Diffraction data were collected at 100 K at the Argonne National Laboratory beamline SER-CAT 20ID and processed with HKL-3000 (ref. 42 (link)). The rosiglitazone-containing structure was solved using phases obtained from a SAD experiment. Both Refmac5 (CCP4) and CNS 1.2 were used for initial structure refinement, during which restraints were placed on DNA geometry43 (link)–45 (link). The rosiglitazone structure was used to solve the BVT.13 and GW9662 structures by molecular replacement using PHASER46 (link).
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GW9662
GW9662
GW9662 is a potent and selective peroxisome proliferator-activated receptor gamma (PPAR-γ) antagonist.
It has been widely used in research to investigate the role of PPAR-γ in various biological processes and disease models.
PubCompare.ai can help optimize your GW9662 protocols by enabling easy access to and comparison of relevant research from literature, preprints, and patents.
This AI-driven tool enhances reproducibility and efficiency in your research by ensuring you find the best possible approach for your GW9662 studies.
It has been widely used in research to investigate the role of PPAR-γ in various biological processes and disease models.
PubCompare.ai can help optimize your GW9662 protocols by enabling easy access to and comparison of relevant research from literature, preprints, and patents.
This AI-driven tool enhances reproducibility and efficiency in your research by ensuring you find the best possible approach for your GW9662 studies.
Most cited protocols related to «GW9662»
GW9662
Molecular Structure
Rosiglitazone
Albumins
Biological Factors
Cells
Fatty Acids
GW9662
Hepatocellular Carcinomas
Hep G2 Cells
Homo sapiens
Nonesterified Fatty Acids
Salts
Serum
Serum Albumin, Bovine
Sodium
Syringes
To investigate the effect of astaxanthin, the AGS cells (1.0–1.5 × 105/mL) were pre-treated with astaxanthin (1 or 5 μM) for 3 h before adding the H. pylori. Following 1 h of incubation the ROS levels, mitochondrial membrane potential, ATP level, IκBα level, NF-κB DNA binding activity, PPAR DNA binding activity, protein expression of PPAR-γ and catalase, and the activities of NADPH oxidase and catalase were determined. Following a 4 h incubation period, the IL-8 mRNA expression was measured, and following 24 h, the IL-8 level in the medium was assayed. To determine the involvement of NADPH oxidase, the cells were pre-treated with apocynin (0.2 or 1 μM), a NADPH oxidase inhibitor, for 3 h before exposure to the H. pylori. To ensure the involvement of PPAR-γ, the PPAR-γ antagonist GW9662 (5 μM) and astaxanthin (5 μM) were preincubated with the AGS cells for 3 h prior to the addition of the H. pylori
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acetovanillone
alpha, NF-KappaB Inhibitor
astaxanthin
Catalase
Cells
GW9662
Helicobacter pylori
Membrane Potential, Mitochondrial
NADPH Oxidase
Peroxisome Proliferator-Activated Receptors
PPAR gamma
Proteins
RELA protein, human
RNA, Messenger
Neonatal rat CFs and cardiomyocytes were prepared by the methods according to previous literatures58 (link),59 (link). Bromodeoxyuridine (0.1 mM) was employed to inhibit proliferation of CFs in neonatal rat cardiomyocytes. Cardiomyocytes were seeded into 6- and 24-well plates and cultured in Dulbecco’s modified Eagle’s medium (DMEM)/F12 (GIBCO, C11995) supplemented with 10% fetal bovine serum (FBS, GIBCO, 10099) for 48 h. After grown to 70–80% confluency and serum deprived for 16 h to synchronize, cardiomyocytes were assigned randomly to incubate with RA (20 μg/ml)21 (link) or equal volume of vehicle for 24 h in the presence or absence of PE (50 μM). Eventually, cells were collected for western blot, quantitative real-time PCR, and immunofluorescence staining without awareness of the sample group allocation during the experiment.
The purity of cultured CFs was measured by a negative result of anti-α-actinin and positive result of anti-vimentin via immunofluorescence staining. CFs in passages 2 and 3 were used for all studies. After cultured in DMEM/F12 with 15% FBS for 48 h and synchronization, CFs were randomly treated with the indicated concentration of RA with or without TGF-β (10 ng/ml) stimulation for 24 h. To investigate the effect of RA on the phosphorylation and nuclear translocation of Smad3, CFs seeded in six-well plates or coverslips were pretreated with RA (30 μg/ml) for 30 min before addition of TGF-β (10 ng/ml) to the medium and incubation for an additional 1 h14 (link). RA was dissolved in 0.1% DMSO as a stock solution (20 mg/ml) and diluted to the desired final concentrations. For evaluating the effect of RA on the proliferation capacity of CFs, cell counting kit (CCK-8; Dojindo Molecular Technologies, Rockville, MD, USA) was used referring to the manufacturer′s protocol.
We knocked down the expression of AMPKα2 via shAmpkα2 carried by adenovirus as our previous study52 (link). In brief, CFs were infected with shAmpkα2 or shRNA for 4 h at a multiplicity of infection (MOI) of 50, then rinsed and synchronized with serum-free medium for 16 h before further studies.
For PPAR-γ inhibition, CFs were treated with GW9662 (10 μM), a specific antagonist of PPAR-γ, for 24 h prior to interventions60 (link). Moreover, genetic ablation targeting Ppar-γ with small interfering RNA (siPpar-γ) was performed to knockdown the expression of PPAR–γ referring to a previous study61 (link).
The purity of cultured CFs was measured by a negative result of anti-α-actinin and positive result of anti-vimentin via immunofluorescence staining. CFs in passages 2 and 3 were used for all studies. After cultured in DMEM/F12 with 15% FBS for 48 h and synchronization, CFs were randomly treated with the indicated concentration of RA with or without TGF-β (10 ng/ml) stimulation for 24 h. To investigate the effect of RA on the phosphorylation and nuclear translocation of Smad3, CFs seeded in six-well plates or coverslips were pretreated with RA (30 μg/ml) for 30 min before addition of TGF-β (10 ng/ml) to the medium and incubation for an additional 1 h14 (link). RA was dissolved in 0.1% DMSO as a stock solution (20 mg/ml) and diluted to the desired final concentrations. For evaluating the effect of RA on the proliferation capacity of CFs, cell counting kit (CCK-8; Dojindo Molecular Technologies, Rockville, MD, USA) was used referring to the manufacturer′s protocol.
We knocked down the expression of AMPKα2 via shAmpkα2 carried by adenovirus as our previous study52 (link). In brief, CFs were infected with shAmpkα2 or shRNA for 4 h at a multiplicity of infection (MOI) of 50, then rinsed and synchronized with serum-free medium for 16 h before further studies.
For PPAR-γ inhibition, CFs were treated with GW9662 (10 μM), a specific antagonist of PPAR-γ, for 24 h prior to interventions60 (link). Moreover, genetic ablation targeting Ppar-γ with small interfering RNA (siPpar-γ) was performed to knockdown the expression of PPAR–γ referring to a previous study61 (link).
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5-bromouridine
Actinin
Adenoviruses
Awareness
Cardiac Arrest
Cells
Eagle
GW9662
Immunofluorescence
Infant, Newborn
Infection
Myocytes, Cardiac
Phosphorylation
PPAR gamma
Psychological Inhibition
Real-Time Polymerase Chain Reaction
RNA, Small Interfering
Serum
Short Hairpin RNA
Sincalide
SMAD3 protein, human
Sulfoxide, Dimethyl
Transforming Growth Factor beta
Translocation, Chromosomal
Vimentin
Western Blotting
Stromal vascular cells were obtained from iBAT and iWAT excised from 3-week-old C57BL6 mice (males and females), primary cultures were generated and the cells were induced to differentiate into brown and beige adipocytes, respectively, following the previously reported procedures25 (link)26 (link). Brown adipocyte differentiation was achieved by exposing confluent precursor cells from iBAT in DMEM/F12 medium containing 10% foetal bovine serum (FBS) and supplemented with 20 nM insulin, 2 nM T3 and 0.1 mM ascorbic acid (ITA).
For beige cell differentiation, confluent precursor cells from iWAT and eWAT were maintained in DMEM/F12 containing 10% newborn calf serum (NCS). For differentiarion, 850 nM insulin, 3 μM T3, 35 nM dexamethasone and 10 μM rosiglitazone were added. When indicated, pre-adipocytes were cultured in the presence of delipidated serum (Charcoal Stripped Serum-GIBCO) instead of FBS/NCS
Cells were treated either across the differentiation process or were treated acutely (24 h), when already differentiated. Treatments included TUG-891 (200 μM), grifolic acid (100 μM), GW9508 (100 μM), ALA (100 μM), EPA (100 μM), NE (0.5 μM), dibutyryl-cAMP (1 mM), SB202190 (10 μM), H89 (20 μM), GW7647 (1 μM), GW9662 (30 μM), AH-7614 (100 μM), U-0128 (10 μM), compound C (10 μM), wortmannin (2 μM) and CL316,243 (1 μM). All reagents were obtained from Sigma with the exception of TUG-891, AH-7614, GW9662 (from Tocris), GW9508 (from Cayman Chemical), compound C (Calbiochem) and U-0128 (Enzo). When indicated, cells were subjected to dynamic measurements (see below) and/or further collected for RNA extraction.
For beige cell differentiation, confluent precursor cells from iWAT and eWAT were maintained in DMEM/F12 containing 10% newborn calf serum (NCS). For differentiarion, 850 nM insulin, 3 μM T3, 35 nM dexamethasone and 10 μM rosiglitazone were added. When indicated, pre-adipocytes were cultured in the presence of delipidated serum (Charcoal Stripped Serum-GIBCO) instead of FBS/NCS
Cells were treated either across the differentiation process or were treated acutely (24 h), when already differentiated. Treatments included TUG-891 (200 μM), grifolic acid (100 μM), GW9508 (100 μM), ALA (100 μM), EPA (100 μM), NE (0.5 μM), dibutyryl-cAMP (1 mM), SB202190 (10 μM), H89 (20 μM), GW7647 (1 μM), GW9662 (30 μM), AH-7614 (100 μM), U-0128 (10 μM), compound C (10 μM), wortmannin (2 μM) and CL316,243 (1 μM). All reagents were obtained from Sigma with the exception of TUG-891, AH-7614, GW9662 (from Tocris), GW9508 (from Cayman Chemical), compound C (Calbiochem) and U-0128 (Enzo). When indicated, cells were subjected to dynamic measurements (see below) and/or further collected for RNA extraction.
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Adipocytes
Adipocytes, Beige
Adipocytes, Brown
Ascorbic Acid
Blood Vessel
Caimans
Cells
Charcoal
Dexamethasone
Females
Fetal Bovine Serum
grifolic acid
GW 7647
GW9508
GW9662
Infant, Newborn
Insulin
Males
Mus
Rosiglitazone
SB 202190
Serum
Stem Cells, Hematopoietic
Stromal Cells
TUG-891
Wortmannin
Most recents protocols related to «GW9662»
Thirty mice were randomized into four groups: TBI + ω-3 and TBI + ω-3 + GW9662 groups (n = 15/group). TBI + ω-3 and TBI + ω-3 + GW9662 groups received same dosage ω-3 PUFA. Mice in the TBI + ω-3 group received intraperitoneal injection of normal saline, TBI + ω-3 + GW9662 group received intraperitoneal injection of GW9662 (1 mg/kg, M2748, AbMole) once daily for 5 consecutive days, beginning about 2 days before the TBI.
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GW9662
Injections, Intraperitoneal
Mice, House
Normal Saline
Omega-3 Fatty Acids
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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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
HC was purchased from Yamakawa (Tokyo, Japan). HC extracted from horse spinal cord is a mixture of lipids containing GalCer(72~82%) as the main component along with sphingomyelin, phosphatidylethanolamine, lecithin (combined 8~25%) and cholesterol (0.1~0.6%). The GalCer of HC contains more than 11 types of molecular species. The structures with the highest content in HC are d18:14E-C24:0GalCer and d18:14E-C24h:0 GalCer.
Ceramide standards, Cer[NS/NDS], Cer[NP] and Cer[AS], used for quantitative determination, were purchased from Takasago International Corp. (Tokyo, Japan), Evonik Industries (Essen, Germany) and Matreya (State College, PA, USA). RHEEs (LabCyte EPIMODEL 6D) and assay medium were purchased from Japan Tissue Engineering (Aichi, Japan). NHKs and assay medium (Humedia-KG2) were purchased from Kurabo (Tokyo, Japan). PBS (-) was purchased from Fujifilm Wako Pure Chemical Corp. (Osaka, Japan), 0.05% Trypsin-EDTA was purchased from Gibco (BRL, Palo Alto, CA, USA) and fetal bovine serum (FBS) was obtained from Sigma-Aldrich (St. Louis, MO, USA). Isogen was purchased from Nippon Genes (Tokyo, Japan). The One-step Syber Prime Script PLUS RT-PCR kit was purchased from Takara Bio (Shiga, Japan). PCR primers were purchased from Hokkaido System Science (Hokkaido, Japan). IGEPAL™ CA-630 and cOmpl™TM) Mini Protease Inhibitor Cocktail Tablets were purchased from Sigma-Aldrich (St. Louis, MO, USA). The DC Protein Assay Kit, Laemmli sample buffer and Clarity Western ECL Substrate were from Bio-Rad Laboratories (Hercules, CA, USA). Can Get Signal solutions 1 and 2 were purchased from Toyobo (Osaka, Japan). Antibodies to ELOVL4 (DF4037) were obtained from Affinity Biosciences (Cincinnati, OH, USA). Antibodies to CERS3 (Anti-LASS3: ab169259), ASM (ab83354) and INV (ab53112) were obtained from Abcam (Cambridge, UK) and TGM3(NBP1-86950) was from Novus Biologicals (Littleton, CO, USA). Antibodies to SMS1 (bs-4216R) and GCS (bs-8593R) were obtained from Bioss (Beijing, China). Antibodies to GBA (G4171) and beta-Actin (A1978) and horseradish peroxidase (HRP) conjugated goat anti-mouse IgG and HRP conjugated goat anti-rabbit IgG were obtained from Sigma-Aldrich (St. Louis, MA, USA). Antibodies to TGM1 (12912-3-AP) were obtained from Proteintech Group (Rosemont, IL, USA). Agonists and antagonists to PPARs, WY14643/GW501516, GW6471/GSK0660 and Rosiglitazone/GW9662 were obtained from Adipogen Life Sciences (San Diego, CA, USA), Cayman Chemical (Ann Arbor, MI, USA) and Fujifilm Wako Pure Chemical Corp. (Osaka, Japan), respectively. TLC plates for HPTLC were obtained from Merck Millipore (Darmstadt, Germany). All other reagents were obtained commercially and used without further purification.
Ceramide standards, Cer[NS/NDS], Cer[NP] and Cer[AS], used for quantitative determination, were purchased from Takasago International Corp. (Tokyo, Japan), Evonik Industries (Essen, Germany) and Matreya (State College, PA, USA). RHEEs (LabCyte EPIMODEL 6D) and assay medium were purchased from Japan Tissue Engineering (Aichi, Japan). NHKs and assay medium (Humedia-KG2) were purchased from Kurabo (Tokyo, Japan). PBS (-) was purchased from Fujifilm Wako Pure Chemical Corp. (Osaka, Japan), 0.05% Trypsin-EDTA was purchased from Gibco (BRL, Palo Alto, CA, USA) and fetal bovine serum (FBS) was obtained from Sigma-Aldrich (St. Louis, MO, USA). Isogen was purchased from Nippon Genes (Tokyo, Japan). The One-step Syber Prime Script PLUS RT-PCR kit was purchased from Takara Bio (Shiga, Japan). PCR primers were purchased from Hokkaido System Science (Hokkaido, Japan). IGEPAL™ CA-630 and cOmpl™TM) Mini Protease Inhibitor Cocktail Tablets were purchased from Sigma-Aldrich (St. Louis, MO, USA). The DC Protein Assay Kit, Laemmli sample buffer and Clarity Western ECL Substrate were from Bio-Rad Laboratories (Hercules, CA, USA). Can Get Signal solutions 1 and 2 were purchased from Toyobo (Osaka, Japan). Antibodies to ELOVL4 (DF4037) were obtained from Affinity Biosciences (Cincinnati, OH, USA). Antibodies to CERS3 (Anti-LASS3: ab169259), ASM (ab83354) and INV (ab53112) were obtained from Abcam (Cambridge, UK) and TGM3(NBP1-86950) was from Novus Biologicals (Littleton, CO, USA). Antibodies to SMS1 (bs-4216R) and GCS (bs-8593R) were obtained from Bioss (Beijing, China). Antibodies to GBA (G4171) and beta-Actin (A1978) and horseradish peroxidase (HRP) conjugated goat anti-mouse IgG and HRP conjugated goat anti-rabbit IgG were obtained from Sigma-Aldrich (St. Louis, MA, USA). Antibodies to TGM1 (12912-3-AP) were obtained from Proteintech Group (Rosemont, IL, USA). Agonists and antagonists to PPARs, WY14643/GW501516, GW6471/GSK0660 and Rosiglitazone/GW9662 were obtained from Adipogen Life Sciences (San Diego, CA, USA), Cayman Chemical (Ann Arbor, MI, USA) and Fujifilm Wako Pure Chemical Corp. (Osaka, Japan), respectively. TLC plates for HPTLC were obtained from Merck Millipore (Darmstadt, Germany). All other reagents were obtained commercially and used without further purification.
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agonists
antagonists
anti-IgG
Antibodies
beta-Actin
Biological Assay
Biological Factors
Caimans
Ceramides
Cholesterol
Edetic Acid
Equus caballus
Fetal Bovine Serum
Galactosylceramides
Genes
Goat
GSK0660
GW 6471
GW9662
GW 501516
Horseradish Peroxidase
Igepal CA-630
Laemmli buffer
Lecithin
Lipid A
Mice, House
Novus
Oligonucleotide Primers
Peroxisome Proliferator-Activated Receptors
Phosphatidylethanolamines
Protease Inhibitors
Proteins
Rabbits
Reverse Transcriptase Polymerase Chain Reaction
Rosiglitazone
Sphingomyelins
Spinal Cord
Trypsin
Simvastatin, lovastatin, rosuvastatin, atorvastatin, GW9662, GSK2033, A967079, HC030031, and activity assay kits for peroxisome proliferator-activated receptor γ (PPARγ) and liver X receptor α (LXRα) were purchased from Cayman Chemical (Ann Arbor, MI, USA). Di-(2-ethylhexyl) phthalate, mono-(2-ethylhexyl) phthalate (MEHP), 2-ethyl-1-hexanol (2-EH), phthalic acid (PA), N-acetylcysteine (NAC), apocynin (APO), and mouse antibody for α-tubulin were obtained from Sigma-Aldrich (St Louis, MO, USA). 5OH-MEHP, 5oxo-MEHP, and 5cx-MEHP were obtained from Toronto Research Chemicals (Toronto, ON, Canada). Control small interfering RNA (siRNA), PCSK9 (proprotein convertase subtilisin/kexin type 9, sc45482) siRNA, and IDOL (inducible degrader of the low-density lipoprotein receptor, sc95314) siRNA were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Rabbit and mouse antibodies for low-density lipoprotein receptor (LDLR, ab52818), PCSK9 (ab31762), PPARγ (ab209350), IDOL (MYLIP, ab74562), and LXRα (ab41902) were obtained from Abcam (Cambridge, MA, USA). Sterol regulatory element-binding protein 2 (SREBP2, 557037) was obtained from BD Bioscience (SanJose, CA, USA). The QuestTM Fluo-8 NW, a calcium assay kit, was obtained from AAT Bioquest (Sunnyvale, CA, USA). The Boyden Chamber was obtained from Thermo Fisher Scientific Inc. (Waltham, MA, USA). Dihydroethidium (DHE) and 2′,7′-dichlorofluorescin diacetate (DCFH-DA) were obtained from Molecular Probes (Eugene, OR, USA). The EnzyChrom NADP+/NAD(P)H assay kit was obtained from BioAssay Systems (Hayward, CA, USA). Dil-LDL was purchased from Biomedical Technologies (Stoughton, MA, USA). Lipofectamine® RNAMAX reagent was obtained from Thermo Fisher Scientific (Lafayette, CO, USA).
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2-ethylhexanol
A 967079
acetovanillone
Acetylcysteine
alpha-Tubulin
Antibodies
Atorvastatin
Biological Assay
Biomedical Technology
Caimans
Calcium
dichlorofluorescin
Diethylhexyl Phthalate
dihydroethidium
FLUOS
GSK 2033
GW9662
HC 030031
Immunoglobulins
LDLR protein, human
Lipofectamine
Lovastatin
Low Density Lipoprotein Receptor
LXR-Alpha Protein
Molecular Probes
mono-(2-ethylhexyl)phthalate
Mus
NADH
NADP
PCSK9 protein, human
Peroxisome Proliferator-Activated Receptors
phthalic acid
Rabbits
RNA, Small Interfering
Rosuvastatin
Simvastatin
Sterol Regulatory Element Binding Protein 2
Male C57BL/6 wild‐type mice (4 weeks old, weighing 15 ± 3 g, SPF grade) were purchased from Chongqing Enswell Biotechnology Co., LTD (Chongqing, China). All protocols in this study were approved by the Laboratory Animal Care Committee of Three Gorges Hospital, affiliated with Chongqing University. The mice were fed adaptively for 2–12 h, alternating day and night, temperature of 20–22°C, humidity of 40%–60%, drinking water freely and eating ordinary feed. After 1 week, 32 mice were randomly divided into wild‐type general feeding, wild‐type high‐fat diet, JAZF‐1 transgenic general feeding and JAZF‐1 transgenic high‐fat diet groups (n = 8). The weight and energy compositions between the general diet and high‐fat diet are shown in Table 1 . Transgenic mice overexpressing JAZF‐1 were obtained by continuously injecting AAV‐JAZF‐1 in their tail vein for 3 days. Another 32 mice were injected with AAV‐JAZF‐1 and randomly assigned to general feeding plus normal saline, high‐fat diet plus normal saline, general feeding plus PPAR‐γ inhibitor (GW9662) and high‐fat diet plus PPAR‐γ inhibitor (n = 8). The insulin resistance model was constructed using a high‐fat diet, while an ordinary diet was given to the control group, and the body weight of mice was recorded weekly.
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Animal Care Committees
Animals, Transgenic
Body Weight
Diet, High-Fat
GW9662
Humidity
Insulin Resistance
Males
Mice, Inbred C57BL
Mice, Laboratory
Mice, Transgenic
Normal Saline
PPAR gamma
Tail
Therapy, Diet
Veins
Top products related to «GW9662»
Sourced in United States, Germany, United Kingdom, China, Macao
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).
Sourced in United States
GW9662 is a synthetic organic compound that functions as a selective and irreversible peroxisome proliferator-activated receptor gamma (PPARγ) antagonist.
Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal
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.
Sourced in United States, Germany, China, France, Macao, Italy, Sao Tome and Principe
Rosiglitazone is a synthetic compound used as a laboratory reagent. It is a member of the thiazolidinedione class of drugs and functions as a selective agonist for the peroxisome proliferator-activated receptor gamma (PPAR-gamma). Rosiglitazone is commonly used in research studies to investigate its effects on cellular and metabolic processes.
Sourced in United States, China
GW9662 is a lab equipment product manufactured by MedChemExpress. It functions as a high-affinity antagonist for the peroxisome proliferator-activated receptor gamma (PPARγ).
Sourced in United States, United Kingdom, Germany
Rosiglitazone is a research-use-only chemical compound. It is a synthetic thiazolidinedione compound. The primary function of Rosiglitazone is to act as a selective agonist for the peroxisome proliferator-activated receptor gamma (PPAR-γ).
Sourced in United Kingdom, United States
GW9662 is a lab equipment product manufactured by Bio-Techne. It is a synthetic compound that functions as a selective and potent antagonist of the peroxisome proliferator-activated receptor gamma (PPAR-γ).
Sourced in United States, Germany, United Kingdom, China, Canada, France, Japan, Australia, Switzerland, Israel, Italy, Belgium, Austria, Spain, Gabon, Ireland, New Zealand, Sweden, Netherlands, Denmark, Brazil, Macao, India, Singapore, Poland, Argentina, Cameroon, Uruguay, Morocco, Panama, Colombia, Holy See (Vatican City State), Hungary, Norway, Portugal, Mexico, Thailand, Palestine, State of, Finland, Moldova, Republic of, Jamaica, Czechia
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.
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
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.
Sourced in United States, China
GW9662 is a synthetic organic compound that functions as a selective antagonist of the peroxisome proliferator-activated receptor gamma (PPARγ). It is commonly used in scientific research applications.
More about "GW9662"
GW9662 is a powerful and selective antagonist of the peroxisome proliferator-activated receptor gamma (PPAR-γ), a critical regulator of various biological processes and disease models.
Researchers have widely utilized GW9662 to investigate the role of PPAR-γ in areas such as metabolism, inflammation, and cancer.
Optimizing your GW9662 protocols is essential for ensuring reproducibility and efficiency in your research.
PubCompare.ai, an AI-driven tool, can help you achieve this by providing easy access to and comparison of relevant protocols from the literature, preprints, and patents.
When working with GW9662, it's important to consider the appropriate cell culture conditions, including the use of fetal bovine serum (FBS) and antibiotics like penicillin/streptomycin.
Additionally, the solvent dimethyl sulfoxide (DMSO) is commonly used to dissolve GW9662 for in vitro studies.
Rosiglitazone, another PPAR-γ agonist, may also be of interest in your research.
By leveraging the insights from PubCompare.ai and incorporating relevant terms and concepts, you can enhance your understanding and optimize your GW9662 protocols, leading to more robust and reliable research outcomes.
Researchers have widely utilized GW9662 to investigate the role of PPAR-γ in areas such as metabolism, inflammation, and cancer.
Optimizing your GW9662 protocols is essential for ensuring reproducibility and efficiency in your research.
PubCompare.ai, an AI-driven tool, can help you achieve this by providing easy access to and comparison of relevant protocols from the literature, preprints, and patents.
When working with GW9662, it's important to consider the appropriate cell culture conditions, including the use of fetal bovine serum (FBS) and antibiotics like penicillin/streptomycin.
Additionally, the solvent dimethyl sulfoxide (DMSO) is commonly used to dissolve GW9662 for in vitro studies.
Rosiglitazone, another PPAR-γ agonist, may also be of interest in your research.
By leveraging the insights from PubCompare.ai and incorporating relevant terms and concepts, you can enhance your understanding and optimize your GW9662 protocols, leading to more robust and reliable research outcomes.