U0126-EtOH

カタログ番号 T6223 CAS 1173097-76-1

別名: U0126 Ethanol, U0126

U0126-EtOH (U0126 Ethanol) is a non-ATP competitive specific inhibitor of MEK1/2 (IC50: 0.07/0.06 μM).

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U0126-EtOH, CAS 1173097-76-1

パッケージサイズ	在庫状況	単価(税別)
サンプルについてお問い合わせ
5 mg	在庫あり	￥ 7,000
10 mg	在庫あり	￥ 11,000
25 mg	在庫あり	￥ 15,000
50 mg	在庫あり	￥ 18,000
100 mg	在庫あり	￥ 22,500
1 mL * 10 mM (in DMSO)	在庫あり	￥ 11,500

バルクのお問い合わせ

バッチを選択

純度: 99.82%

COA DATASHEET SDS HNMR HPLC

純度: 99.72%

COA DATASHEET SDS HPLC

純度: 98.65%

COA DATASHEET SDS HPLC HNMR

COA DATASHEET SDS HNMR

DATASHEET SDS

COA DATASHEET SDS

DATASHEET SDS

バッチの詳細情報はお問い合わせください

生物学的特性に関する説明

化学的特性

保存条件 & 溶解度情報

説明	U0126-EtOH (U0126 Ethanol) is a non-ATP competitive specific inhibitor of MEK1/2 (IC50: 0.07/0.06 μM).
ターゲット＆IC50	MEK2:60 nM (cell free), MEK1:70 nM (cell free)
In vitro	U0126 antagonized AP-1 transcriptional activity via noncompetitive inhibition of the dual specificity kinase MEK with an IC50 of 0.07 microM for MEK 1 and 0.06 microM for MEK 2 [1]. In fibroblasts treated with TPA/serum, U0126 suppressed the up-regulation of c-Fos and c-Jun proteins by 50–80%. Treatment with 10 μM U0126 did not affect the protein levels of the constitutively expressed transcription factors SP-1 or JunD and Fra-1 [2]. U0126 caused phosphorylation and activation of AMPK) and increased phosphorylation of its downstream target acetyl-CoA carboxylase, in HEK293 cells. This effect only occurred in cells expressing the upstream kinase, LKB1 [3].
In vivo	Treatment of mice with U0126 via the aerosol route led to (i) inhibition of MEK activation in the lung (ii) reduction of progeny IAV titers compared to untreated controls (iii) protection of IAV infected mice against a 100× lethal viral challenge [4]. In all U0126 (10.5 mg/kg) experiments, engraftment and early tumor growth were significantly decreased. Furthermore, a 60–70% reduction in the volume of tumors treated with U0126 was obtained 9 days after injection and thereafter. Cdk1 expression was also strongly reduced in U0126-treated mice [5].
キナーゼ試験	The amount of immunoprecipitated wild type MEK used in these assays was adjusted to give a similar amount of activity units as obtained with 10 nM recombinant MEK. All other assays were performed with a recombinant, constitutively activated mutant MEK-1 (ΔN3-S218E/S222D) or constitutively active MEK-2(S222E/S226D). Reaction velocities were measured using a 96-well nitrocellulose filter apparatus as described below. Unless otherwise noted, reactions were carried out at an enzyme concentration of 10 nM, in 20 mM Hepes, 10 mM MgCl2, 5 mM β-mercaptoethanol, 0.1 mg/ml BSA, pH 7.4, at room temperature. Reactions were initiated by the addition of [γ-33P]ATP into the premixed MEK/ERK/inhibitor reaction mixture, and an aliquot of 100 μl was taken every 6 min and transferred to the 96-well nitrocellulose membrane plate which had 50 mM EDTA to stop the reaction. The membrane plate was drawn and washed 4 times with buffer under vacuum. Wells were then filled with 30 μl of Microscint-20 scintillation fluid, and the radioactivity of33P-phosphorylated ERK was counted with a Top Count scintillation counter. Velocities were obtained from the slopes of radioactivity versus time plots. Concentrations of ERK and ATP were 400 nM and 40 μM, respectively, unless otherwise indicated [2].
細胞研究	HEK293 cells were maintained in Dulbecco's modification of Eagle's medium (low glucose) plus 10% foetal bovine serum. HeLa cells stably expressing wild type or kinase-dead LKB1 have been described. AMPK activity was determined by immunoprecipitate kinase assays using anti-AMPK-a1 and -a2 antibodies. Antibodies recognising AMPK phosphorylated on Thr-172 (anti-pT172), AMPK-α1 and -α2 and acetyl-CoA carboxylase-1 (ACC1) phosphorylated on Ser-80 [16] were described previously. Quantification of ratios of signals from phosphorylated and total protein using these antibodies was performed by dual labelling using the LI-COR Odyssey IR imager as described. Contents of ATP and ADP were determined for cells in 6 cm culture dishes by quickly pouring off the medium, adding 350 μl of ice-cold 5% perchloric acid, scraping the cells off with a plastic scraper, and centrifuging (14 000 · g; 3 min, 4 °C) to remove insoluble material. The perchloric acid was then extracted from the supernatant and nucleotides analysed by capillary electrophoresis of perchloric acid extracts as described previously. All incubations of cells were performed in triplicate and results are expressed as means ± S.E.M [3].
動物実験	Prior to injection, FI cells were labeled with a stable fluorescent dye molecule, DiA at 10 μg/ml for 5 h at 37 1C. After washing to remove free DiA, cells were trypsinized for inoculation (U0126 experiments) or transfection (RNAi experiments). Biliary epithelial cells were injected subcutaneously, at the indicated times, into the tibia of nude mice. In the chemical experiments, 3h after inoculation, mice were treated with U0126 (10.5 mg/kg) daily by intraperitoneal injection. The length and width of each tumor were measured every day by using a caliper. The following formula was used to calculate tumor volumes ? width2 length/2. Mice were killed at the end of experiment. Tumors were immediately frozen in liquid nitrogen [5].

別名	U0126 Ethanol, U0126
分子量	426.6
分子式	C18H16N6S2·C2H6O
CAS No.	1173097-76-1

保存条件

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度情報

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 55 mg/mL (128.93 mM)

5% DMSO+95% Saline: 3.95 mg/mL (9.26 mM, suspension)

参考文献

1. Duncia JV, et al. MEK inhibitors: the chemistry and biological activity of U0126, its analogs, and cyclization products. Bioorg Med Chem Lett. 1998, 8(20), 2839-2844. 2. Favata MF, et al. Identification of a novel inhibitor of mitogen-activated protein kinase kinase. J Biol Chem. 1998 Jul 17;273(29):18623-32. 3. Dokladda K, et al. PD98059 and U0126 activate AMP-activated protein kinase by increasing the cellular AMP:ATP ratio and not via inhibition of the MAP kinase pathway. FEBS Lett. 2005 Jan 3;579(1):236-40. 4. Droebner K, et al. Antiviral activity of the MEK-inhibitor U0126 against pandemic H1N1v and highly pathogenic avian influenza virus in vitro and in vivo. Antiviral Res. 2011 Nov;92(2):195-203. 5. Bessard A, et al. RNAi-mediated ERK2 knockdown inhibits growth of tumor cells in vitro and in vivo. Oncogene. 2008 Sep 11;27(40):5315-25. 6. Ahnstedt H, et al. U0126 attenuates cerebral vasoconstriction and improves long-term neurologic outcome after stroke in female rats. J Cereb Blood Flow Metab. 2015 Mar;35(3):454-60. 7. Zeng H, Pathak J L, Shi Y, et al. Indirect selective laser sintering-printed microporous biphasic calcium phosphate scaffold promotes endogenous bone regeneration via activation of ERK1/2 signaling[J]. Biofabrication. 2020, 12(2): 025032. 8. Shao S, Xia H, Hu M, et al. Isotalatizidine, a C 19-diterpenoid alkaloid, attenuates chronic neuropathic pain through stimulating ERK/CREB signaling pathway-mediated microglial dynorphin A expression[J]. Journal of Neuroinflammation. 2020, 17(1): 1-11. 9. Zeng H, Pathak J L, Shi Y, et al. Indirect selective laser sintering printed microporous biphasic calcium phosphate scaffold promotes endogenous bone regeneration via activation of ERK1/2 signaling[J]. Biofabrication. 2020. 10. Zhou B, Yan J, Guo L, et al. Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma[J]. Theranostics. 2020, 10(14): 6530.

引用文献

1. Shao S, Xia H, Hu M, et al. Isotalatizidine, a C19-diterpenoid alkaloid, attenuates chronic neuropathic pain through stimulating ERK/CREB signaling pathway-mediated microglial dynorphin A expression. Journal of Neuroinflammation. 2020, 17(1): 1-11 2. Zeng H, Pathak J L, Shi Y, et al. Indirect selective laser sintering-printed microporous biphasic calcium phosphate scaffold promotes endogenous bone regeneration via activation of ERK1/2 signaling. Biofabrication. 2020, 12(2): 025032. 3. Zhou B, Yan J, Guo L, et al. Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma. Theranostics. 2020, 10(14): 6530. 4. Zeng H, Pathak J L, Shi Y, et al. Indirect selective laser sintering printed microporous biphasic calcium phosphate scaffold promotes endogenous bone regeneration via activation of ERK1/2 signaling. Biofabrication. 2020 5. Xiao Q, Lei L, Ren J, et al. Mutant NPM1-Regulated FTO-Mediated m6A Demethylation Promotes Leukemic Cell Survival via PDGFRB/ERK Signaling Axis. Frontiers in Oncology. 2022.12 6. Zhu Y, Xiao Y, Kong D, et al. Down-Regulation of miR-378d Increased Rab10 Expression to Help Clearance of Mycobacterium tuberculosis in Macrophages. Frontiers in cellular and infection microbiology. 2020, 10: 108. 7. Meng Y, Lv T, Zhang J, et al.Temporospatial inhibition of Erk signaling is required for lymphatic valve formation.Signal Transduction and Targeted Therapy.2023, 8(1): 342.

投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください

投与量

mg/kg

動物の平均体重

動物あたりの投与量

動物数

溶媒の組成を入力してください

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

計算するリセット

計算結果:

作業濃度: mg/ml;

DMSO溶液の作成方法: mg あらかじめ溶解した薬剤 μL DMSO (マスター溶液の濃度 mg/mL)，濃度がそのバッチの薬剤のDMSO溶解度を超える場合は、まずご連絡ください。

生体内薬剤の調合法：取る μL DMSO マスター溶液、次に追加 μL PEG300，確実に混ぜてから加える μL Tween 80，確実に混ぜてから加える μL ddH₂O, 確実に混ぜる

お問合せ内容:

必ず順番通りに溶媒を加えてください。ボルテックスミキサーや超音波、湯煎することで溶解しやすくなります

計算器

モル濃度計算機

希釈計算機

再構成計算

分子量計算機

質量

濃度

体積

分子量

モル度計算機では以下の計算が可能です

既知の体積と濃度の溶液を調製するために必要な化合物の質量
質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度

参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか？
［分子量（MW）］の欄に［197.13］と入力してください
[濃度]ボックスに10と入力し、正しい単位（millimolar）を選択します
[容量]ボックスに10と入力し、正しい単位（milliliter）を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

濃度 (開始)

体積 (開始)

濃度 (終了)

体積 (終了)

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2＆V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか？
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度（開始）ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度（終了）ボックスに50を入力し正しい単位(millimolar)を選択してください
体積（終了）ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積（開始）ボックスに表示されます。

分子式

分子量 g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント：化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量（分子量）を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量（分子量）とは、物質の1分子の質量であり、統一された原子質量単位（u）で表されます。(1uは炭素12の1原子の質量の1/12に等しい）
モル質量（molar weight）とは、ある物質の1モルの質量のことで、単位はg/molです。

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技術サポート

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.

Keywords

U0126-EtOH 1173097-76-1 Autophagy MAPK Microbiology/Virology Influenza Virus Mitophagy MEK Mitogen-activated protein kinase kinase MAP2K U-0126-EtOH inhibit competitive virus U0126 Ethanol U0126EtOH MAPKK Mitochondrial Autophagy U 0126 Inhibitor progeny non-ATP U0126 EtOH U-0126 U0126 inhibitor

本ウェブサイトに掲載されている製品は全て研究用試薬です。研究目的以外の用途にはご使用できません。

U0126-EtOH

保存条件

溶解度情報

参考文献

引用文献

関連化合物ライブラリー

関連製品

投与量変換

In vivo投与量計算 (透明溶液)

計算器

モル度計算機では以下の計算が可能です

溶液を作るのに必要な希釈率の計算

バイアルを再構成するのに必要な溶媒の量を計算する.

化合物の化学式を入力して、そのモル質量や元素組成を計算します

技術サポート

Keywords