel Organoids Sphenoid Bone Sulfoxide, Dimethyl Troglitazone Trypsin
Rosiglitazone was purchased from Cayman Chemical, pioglitazone and troglitazone from Sigma-Aldrich. MAO A and B recombinant proteins were over-expressed in Pichia pastoris and purified following previously published procedures.15 ,16 Enzymatic activities were measured spectrophotometrically using the horseradish peroxidase coupled Amplex red assay (ΔⲈ = 54,000 M−1-cm−1, λ = 560 nm) with p-CF3-benzylamine and benzylamine or phenethylamine as substrates for MAO A and MAO B, respectively. Inhibitor Ki values were determined by measuring the initial rates of substrate oxidation (six different concentrations) in the presence of varying concentrations of inhibitor (a minimum of four different concentrations). Ki values were determined using global fit analysis of the hyperbolic fits of enzyme activity with inhibitor concentrations using Graphpad Prism 5.0 software. Crystals of MAO B complexes were grown under conditions described previously14 (link) in the presence of ~500 μM inhibitors. X-ray diffraction data were collected at the ESRF (Grenoble, France) and at the SLS (Villigen, Switzerland) synchrotrons. Data processing and structure refinement were performed using programs of the CCP4 package following standard protocols (Table S1).25 (link) Structural representations were generated with CCP4mg.26 (link) Purification of recombinant human LSD1/CoREST complex and inhibition assays against this enzyme were carried out as described.27 (link)
Publication 2011
Benzylamines Biological Assay Caimans enzyme activity Enzyme Assays Homo sapiens Horseradish Peroxidase inhibitors KDM1A protein, human Komagataella pastoris MAOA protein, human Monoamine Oxidase B Phenethylamines Pioglitazone prisma Psychological Inhibition Recombinant Proteins Rosiglitazone Seizures Seizures, Generalized Troglitazone X-Ray Diffraction
Figure 1 presents a timeline that defines the intervention periods from randomization through the end of DPP, the transitional bridge period and the start of DPPOS.
The Diabetes Prevention Program examined the effects of four treatment arms to prevent or delay type 2 diabetes in high-risk adults. Overweight or obese individuals with elevated fasting glucose and impaired glucose tolerance were randomly assigned to an individually administered intensive lifestyle weight loss program (ILS), metformin (MET), troglitazone (TROG) or placebo (PLAC) arm. Descriptions of the treatments and major outcomes have been previously reported.9 (link)
The first phase of DPP was terminated early after 3.2 years of average follow-up when ILS efficacy was clearly demonstrated. Briefly, 95% of all participants, randomized to the lifestyle arm of the DPP, completed the individually administered 16-session core curriculum with a median time to program completion of 24 weeks. The mean weight loss for this treatment period was 6.5±4.7 kg. After 3.2 years, ILS reduced the incidence of diabetes by 55%, compared with PLAC; and MET reduced incidence of diabetes by 31%, compared with PLAC. Treatment with TROG was stopped after an average of only 0.9 years of follow-up (due to toxicity) and after drug treatment was withdrawn, this group was offered lifestyle sessions and handouts with no additional behavioral coaching on self-management strategies. Subsequent analyses of the DPP data have shown weight loss to be the dominant factor in the efficacy of ILS.10 (link)
Publication 2008
Adult Diabetes Mellitus Diabetes Mellitus, Non-Insulin-Dependent Factor X Glucose Intolerances, Glucose Metformin Obesity Pharmaceutical Preparations Placebos Preventive Health Programs Self-Management TimeLine Troglitazone Weight Reduction Programs
The 3T3-L1 preadipocytes (#EC86052701-G0, KAK) were grown in 2D culture medium (HG-DMEM containing 100 U/mL penicillin, 100 μg/mL streptomycin and 10% CS) in 150 mm dish until confluence at 37℃.
To obtain 3T3-L1 organoids, 3T3-L1 preadipocytes were grown in 3D pre-culture medium (HG-DMEM containing 8 mg/L d-biotin, 4 mg/L calcium pantothenate, 100 U/mL penicillin, 100 μg/mL streptomycin and 10% CS) in 150 mm dish as above. When the cultures reached approximately a 90% confluence, the cells were washed with phosphate buffered saline (PBS), detached using 0.25% Trypsin/EDTA and resuspended in 3D pre-culture medium containing 0.25% w/v Methocel A4M (3D organoid medium). Approximately 20,000 cells in the 28μL 3D organoid medium were placed into each well of the drop culture plate (defined as 3D/Day 0). On alternate days, 14 μL of the medium was substituted with 14 μL of fresh medium in each well.
For the induction of adipogenic differentiation, two days after the 2D cells in the 2D culture medium or 3D organoids at Day 1 in the 3D organoid medium reached confluence, there were processed by supplementation with 250 nM dexamethasone, 10 nM T3, 10 μM troglitazone, and 1 μg/ml insulin during the initial two days, and during the following 4 days with 10 μM troglitazone and 1 μg/ml insulin. To study the efficacy of several drugs, 100 nM prostaglandin F2α (PGF2α), 100 nM omidenepag (OMD), or 100 nM butaprost (Buta) were added during their adipogenic differentiation. In terms of their corresponding receptor, PF and EP2 receptors, of these drugs, we confirmed their positive expressions with the 2D and 3D cultured 3T3-L1 cells (Supplemental Fig. 1).
Phase contrast images of the 3D organoids were captured in a × 4 objective lens using an inverted microscope (Nikon ECLIPSE TS2; Tokyo, Japan). For measurement of each organoid size, the largest cross-sectional area (CSA) was calculated using the Image-J software version 1.51n (National Institutes of Health, Bethesda, MD).
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Publication 2020
3T3-L1 Cells Adipogenesis Biotin butaprost Cells Dexamethasone Dinoprost Edetic Acid Hyperostosis, Diffuse Idiopathic Skeletal Insulin Lens, Crystalline Methocel Microscopy Microscopy, Phase-Contrast Organoids Pantothenate, Calcium Penicillins Pharmaceutical Preparations Phosphates Saline Solution Streptomycin Troglitazone Trypsin

Most recents protocols related to «Troglitazone»

Example 8

Cells were treated with troglitazone, followed by incubation with the various fluorescence dyes (CALCEIN AM, MBBR, MITOSOX™ and CYTOSOX™). For each non-control well, the quadratic chi-distance distance to positive and negative control templates (for each fluorescence channel) was calculated and normalized with the scaling factor. The normalized data are reorganized into tensors, and the distance from positive and negative control templates are calculated. The similarities of the trioglitazone tensor to another compound tensor can be computed using known techniques by comparing the fiber columns of the tensors using dynamic time warping distance (see, Giorgino et al. “Computing and Visualizing Dynamic Time Warping Alignments in R: The dtw Package.” Journal of Statistical Software, 31(7), 1-24, 2009). Dissimilarities or distances to all other compounds can be calculated this way.

Results are shown in FIG. 12.

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Patent 2024
Cells Fibrosis Fluorescence Fluorescent Dyes fluorexon MitoSOX monobromobimane Troglitazone
NHKs were seeded at 1.6 × 105 cells/well in 6-well culture plates and were maintained in Humedia-KG2 at 37 °C in a 5% CO2 atmosphere. After overnight incubation, the medium was exchanged with proliferation medium (Humedia-KG2, final Ca2+ concentration: 0.15 mM) or differentiation medium (excluding insulin, hEGF, hydrocortisone and BPE from Humedia-KG2 and final Ca2+ concentration: 1.5 mM), and then HC (final concentration of 200 µg/mL), agonists of PPARs (WY14643, GW501516 and troglitazone at final concentrations of 20, 20 and 5 µg/mL, respectively) or antagonists of PPARs (GW6471, GSK0660 and GW9662 at final concentrations of 4, 20 and 20 µg/mL, respectively) dissolved in 0.2% dimethyl sulfoxide were added to the medium. An amount of 0.2% dimethyl sulfoxide was added as a control. The NHKs were then cultured for 6, 12, 24 or 48 h and analyzed using real-time RT-PCR.
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Publication 2023
agonists antagonists Atmosphere Cell Culture Techniques GSK0660 GW 6471 GW9662 GW 501516 Insulin Peroxisome Proliferator-Activated Receptors Real-Time Polymerase Chain Reaction Sulfoxide, Dimethyl Troglitazone
The contributions of CYPs and UGTs to the metabolism of PND in rat, mouse and human LMs were investigated by using specific chemical inhibitors: furafyllin (50 μM) for CYP1A2, ticlopipidine (25 μM) for CYP2C11 (CYP2C19), quinidine (50 μM) for CYP2D2 (CYP2D6), sulfaphenazole (100 μM) for CYP2C6 (CYP2C9), ketoconazole (2 μM) for CYP3A4, disulfiram (50 μM) for CYP2E1, bilirubin (100 μM) for UGT1A1, lithocholic acid (50 μM) for UGT1A3, hecogenin (10 μM) for UGT1A4, troglitazone (250 μM) for UGT1A6, niflumic acid (5 μM) for UGT1A9, fluconazole (10 μM) for UGT2B7. PND (2 µM) was incubated with rat, mouse and human LMs (0.5 mg protein/mL) with or without specific chemical inhibitors at 37 °C for 30 (for RLM and MLM CYPs) or 60 min (for HLM CYPs) and 90 min (for UGTs) with shaking. Then, 100 μL of each incubation mixture was taken and mixed with 900 μL of ice-cold acetonitrile (containing IS, 20 ng/mL). The validation of LMs system was confirmed by specific probe substrates (metabolite determination were shown in Supplementary Section: Substrates Metabolite Quantification and Tables S1–S6).
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Publication 2023
acetonitrile Bilirubin Cold Temperature CYP2C11 protein, rat CYP2C19 protein, human Cytochrome P-450 CYP1A2 Cytochrome P-450 CYP2D6 Cytochrome P-450 CYP2E1 Cytochrome P-450 CYP3A4 Cytochrome P450 Disulfiram Fluconazole hecogenin Homo sapiens inhibitors Ketoconazole Lithocholic Acid Metabolism Mice, House Niflumic Acid Proteins Quinidine Sulfaphenazole Troglitazone UGT1A1 protein, human UGT1A6 protein, human UGT1A9 protein, human
Penindolone and its derivatives HDYL-GQQ-2399, QL-Vir-09 and lbh3-78-2 (all HPLC purity > 95%, Figure S1), were synthesized by Laboratory of Natural Product Chemistry (School of Medicine, Ocean University of China). Mephenytoin, diclofenac sodium, chlorzoxazone, 6-hydroxychlorzoxazone, 4-acetaminophen were purchased from J&K Scientific (Beijing, China). Dextromethorphan, midazolam, 4-hydroxymephenytoin, 1-hydroxymidazolam, chenodeoxycholic acid 24-acyl-β-D-glucuronide, serotonin-β-D-glucuronide and 3′-azido-3′-deoxythymidine-β-D-glucuronide were acquired from Toronto Research Chemicals (Toronto, Canada). Glucose-6-phosphate (G-6-P), β-nicotinamide adenine dinucleotide phosphate (β-NADP), glucose-6-phosphate dehydrogenase (G-6-P-DH), phenacetin, 4-hydroxydiclofenac sodium, ticlopidine, β-glucuronidase (Type HP-2, aqueous solution, ≥100,000 units/mL) and trifluoperazine N-glucuronide were purchased from Sigma-Aldrich (Shanghai, China). Paeonol, estradiol, chenodeoxycholic acid, trifluoperazine, serotonin, propofol, zidovudine, bilirubin, lithocholic acid, hecogenin, troglitazone, niflumic acid, fluconazole, alamethicin and formic acid (FA) were acquired from Aladdin Biochemical (Shanghai, China). β-Estradiol-3-glucuronide was obtained from APExBIO (Shanghai, China). Propofol-β-D-glucuronide was purchased from GlpBio (Shanghai, China). Ibrutinib, UDP-D-glucuronide trisodium salt (UDPGA) and theophylline were obtained from Macklin Biochemical (Shanghai, China). PEG 300 was purchased from Sinopharm Chemical Reagent. (Shanghai, China). Dimethyl sulfoxide (DMSO) was obtained from Sangon Biotech (Shanghai, China). Isopropanol, methanol, acetonitrile and water were purchased from Merck (Darmstadt, Germany).
Mouse and rat liver microsomes (LMs) were prepared following previously established methods [16 (link)]. Mouse liver microsomes (MLM) were prepared with 10 Kunming males (6–8 weeks), and rat liver microsomes (RLMs) were prepared with 6 Sprague-Dawley males (6–8 weeks). Male Mongolia human microsomes (HLM), prepared from 30 male donors (19–78 years old), were obtained from RILD Liver Disease Research Co., Ltd. (Shanghai, China). LMs were activated by preincubation with alamethicin (50 μg/mg protein) on ice for 30 min before their use in UGTs incubations [17 (link)].
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Publication 2023
1-hydroxymethylmidazolam 4'-hydroxydiclofenac 4-hydroxymephenytoin 6-hydroxychlorzoxazone Acetaminophen acetonitrile Alamethicin beta-Glucuronidase Bilirubin Chenodeoxycholic Acid Chlorzoxazone derivatives Dextromethorphan Diclofenac Sodium Donors Estradiol estradiol-3-glucuronide Fluconazole formic acid Glucose-6-Phosphate Glucosephosphate Dehydrogenase Glucuronides hecogenin Hepatobiliary Disorder High-Performance Liquid Chromatographies ibrutinib Isopropyl Alcohol Lithocholic Acid Males Mephenytoin Methanol Mice, House Microsomes Microsomes, Liver Midazolam NADP Natural Products Niflumic Acid paeonol Phenacetin polyethylene glycol 300 Propofol Proteins Serotonin Sodium Sodium Chloride Sulfoxide, Dimethyl Theophylline Ticlopidine Trifluoperazine Troglitazone Uridine Diphosphate Glucuronic Acid Zidovudine
Primary isolated FAPs were routinely cultured in FAP growth media containing DMEM Low glucose (22320022, ThermoFisher Scientific) supplemented with 20% fetal bovine serum (FBS) (10270-106, ThermoFisher Scientific), 1% Penicillin-Streptomycin (10,000 U/ml) (15140122, Thermo Fisher Scientific), and 5 ng/mL basic-FGF (PHG0266, ThermoFisher Scientific). Cells were expanded once before seeding for experiment unless otherwise noted. Full medium adipogenic differentiation was performed using white adipogenic induction medium containing DMEM high glucose (41966052, ThermoFisher Scientific) supplemented with 10% FBS, 1% Penicillin-Streptomycin, 0.5 mM IBMX (I5879, Sigma-Aldrich), 5 μM Troglitazone (T2573, Sigma-Aldrich), 0.25 μM dexamethasone (D2915, Sigma-Aldrich), and 5 ug/mL insulin (Sigma-Aldrich, I9278) during days 0–2. From days 2–7 cells were maintained in white adipogenic maintenance medium containing high glucose DMEM supplemented with 10% FBS, 1% Penicillin-Streptomycin, and 5 μg/mL insulin. Medium was changed every 48 h and collected on day 7 for imaging or RNA extraction. For low insulin adipogenic differentiation, cells were seeded at a density of 30,000 cells/well in a 96-well plate in FAP growth medium and allowed to attach overnight. Insulin was then added to the wells to a final concentration of 156 ng/mL. Medium was changed every 3 days before harvesting on day 5 for imaging or RNA extraction. For brown adipogenic differentiation, cells were induced from days 0–2 using brown adipogenic medium containing DMEM high glucose supplemented with 10% FBS, 1% Penicillin-Streptomycin, 5 ug/mL insulin, 1 nM T3 (T6397, Sigma-Aldrich), 1 μM rosiglitazone (AG-CR1-3570, Adipogen), 125 μM indomethacin (I8280, Sigma-Aldrich), 5 μM dexamethasone, and 0.5 mM IBMX. From days 2–10 cells were maintained in brown adipogenic maintenance medium containing high glucose DMEM supplemented with 10% FBS, 1% Penicillin-Streptomycin, and 5 μg/mL insulin, 1 nM T3, and 1 μM rosiglitazone. Medium was changed every 48 h and collected on day 10 for RNA extraction. Chondrogenic differentiation was performed using Mesenchymal Stem Cell Chondrogenic Differentiation Medium (with Inducers) (PromoCell Inc., c-28012) according to the manufacturer’s protocol and harvested on day 21 for RNA extraction. Osteogenic differentiation was performed using Mesenchymal Stem Cell Osteogenic Differentiation Medium (PromoCell Inc., c-28013) according to the manufacturer’s protocol and harvested on day 14 for RNA extraction. Fibrogenic differentiation was performed using fibrogenic induction medium consisting of low glucose DMEM supplemented with 5% horse serum (HS, 16050-122, ThermoFisher Scientific), 1% Penicillin-Streptomycin, 5 ng/mL TGFβ (eBioscience, 14-8342-82) for 3 days when cells were harvested for RNA extraction.
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Publication 2023
1-Methyl-3-isobutylxanthine Adipogenesis Cells Chondrogenesis Dexamethasone Epiphyseal Cartilage Equus caballus Fetal Bovine Serum Glucose Indomethacin Insulin Mesenchymal Stem Cells Osteogenesis Penicillins Rosiglitazone Serum Streptomycin Transforming Growth Factor beta Troglitazone

Top products related to «Troglitazone»

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Troglitazone is a laboratory equipment product manufactured by Merck Group. It is a chemical compound used in research and scientific experiments. The core function of Troglitazone is to serve as a research tool, without further interpretation on its intended use.
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Dexamethasone is a synthetic glucocorticoid medication used in a variety of medical applications. It is primarily used as an anti-inflammatory and immunosuppressant agent.
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Insulin is a lab equipment product designed to measure and analyze insulin levels. It provides accurate and reliable results for research and diagnostic purposes.
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Troglitazone is a synthetic organic compound used as a laboratory reagent. It is a member of the thiazolidinedione class of compounds and serves as a peroxisome proliferator-activated receptor gamma (PPARγ) agonist.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
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GW9662 is a laboratory equipment product manufactured by Merck Group. It is a selective and irreversible antagonist of the peroxisome proliferator-activated receptor gamma (PPAR-γ).
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IBMX is a laboratory product manufactured by Merck Group. It is a chemical compound that functions as a phosphodiesterase inhibitor. The core function of IBMX is to inhibit the activity of phosphodiesterase enzymes, which are involved in the regulation of cellular processes. This product is intended for use in research and laboratory settings.
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GW9662 is a synthetic organic compound that functions as a selective and irreversible peroxisome proliferator-activated receptor gamma (PPARγ) antagonist.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

More about "Troglitazone"

Troglitazone is a member of the thiazolidinedione (TZD) class of antidiabetic drugs, also known as glitazones.
It acts as an agonist of the peroxisome proliferator-activated receptor gamma (PPAR-γ), which plays a crucial role in glucose and lipid metabolism.
Troglitazone was once used to treat type 2 diabetes mellitus (T2DM) by enhancing insulin sensitivity and improving glucose homeostasis.
However, troglitazone has been associated with rare but serious liver toxicity, leading to its withdrawal from the market in many countries.
This underscores the importance of rigorous experimental design and optimization when studying troglitazone and other diabetes medications.
Researchers investigating troglitazone must carefully consider factors such as cell lines (e.g., hepatocytes), culture conditions (e.g., media components like Dexamethasone, Insulin, Penicillin/streptomycin), and the use of PPAR-γ antagonists (e.g., GW9662) or activators (e.g., IBMX) to ensure the reproducibility and accuracy of their findings.
The use of AI-driven platforms like PubCompare.ai can greatly assist in this process by helping researchers identify the best published protocols and products for their troglitazone studies.
By leveraging the power of PubCompare.ai's cutting-edeg AI comparisons, scientists can enhance the rigor and reliability of their troglitazone research, leading to a better understanding of its pharmacology, toxicology, and potential therapeutic applications in the management of type 2 diabetes and related metabolic disorders.