Molecular Weight(MW): 426.56
U0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM in cell-free assays, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059.
Cited by 61 Publications
12 Customer Reviews
Melanoma cell viability and in vivo growth by cyclindependent kinase 2/4 inhibition. Western blot analysis for c-Jun, phosphorylated-ERK1/2 (Thr202/Tyr204) (p-ERK1/2), and total ERK1/2 protein levels was done for human melanoma cell lines treated with the BRAFV600E inhibitor GDC-0879 (1 μM), or MEK inhibitors CI-1040 (1 μM), U0126 (1 μM), and PD98059 (10 μM) for 18 hours.
J Natl Cancer Inst 2012 104(21), 1673-9. U0126-EtOH purchased from Selleck.
Successful test of decision tree model prediction that reducing ERK signal on Cn/tEGF substrates will enhance MSC migration persistence and mean free path. (A) mean free path, (B) persistence time, and (C) speed under partial and total ERK inhibition with MEK inhibitor U0126
Biomaterials 2011 32, 7524-7531. U0126-EtOH purchased from Selleck.
Inhibition of the ERK1/2 pathway prevents FLIPL downregulation and sensitivity to TRAIL induced by EGF. MCF10A cells were preincubated in the absence of EGF for 48 h before re-addition of EGF ( -/+ ) and incubated in the presence or absence of ( a) the PI3K inhibitor LY294002 (LY, 10 μM), or (b) the MEK1 inhibitor U0126 (10 μM), for 15 h. Other cultures were incubated in parallel with (+/+ ) or without ( -/- ) EGF for the entire experimental period (preincubation/incubation). FLIPL , p-AKT, AKT, p-ERK1/2, ERK1/2 and BimEL levels were assessed by western blotting. GAPDH and tubulin levels were used as protein loading controls. FLIPL mRNA levels were measured by quantitative PCR (b , lower panel). Results are representative of two independent experiments. (c ) Cells were preincubated/incubated as in (b) and then TRAIL (500 ng/ml) was added to some cultures for 6 h. Apoptosis was determined as described in Materials and Methods. Error bars represent S.D. from three independent experiments.
Cell Death Differ 2012 19, 1908-16. U0126-EtOH purchased from Selleck.
UACC62 cells were treated for 6 hours as indicated, followed by assessment of phospho-p90RSK1 and p90RSK1 levels by western blotting.
J Invest Dermatol 2012 132, 2780-90. U0126-EtOH purchased from Selleck.
ERK activation is increased in Il6ra2/2 mice compared with WT mice. A, Total and phosphorylated (p) Stat3 and ERK were assessed in small punch biopsy wounds collected after 30 min (Stat3) or 1 d (ERK) by Western blotting. Densitometry results for the blots are provided to the right. pp , 0.05. B, Total and p-ERKs were assessed in small wounds generated in WTand Il6ra2/2 mice treated topically with vehicle (DMSO) or with the MEK inhibitor U0126.Wounds were harvested after 1 d, and western blotting was performed on lysates. C, Wound contraction was assessed macroscopically in large wounds of WT (left panel) and Il6ra2/2 mice treated daily with vehicle (DMSO) or U0126. pp , 0.05.
J Immunol 2010 184, 7219-7228. U0126-EtOH purchased from Selleck.
Dose response curves and cytotoxic CI plots for A549 in 72 h combined treatment of gemcitacine, AG1478 and U0126 are shown in (A) and (B), respectively. These are also shown for H322 in (C) and (D). Gemcitabine concentration was set constant at 10 nM for A549 and 500 nM for H322. U0126 concentration was 2.5 μM and AG1478.
Lung Cancer 2011 73, 274-82. U0126-EtOH purchased from Selleck.
Some of the mice received intra-peritoneal administration of U0126 (10 mg/kg BW) or vehicle beginning at 24 h after I/R or sham until 24 h prior to harvest daily. Antibodies used was: Na,K-ATPase.
Biochim Biophys Acta 2013 1832(12):1998-2008. U0126-EtOH purchased from Selleck.
Some of the mice received intra-peritoneal administration of U0126 (10 mg/kg BW) or vehicle beginning at 24 h after I/R or sham until 24 h prior to harvest daily. kidneys were snap-frozen in liquid nitrogen and perfusion-fixed with 30 mL of phosphate buffered saline (PBS) for 2 min and then PLP (4% paraformaldehyde, 75 mM l-lysine, 10 mM sodium periodate) solution, respectively.
Biochim Biophys Acta 2013 1832(12):1998-2008. U0126-EtOH purchased from Selleck.
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of U0126 for 24 hours.
2010 Dr. Zhang of Tianjin Medical University. U0126-EtOH purchased from Selleck.
Purity & Quality Control
Choose Selective MEK Inhibitors
|Description||U0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM in cell-free assays, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059.|
|Features||A chemically synthesized and highly selective inhibitor of both MEK1 and MEK2.|
U0126-EtOH functionally antagonizes AP- 1 transcriptional activity and blocks the production of a variety of cytokines and metalloproteinases involved in the inflammatory response.  U0126-EtOH inhibits T cell proliferation in response to antigenic stimulation or cross-linked anti-CD3 plus anti-CD28 Abs without effect on IL-2-induced proliferation by down-regulating IL-2 mRNA levels.  A recent study shows that U0126-EtOH antagonizes resveratrol-induced apoptosis in castration-resistant human prostate cancer C4-2 cells, inhibits mitochondrial function and shifts cells to aerobic glycolysis independently of MEK. 
|In vivo||U0126-EtOH, as the inhibitor of intracellular Raf/MEK/ERK signaling pathway, demonstrates antiviral activity by suppressing propagation of the 2009 pandemic IV H1N1 variant and highly pathogenic avian influenza viruses (HPAIV) in vivo in the mouse lung by inhibiting.  U0126-EtOH shows the potential neuroprotective effect and improving spatial learning in Morris water maze (MWM) by activating peroxisome proliferator-activated receptor gamma coactivator-1a, nuclear respiratory factor 1, and mitochondrial transcription factor A in Aβ-injected rats. |
In Vitro Kinase Assays :The amount of immunoprecipitated wild type MEK used in these assays is adjusted to give a similar amount of activity units as obtained with 10 nM recombinant MEK. Reaction velocities are measured using a 96-well nitrocellulose filter apparatus as described below. Unless otherwise noted, reactions are 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 are initiated by the addition of [γ-33P]ATP into the premixed MEK/ERK/inhibitor reaction mixture, and an aliquot of 100 μL is taken every 6 minutes and transferred to the 96-well nitrocellulose membrane plate which has 50 mM EDTA to stop the reaction. The membrane plate is drawn and washed 4 times with buffer under vacuum. Wells are then filled with 30 μL of Microscint-20 scintillation fluid, and the radioactivity of 33P-phosphorylated ERK is counted with a Top Count scintillation counter. Velocities are obtained from the slopes of radioactivity versus time plots. Concentrations of ERK and ATP are 400 nM and 40 μM, respectively, unless otherwise indicated. For all of the in vitro enzyme assays, the percent inhibition is calculated 100 (1 −Vi/Vo) where Vi and Vo are the initial reaction velocities in the presence and absence of inhibitor, respectively. The data are then plotted as percent inhibition as a function of inhibitor concentration and fit, by nonlinear least squares regression, to the standard equation for a Langmuir isotherm to determine the IC50. As reported, enzyme concentrations are based upon molecular weights and mass of protein used in the final assay volume and not on active site titration. Thus, the actual enzyme active site concentration may differ from that reported.
-  Duncia JV, et al. Bioorg Med Chem Lett. 1998, 8(20), 2839-2844.
-  DeSilva DR, et al. J Immunol. 1998, 160(9), 4175-4181.
-  Freeman MR, et al. Cancer Biol Ther. 2011, 12(11), 966-977.
|In vitro||DMSO||85 mg/mL warmed (199.26 mM)|
|In vivo||10% DMSO+50% PEG 300+ddH2O||28mg/mL|
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