U0126-EtOH

MEK1/2 inhibitor CAS# 1173097-76-1

U0126-EtOH

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Chemical structure

U0126-EtOH

3D structure

Chemical Properties of U0126-EtOH

Cas No. 1173097-76-1 SDF Download SDF
PubChem ID 16220066 Appearance Powder
Formula C20H22N6OS2 M.Wt 426.56
Type of Compound N/A Storage Desiccate at -20°C
Synonyms U0126-EtOH
Solubility DMSO : ≥ 49 mg/mL (114.87 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.
Chemical Name (2Z,3Z)-2,3-bis[amino-(2-aminophenyl)sulfanylmethylidene]butanedinitrile;ethanol
SMILES CCO.C1=CC=C(C(=C1)N)SC(=C(C#N)C(=C(N)SC2=CC=CC=C2N)C#N)N
Standard InChIKey CFQULUVMLGZVAF-OYJDLGDISA-N
Standard InChI InChI=1S/C18H16N6S2.C2H6O/c19-9-11(17(23)25-15-7-3-1-5-13(15)21)12(10-20)18(24)26-16-8-4-2-6-14(16)22;1-2-3/h1-8H,21-24H2;3H,2H2,1H3/b17-11+,18-12+;
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of U0126-EtOH

DescriptionU0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059.
TargetsMEK1MEK2    
IC500.07 μM0.06 μM    

Protocol

Cell experiment: [1]

Cell lines

HT22 cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reacting condition

10 μM, 24 hours

Applications

Cells were exposed to 5 mM glutamate with or without different concentrations of the inhibitor. The viability of HT22 cells was determined by MTT assay 24 h after the treatment. The results showed that U0126 inhibited cell death induced by glutamate toxicity dose-dependently. The complete inhibition of cell injury was achieved at 10 μM, a concentration that specifically inhibits MEK1/2.

Animal experiment: [2]

Animal models

Male BALB/c mice

Dosage form

Intraperitoneal injection; 7.5, 15 and 30 mg/kg

Application

Mice were sensitized by i.p. injections of 20 μg of OVA and 4 mg of Al(OH)3. BAL fluid was collected 24 h after the last OVA aerosol challenge. U0126 (7.5, 15, and 30 mg/kg) substantially reduced the total cell number recovered in BAL fluid as compared with PEG control, which was mainly due to a significant reduction in eosinophils in the U0126-treated mice in a dose-dependent manner. U0126 did not show any inhibitory effects on BAL fluid cell counts from sensitized mice challenged with saline aerosol.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Satoh T, Nakatsuka D, Watanabe Y, et al. Neuroprotection by MAPK/ERK kinase inhibition with U0126 against oxidative stress in a mouse neuronal cell line and rat primary cultured cortical neurons. Neuroscience letters, 2000, 288(2): 163-166.

[2] Duan W, Chan J H P, Wong C H, et al. Anti-inflammatory effects of mitogen-activated protein kinase kinase inhibitor U0126 in an asthma mouse model. The Journal of Immunology, 2004, 172(11): 7053-7059.

U0126-EtOH Dilution Calculator

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U0126-EtOH Molarity Calculator

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Preparing Stock Solutions of U0126-EtOH

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3443 mL 11.7217 mL 23.4434 mL 46.8867 mL 58.6084 mL
5 mM 0.4689 mL 2.3443 mL 4.6887 mL 9.3773 mL 11.7217 mL
10 mM 0.2344 mL 1.1722 mL 2.3443 mL 4.6887 mL 5.8608 mL
50 mM 0.0469 mL 0.2344 mL 0.4689 mL 0.9377 mL 1.1722 mL
100 mM 0.0234 mL 0.1172 mL 0.2344 mL 0.4689 mL 0.5861 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on U0126-EtOH

U0126-EtOH is a selective inhibitor of MEK1 and MEK2 with IC50 values of 70 nM and 60 nM, resepctively [1].

U0126 was screened out as an anti-inflammatory agent that inhibited AP-1 transcription with IC50 value of 1μM and had no interactions with GREs. U0126 binds MEK1/2 in a unique site. This inhibition of MEK1/2 is noncompetitive with ERK and ATP. U0126 showed no effects on other MAPKKs. In HT22 cells, U0126 treatment significantly inhibited the cell injury caused by oxidative glutamate toxicity and remarkably blocked the phosphorylation of ERK1/2. Besides that, U0126 exerted no neuroprotection against other stimuli such as TNFα and actinomycin D. U0126 treatment also protected the primary cultured cortical neurons from oxidative glutamate toxicity and hypoxia/reoxygenation [1, 2].

References:
[1] Duncia J V, Santella III J B, Higley C A, et al. MEK inhibitors: the chemistry and biological activity of U0126, its analogs, and cyclization products. Bioorganic & Medicinal Chemistry Letters, 1998, 8(20): 2839-2844.
[2] Satoh T, Nakatsuka D, Watanabe Y, et al. Neuroprotection by MAPK/ERK kinase inhibition with U0126 against oxidative stress in a mouse neuronal cell line and rat primary cultured cortical neurons. Neuroscience letters, 2000, 288(2): 163-166.

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References on U0126-EtOH

Netrin-1 induces the migration of Schwann cells via p38 MAPK and PI3K-Akt signaling pathway mediated by the UNC5B receptor.[Pubmed:26116534]

Biochem Biophys Res Commun. 2015 Aug 14;464(1):263-8.

Schwann cells (SCs) play an essentially supportive role in the regeneration of injured peripheral nerve system (PNS). As Netrin-1 is crucial for the normal development of nervous system (NS) and can direct the process of damaged PNS regeneration, our study was designed to determine the role of Netrin-1 in RSC96 Schwann cells (an immortalized rat Schwann cell line) proliferation and migration. Our studies demonstrated that Netrin-1 had no effect on RSC96 cells proliferation, while significantly promoted RSC96 cells migration. The Netrin-1-induced RSC96 cells migration was significantly attenuated by inhibition of p38 and PI3K through pretreatment with SB203580 and LY294002 respectively, but not inhibition of MEK1/2 and JNK by U0126-EtOH and SP600125 individually. Treatment with Netrin-1 enhanced the phosphorylation of p38 and Akt. QRT-PCR indicated that Netrin-1 and only its receptors Unc5a, Unc5b and Neogenin were expressed in RSC96 cells, among which Unc5b expressed the most. And UNC5B protein was significantly increased after stimulated by Netrin-1. In conclusion, we show here that Netrin-1-enhanced SCs migration is mediated by activating p38 MAPK and PI3K-Akt signal cascades via receptor UNC5B, which suggests that Netrin-1 could serve as a new therapeutic strategy and has potential application value for PNS regeneration.

[Effect of Picroside II on ERK1/2 Signal Pathway in Cerebral lschemic Injury Rats].[Pubmed:27323616]

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2016 Apr;36(4):437-44.

OBJECTIVE: To explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into middle cerebral artery. Totally 96 successfully modeled Wistar rats were divided into the modelgroup, the treatment (picroside II) group, the Lipopolysachcaride (LPS) group, and the U0126 group according to random digit table. Each group was further divided into 3 subgroups, i.e. 6, 12, and 24 h sub-groups. Picroside II (20 mg/kg) was peritoneally injected to rats in the treatment group 2 h after ischemia.LPS (20 mg/kg) and Picroside II (20 mg/kg) were peritoneally injected to rats in the LPS group 2 h after ischemia. U0126-EtOH (20 mg/kg)and Picroside II (20 mg/kg) were peritoneally injected to rats in the U0126group 2 h after ischemia. Equal volume of normal saline was peritoneally injected to rats in the control groupand the model group. The neurobehavioral function was evaluated by modified neurological severity score(mNSS) test. The structure of neurons was observed using hematoxylin-eosinstaining (HE) staining. Theapoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of phosphorylated extracellular signal-regulated protein kinase1,2 (pERK1,2) in cortex was detected using immunohistochemistry (IHC) and Western blot. RESULTS: After cerebral ischemia injury neurological impairment score increased, the damage of neuron in the cortical area was aggravated, apoptotic cells increased in the model group as time went by. The expression of pERK1/2 increased more significantly in the model group than in the control group (P <0.05). The damage of neuron in the cortical area was milder, while apoptotic cells decreased, the expression of pERK1f2 obviously decreased more in the treatment group and the U0126 group (P < 0.05). The early damage of neuron in the cortical area was more severe, apoptotic cells and the expression of pERK12 were comparatively higher in early stage of the LPS group, but the expression of pERK1/2 was somewhat decreased in late stage. CONCLUSIONS: Activating ERK12 pathway could mediate apoptosis and inflammatory reactions of neurons after cerebral ischemia injury. Picroside II could protect the nerve system possibly through reducing activation of ERKI2 pathway, inhibiting apoptosis of neurons and inflammation reaction.

Description

U0126-EtOH is a potent, non-ATP competitive and selective MEK1 and MEK2 inhibitor, with IC50s of 72 nM and 58 nM, respectively. U0126-EtOH is an autophagy and mitophagy inhibitor.

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