- 阻害剤
- 研究分野別
- PI3K/Akt/mTOR
- Epigenetics
- Methylation
- Immunology & Inflammation
- Protein Tyrosine Kinase
- Angiogenesis
- Apoptosis
- Autophagy
- ER stress & UPR
- JAK/STAT
- MAPK
- Cytoskeletal Signaling
- Cell Cycle
- TGF-beta/Smad
- 化合物ライブラリー
- 抗体
- 新製品
- お問い合わせ
T0070907
T0070907 is a potent inhibitor of PPARγ (peroxisome proliferator activator receptor γ ) that induces G2/M arrest and enhances the effect of radiation in human cervical cancer cells through mitotic catastrophe. It also acts as an antagonist of PPARγ that suppresses breast cancer cell proliferation and motility via both PPARgamma-dependent and -independent mechanisms.
CAS No. 313516-66-4
文献中Selleckの製品使用例（83）
製品安全説明書
現在のバッチを見る：
純度：
99.96%
99.96
T0070907関連製品
シグナル伝達経路
PPAR阻害剤の選択性比較
Cell Data
| Cell Lines | Assay Type | Concentration | Incubation Time | 活性情報 | PMID |
|---|---|---|---|---|---|
| OR6 | Cytotoxicity assay | 72 hrs | Cytotoxicity against african green monkey OR6 cells after 72 hrs by WST1 assay, CC50=2.7μM. | 23891183 | |
| OR6 | Antiviral assay | 72 hrs | Antiviral activity against HCV infected in african green monkey OR6 cells assessed as inhibition of viral RNA replication after 72 hrs by luciferase reporter gene assay, ED50=4.9μM. | 23891183 | |
| 他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい | |||||
生物活性
| 製品説明 | T0070907 is a potent inhibitor of PPARγ (peroxisome proliferator activator receptor γ ) that induces G2/M arrest and enhances the effect of radiation in human cervical cancer cells through mitotic catastrophe. It also acts as an antagonist of PPARγ that suppresses breast cancer cell proliferation and motility via both PPARgamma-dependent and -independent mechanisms. | |
|---|---|---|
| Targets |
|
| In Vitro | ||||
| In vitro |
T0070907 is a potent and selective PPARγ antagonist. With an apparent binding affinity of 1 nM, T0070907 covalently modifies PPARγ on cysteine 313 in helix 3 of human PPARγ2. T0070907 blocks PPARγ function in both cell-based reporter gene and adipocyte differentiation assays. Consistent with its role as an antagonist of PPARγ, T0070907 blocks agonist-induced recruitment of coactivator-derived peptides to PPARγ in a homogeneous time-resolved fluorescence-based assay and promotes recruitment of the transcriptional corepressor NCoR to PPARγ in both glutathione S-transferase pull-down assays and a PPARγ/retinoid X receptor (RXR) α-dependent gel shift assay. Studies with mutant receptors suggest that T0070907 modulates the interaction of PPARγ with these cofactor proteins by affecting the conformation of helix 12 of the PPARγ ligand-binding domain. Interestingly, whereas the T0070907-induced NCoR recruitment to PPARγ/RXRα heterodimer can be almost completely reversed by the simultaneous treatment with RXRα agonist LGD1069, T0070907 treatment has only modest effects on LGD1069-induced coactivator recruitment to the PPARγ/RXRα heterodimer. [1] T0070907 treatment inhibits proliferation, invasion and migration but does not significantly affect apoptosis. Molecular inhibition using a dominant negative (Δ462) receptor yields similar results. T007 also mediates a dose-dependent decrease in phosphorylation of PPARγ, and its ability to bind to DNA, and may directly affect mitogen-activated protein kinase signaling. [2] |
|||
|---|---|---|---|---|
| Kinase Assay | Ligand Binding Assay | |||
| To determine the binding affinity of T0070907 to the PPARs, scintillation proximity assay (SPA) is performed with the following modifications. A 90-μl reaction contains SPA buffer (10 mm KH2PO4, 10 mm KH2PO4, 2 mm EDTA, 50 mm NaCl, 1 mm dithiothreitol, 2 mmCHAPS, 10% (v/v) glycerol, pH 7.1), 50 ng of GST-PPARγ (or 150 ng of GST-PPARα, GST-PPARδ), 5 nm 3H-labeled radioligands, and 5 μl of T0070907 in Me2SO. After incubation for 1 h at room temperature, 10 μl of polylysine-coated SPA beads (at 20 mg/ml in SPA buffer) are added, and the mixtureis incubated for 1 h before reading in Packard Topcount. | ||||
| 細胞実験 | 細胞株 | MCF-7 cells | ||
| 濃度 | 20 μM and higher concentrations | |||
| 反応時間 | 48 h | |||
| 実験の流れ | MTS assay |
|||
| In Vivo | ||
| In Vivo |
Lipopolysaccharide preconditioning significantly attenuates the development of renal dysfunction, hepatocellular injury, and circulatory failure as well as the increase in the plasma levels of interleukin-1 [beta] caused by severe endotoxemia. T0070907 can attenuate all of these beneficial effects afforded by preconditioning with lipopolysaccharide [3] |
|
|---|---|---|
| 動物実験 | 動物モデル | Preconditioning is performed by administering a low dose (1 mg/kg) of Escherichia coli LPS (serotype 0.127:B8) intraperitoneally 24 hr before the induction of severe endotoxemia. |
| 投与量 | 1 mg/kg | |
| 投与経路 | intraperitoneally | |
化学情報
| 分子量 | 277.66 | 化学式 | C12H8ClN3O3 |
| CAS No. | 313516-66-4 | SDF | Download T0070907 SDFをダウンロードする |
| Smiles | C1=CC(=C(C=C1[N+](=O)[O-])C(=O)NC2=CC=NC=C2)Cl | ||
| 保管 | |||
|
In vitro |
DMSO : 55 mg/mL ( (198.08 mM)； 吸湿したDMSOは溶解度を減少させます。新しいDMSOをご使用ください。) Water : Insoluble Ethanol : Insoluble |
モル濃度計算器 |
|
in vivo Add solvents to the product individually and in order. |
投与溶液組成計算機 | ||||
実験計算
投与溶液組成計算機(クリア溶液)
ステップ１：実験データを入力してください。（実験操作によるロスを考慮し、動物数を1匹分多くして計算・調製することを推奨します）
mg/kg
g
μL
匹
ステップ２：投与溶媒の組成を入力してください。（ロット毎に適した溶解組成が異なる場合があります。詳細については弊社までお問い合わせください）
% DMSO
%
% Tween 80
% ddH2O
%DMSO
%
計算結果：
投与溶媒濃度： mg/ml;
DMSOストック溶液調製方法： mg 試薬を μL DMSOに溶解する（濃度 mg/mL, 注：濃度が当該ロットのDMSO溶解度を超える場合はご連絡ください。 )
投与溶媒調製方法：Take μL DMSOストック溶液に μL PEG300，を加え、完全溶解後μL Tween 80，を加えて完全溶解させた後 μL ddH2O，を加え完全に溶解させます。
投与溶媒調製方法：μL DMSOストック溶液に μL Corn oil，を加え、完全溶解。
注意：１.ストック溶液に沈殿、混濁などがないことをご確認ください；
２.順番通りに溶剤を加えてください。次のステップに進む前に溶液に沈殿、混濁などがないことを確認してから加えてください。ボルテックス、ソニケーション、水浴加熱など物理的な方法で溶解を早めることは可能です。
技術サポート
ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。
他に質問がある場合は、お気軽にお問い合わせください。
* 必須
Tags: T0070907を買う | T0070907 ic50 | T0070907供給者 | T0070907を購入する | T0070907費用 | T0070907生産者 | オーダーT0070907 | T0070907化学構造 | T0070907分子量 | T0070907代理店
納期 国内在庫品：受注日の翌日（15時までの受注分） ＊北海道、九州、沖縄への配送は受注日より２日以上 を要する場合あり 海外在庫品：受注後１〜２週間