T0070907

Manufactured by Cayman Chemical

Sourced in United States

T0070907 is a laboratory product for use in research and development applications. It is a chemical compound that can be utilized in various analytical and experimental procedures. The product's core function is to serve as a research tool, without any specific interpretation or extrapolation on its intended use.

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Lab products found in correlation

23 protocols using t0070907

PPAR Agonists and Antagonists Protocol

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Dihydrotestosterone was purchased from Steraloids. PPAR agonists and antagonists were purchased from: GW1929 (Sigma), Pioglitazone (Santa Cruz), GW9662 (Sigma), T0070907 (Cayman Chemical).

Elix C.C., Salgia M.M., Otto-Duessel M., Copeland B.T., Yoo C., Lee M., Tew B.Y., Ann D., Pal S.K, & Jones J.O. (2019). Peroxisome Proliferator-Activated Receptor Gamma Controls Prostate Cancer Cell Growth through AR-Dependent and -Independent Mechanisms. The Prostate, 80(2), 162-172.

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Neuroprotective Effects of VCE-003.2 in LPS-Lesioned Mice

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LPS-lesioned mice were distributed in three groups and administered i.p. with 10 mg/kg of VCE-003.2, alone or in combination with 5 mg/kg of the PPARγ antagonist T0070907 (Cayman Chemical, Ann Arbor, Michigan, USA) [25 (link)] or vehicle [DMSO (3.3%) + Tween 20 (2%) + saline (94.7%)]. The experiment included a fourth group consisting of sham-operated mice also treated with DMSO-Tween 20-saline. The treatment was initiated approximately 16 h after the LPS lesion and was repeated daily for 21 days. One day after the last injection, mice were killed by rapid and careful decapitation and their brains were rapidly removed and frozen in 2-methylbutane cooled in dry ice and stored at − 80 °C for subsequent immunohistochemical analysis in the substantia nigra and qPCR analysis in the striatum.

García C., Gómez-Cañas M., Burgaz S., Palomares B., Gómez-Gálvez Y., Palomo-Garo C., Campo S., Ferrer-Hernández J., Pavicic C., Navarrete C., Luz Bellido M., García-Arencibia M., Ruth Pazos M., Muñoz E, & Fernández-Ruiz J. (2018). Benefits of VCE-003.2, a cannabigerol quinone derivative, against inflammation-driven neuronal deterioration in experimental Parkinson’s disease: possible involvement of different binding sites at the PPARγ receptor. Journal of Neuroinflammation, 15, 19.

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Cell Culture and Reagent Preparation

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Jurkat, BV2 and RAW264.7 cells were maintained at 37°C in a humidified atmosphere containing 5% CO₂ in RPMI supplemented with 10% fetal calf serum (FCS), 2 mM L-glutamine and 1% (v/v) penicillin/streptomycin (complete medium). VCE-003 was synthesized as previously described [20] (link), while AM630, T0070907 and WIN-55,212-2 were obtained from Cayman Chem (Ann Arbor, MI, USA), and JWH-133 was purchased from Tocris Bioscience (Bristol, UK). All other reagents were from Sigma Co (St Louis, MO, USA).

Carrillo-Salinas F.J., Navarrete C., Mecha M., Feliú A., Collado J.A., Cantarero I., Bellido M.L., Muñoz E, & Guaza C. (2014). A Cannabigerol Derivative Suppresses Immune Responses and Protects Mice from Experimental Autoimmune Encephalomyelitis. PLoS ONE, 9(4), e94733.

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Prostanoid Compound Acquisition and Characterization

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15-Deoxy-Δ^12,14-prostaglandin J2 (15d-PGJ2), CAY10410 (9,10-dihydro-15-deoxy-Δ^12,14-prostaglandin J2), prostaglandin D2, prostaglandin E2, prostaglandin F2α, rosiglitazone, and T0070907 were purchased from Cayman Chemical (Ann Arbor, MI). Prostaglandin A1, prostaglandin J2, 4-cyclopentene-1,3-dione, 2-cyclopentenone, cycloheximide, actinomycin D, indomethacin, buthionine sulfoximine, and N-acetylcysteine and uric acid were from Sigma-Aldrich (St Louis, MO). Cyclopentanone and cyclopentene were obtained from Tokyo Chemical Industry (TCI, Portland, OR). Structures of these prostanoids are shown in Table I. Nigericin, lactacystin, and ultrapure lipopolysaccharide (LPS) were purchased from Calbiochem (San Diego, CA).

Maier N.K., Leppla S.H, & Moayeri M. (2015). The cyclopentenone prostaglandin 15d-PGJ2 inhibits the NLRP1 and NLRP3 inflammasomes. Journal of immunology (Baltimore, Md. : 1950), 194(6), 2776-2785.

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Inhibitor-Based Pharmacokinetic Assay

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Ko143 (a selective inhibitor of BCRP) was purchased from Enzo Life Sciences (Lausen, Switzerland). LY335979 (a selective inhibitor of P-gp) was a generous gift from Eli Lilly and Company. T0070907 (T007, specific inhibitor of PPARγ receptor) was purchased from Cayman Chemical Company (Ann Arbor, MI). Pioglitazone and rosiglitazone (internal standard, IS) were purchased from Cell Molecular Pharmaceutical R&D (Xi'an, China). All other reagents used were analytical grade.

Chang K.L., Pee H.N., Yang S, & Ho P.C. (2015). Influence of drug transporters and stereoselectivity on the brain penetration of pioglitazone as a potential medicine against Alzheimer's disease. Scientific Reports, 5, 9000.

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Pharmacological Agents Preparation

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Phenylephrine hydrochloride and acetylcholine chloride were dissolved in distilled water. NECA, CGS 21680, SCH-58261, Glibenclamide (Sigma Chemicals, St. Louis, MO), Rosiglitazone (Cayman chemicals, Ann Arbor, MI) were dissolved in 100 % DMSO as 10 mM stock solutions, which were followed by serial dilutions in distilled water. T0070907 (Cayman chemicals) and AUDA (gift from Dr. Morisseau, UC Davis) were dissolved in DMSO. sEH (Santa Cruz Biotechnology) was used for Western blot experiments.

Pradhan I., Ledent C., Mustafa S.J., Morisseau C, & Nayeem M.A. (2015). High salt diet modulates vascular response in A2AAR+/+ and A2AAR−/− mice: role of sEH, PPARγ, and KATP channels. Molecular and cellular biochemistry, 404(0), 87-96.

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Oxidative Stress Modulation in MG-63 Cells

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MG-63 cells were treated with indicated concentrations of 15d-PGJ₂ (Cayman, MI, USA) for indicated time periods. Cells were incubated for 30 min with either an inhibitor of p38 MAPK (25 μM PD169316, Merck Biosciences, Darmstadt, Germany), N-acetyl-l-cysteine (NAC, 5 mM), pyrrolidine dithiocarbamate (PDTC, 1 mM), N-2-mercaptopropionylglycine (MPG, 5 mM) (Sigma–Aldrich, MO, USA), Tempol (1 mM, Tocris, MA, USA), PPARγ antagonist (20 μM T0070907), D-type prostanoid receptor (DP1) antagonist (100 nM MK0524), DP2 antagonist (1 μM CAY10471) (Cayman), l-buthionine-(S,R)-sulfoximine (BSO, 5 μM), GSH ethyl ester (10 mM, Sigma–Aldrich), LY294002 (10 μM) or Akt inhibitor (Akt-I, 10 μM) (Calbiochem, CA, USA) prior to 15d-PGJ₂ treatment. Alternatively, cells were treated with 9,10-dihydro-15d-PGJ₂ (dh-15d-PGJ₂, 20 μM, Cayman) for indicated time periods.

Koyani C.N., Kitz K., Rossmann C., Bernhart E., Huber E., Trummer C., Windischhofer W., Sattler W, & Malle E. (2016). Activation of the MAPK/Akt/Nrf2-Egr1/HO-1-GCLc axis protects MG-63 osteosarcoma cells against 15d-PGJ2-mediated cell death. Biochemical pharmacology, 104, 29-41.

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Macrophage Polarization by PPARγ Modulation

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Bone marrow cells isolated from the femur and tibia of PPARγ-MKO or PPARγ-WT mice were matured in RPMI with 20% FBS, 1% Pen-Strep and 50 ng/mL recombinant mouse M-CSF for seven days, which results in a population that is >95% macrophages[12 (link)]. Following differentiation, bone marrow-derived macrophages (BMDM) were treated with the PPARγ agonist pioglitazone (10 μM), the PPARγ antagonist T0070907 (T007: 10 μM, Cayman), a combination of pioglitazone and T007, or vehicle control (DMSO) for 48 hours. In experiments where tumor homogenate was used to stimulate BMDM, whole left lungs were collected from tumor-bearing or naïve mice and snap frozen in liquid nitrogen. Tissues were homogenized in phosphate-buffered saline (PBS) using an overhead stirrer (Wheaton). A final concentration of 0.5 mg/mL protein each from tumor or control homogenate was added to BMDM for 48 hours. BMDM were then washed three times with HBSS and placed into fresh RPMI for 24 hours prior to collecting the culture media. TGF-β1 released into the media was measured by ELISA (R&D Systems). TGF-β1 levels were normalized to total BMDM RNA or protein concentration.

Sippel T.R., Johnson A.M., Li H.Y., Hanson D., Nguyen T.T., Bullock B.L., Poczobutt J.M., Kwak J.W., Kleczko E.K., Weiser-Evans M.C, & Nemenoff R.A. (2019). Activation of PPARγ in Myeloid Cells Promotes Progression of Epithelial Lung Tumors through TGF- β1. Molecular cancer research : MCR, 17(8), 1748-1758.

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Hematopoietic Stem Cell Culture

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Sorted LSKs were cultured in Stem Span SFEM medium (STEMCELL Technologies) supplemented with 100 ng/mL murine stem cell factor and 50 ng/mL murine thrombopoietin (Preprotech). The Pparγ agonist troglitazone or antagonist T0070907 (Cayman) were added at the initiation of culture at the concentration indicated on the figures. For colony-forming assay, 200 LSKs or 5 × 10³ MNC BM cells were cultured into cytokines supplemented Methocult3434 medium (STEMCELL). Colonies were counted on day 7 and replated for the second round in the same condition.

Sertorio M., Du W., Amarachintha S., Wilson A, & Pang Q. (2017). In Vivo RNAi Screen Unveils PPARγ as a Regulator of Hematopoietic Stem Cell Homeostasis. Stem Cell Reports, 8(5), 1242-1255.

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Regulation of Adipogenesis by Twist1

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The 3T3-L1 mouse embryo fibroblasts and Dulbecco’s modified Eagle medium (DMEM) were obtained from ATCC (Rockefeller, Maryland, USA). Bovine serum and fetal Bovine serum (FBS) were purchased from GIBCO (Invitrogen, CA, USA). The primary antibodies (anti-PPARγ and anti-Twist 1) were obtained from Abcam. The HRP-conjugated secondary antibody and the anti-β-actin primary antibody were purchased from ZSGB-BIO. The lentiviral vectors pGLV3/H1/GFP + Puro (LV3), LV4-EF1a-GFP/Puro (LV5), recombinant vectors LV3/Twist 1 shRNA and LV5/Twist 1 complementary DNA (cDNA) were all acquired from GenePharma (Shanghai, China). NE-PER™ Nuclear and Cytoplasmic Extraction Kit was purchased from Pierce (Thermo Scientific). SYBR^® Green Real-time PCR Master Mix (QPK-201 T) was purchased from TOYOBO. T0070907 and pioglitazone were both from Cayman Chemical (MI, USA). Insulin, isobutylmethylxanthine, cycloheximide (CHX), leupeptin, pepstatin A (L/P), proteasomes inhibitors (MG132) and the other reagents in this study were obtained from Sigma (Merck, German).

Ren R., Chen Z., Zhao X., Sun T., Zhang Y., Chen J., Lu S, & Ma W. (2016). A possible regulatory link between Twist 1 and PPARγ gene regulation in 3T3-L1 adipocytes. Lipids in Health and Disease, 15, 189.

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