Research Area
Product Type
United States ( Change Country )
U0126-EtOH Chemical Structure
Recommended Products
AZD6244 (Selumetinib)
AZD6244 (Selumetinib, ARRY-142886) is highly potent to inhibit MEK1 with IC50 of 14 nM.
CI-1040 (PD184352)
CI-1040 (PD184352) is a MEK 1/2 inhibitor. Ki of 300nM
PD0325901
PD0325901 is MEK inhibitor and non-competitive with ATP, Kiapp of 1 nM against activated MEK1 and MEK2.
RDEA119 (BAY 869766)
MEK inhibitor with EC50 of 73 nM.
PD98059
PD 98059 is an inhibitor of MEK1 and MEK2 with IC50 values of 4 μM and 50 μM respectively.
AS703026
AS703026 is a highly selective and potent noncompetitive inhibitor of MEK1/2 with an IC50 range of 5-11 nM.
BIX 02188
BIX02188 is a MEK5-selective inhibitor with an IC50 of 0.8 ± 1.0 μM.
BIX 02189
BIX 02189 is a selective MEK5/ERK5 inhibitor with an IC50 of 59 nM.
PD318088
PD318088 is a non-ATP competitive allosteric MEK1/2 inhibitor.
AZD8330
AZD8330 is an orally active, selective MEK inhibitor with an IC50 of 7 nM.
Biological Activity
U0126-EtOH is an inhibitor of both MEK1(IC50 of 72 nM) and MEK2(IC50 of 58 nM).
U0126-EtOH is a highly selective inhibitor of both MEK1 and MEK2, a type of MAPK/ERK kinase. U0126 was found to functionally antagonize AP-1 transcriptional activity via noncompetitive inhibition of the dual specificity kinase MEK with IC50 of 72 nM for MEK1 and 58 nM for MEK2. [1]
U0126-EtOH inhibited anchorage-independent growth of Ki-ras-transformed rat fibroblasts by simultaneously blocking both extracellular signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR)-p70(S6K) pathways. [2]
The effects of U0126-EtOH on the growth of eight human breast cancer cell lines shown that U0126-EtOH selectively repressed anchorage-independent growth of MDA-MB231 and HBC4 cells, two lines with constitutively activated ERK. Loss of contact with substratum triggers apoptosis in many normal cell types, a phenomenon termed anoikis. U0126 sensitized MDA-MB231 and HBC4 to anoikis, i.e., upon treatment with U0126-EtOH, cells deprived of anchorage entered apoptosis. [3]
References on U0126-EtOH
- [1] Bioorganic & Medicinal Chemistry Letters 1998;8:2839-2844
- [2] Cancer Res 2000;60:2104-2107
Chemical Information
| Molecular Weight (WM): | 426.56 |
|---|---|
| Formula: | C18H16N6S2.C2H6O |
| CAS No.: | 1173097-76-1 |
| Synonyms: |
Uo126
|
| Dissolve in (25°C): | DMSO ≥85mg/mL |
| Water <1mg/mL | |
| Ethanol <1mg/mL | |
| Storage: | 2 years-20°CPowder |
| 1 week-4°Cin DMSO | |
| 1 month-80°in DMSO |
Quality Control & MSDS
Research Area
Notes:
Related Inhibitors
Recommended Screening Libraries
Chemical Library
A collection of 864 bioactive compounds
Inhibitor Library
A collection of 481 inhibitors
Kinase Inhibitor Library
A collection of 194 kinase inhibitors
Tyrosine Kinase Inhibitor Library
A collection of 85 tyrosine kinase inhibitors.
FDA Approved Drug Library
A collection of 426 FDA approved drugs
Natural Product Library
A collection of 139 natural products
Chemotherapeutic Agent Library
A collection of 40 chemotherapeutic agents
Epigenetics Compound library
A unique collection of 17 small molecule modulators
Stem Cell Compound library
A unique collection of 47 small molecule inhibitors
GPCR Compound library
A unique collection of 63 GPCR small molecules
Selleck's high quality products have been used in several published research findings, including the following:
Down-regulation of mitogen-inducible gene 6, a negative regulator of EGFR, enhances resistance to MEK inhibition in KRAS mutant cancer cells.
BRAF Gene Amplification Can Promote Acquired Resistance to MEK Inhibitors in Cancer Cells Harboring the BRAF V600E Mutation
Controlling multipotent stromal cell migration by integrating “course-graining” materials and “fine-tuning” small molecules via decision tree signal-response modeling
Differences in wound healing in mice with deficiency of IL-6 versus IL-6 receptor.
We have 4 customer reviews of U0126-EtOH.
- (4)
- (0)
- (0)
- (0)
- (0)
- (0)
- (0)
- (0)
- (0)
Average Customer Review
(4 customer reviews)
-
Click to enlarge
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 - 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
Data from [Biomaterials 2011 October;32:7524-7531] U0126-EtOH purchased from Selleck
-
Click to enlarge
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of U0126 for 24 hours.
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of U0126 for 24 hours.
Data independently produced by Dr. Zhang of Tianjin Medical University U0126-EtOH purchased from Selleck
-
Click to enlarge
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.
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.
Data from [J. Immunol 2010.May;184;7219-7228] U0126-EtOH purchased from Selleck
- Your product U0126(Cat.NO S1102) works well in our experiments. I hope I can get more excellent products from your company in future.
Dongfeng ChenThe Rausing Lab
This product has been referenced in
Check our customer reviews
| 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 |
Data from [Biomaterials 2011 October;32:7524-7531]
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of U0126 for 24 hours.
|
Data independently produced by Dr. Zhang of Tianjin Medical University
Recently Viewed Items
Keywords:buy U0126-EtOH | U0126-EtOH supplier | purchase U0126-EtOH | U0126-EtOH cost | U0126-EtOH manufacturer | order U0126-EtOH | U0126-EtOH distributor