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- DB07268
- SP 600125
CC-401JNK inhibitor,ATP-competitive |
Sample solution is provided at 25 µL, 10mM.
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Quality Control & MSDS
- View current batch:
- Purity = 98.15%
- COA (Certificate Of Analysis)
- HPLC(Retest)
- NMR (Nuclear Magnetic Resonance)
- MSDS (Material Safety Data Sheet)
- Datasheet
Chemical structure
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CC-401 Dilution Calculator
calculate
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CC-401 Molarity Calculator
calculate
Cas No. | 395104-30-0 | SDF | Download SDF |
Synonyms | N/A | ||
Chemical Name | 3-[3-(2-piperidin-1-ylethoxy)phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole | ||
Canonical SMILES | C1CCN(CC1)CCOC2=CC=CC(=C2)C3=NNC4=C3C=C(C=C4)C5=NC=NN5 | ||
Formula | C22H24N6O | M.Wt | 388.47 |
Solubility | ≥19.4mg/mL in DMSO | Storage | Store at -20°C |
Physical Appearance | A solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
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. |
CC-401 is a specific inhibitor of JNK with Ki values of 25-50nM [1].
CC-401 is a second generation ATP-competitive inhibitor of all three forms of JNK. It is selective against JNK over other kinases such as p38, ERK, IKK2 and ZAP70. CC-401 potently inhibits JNK in cell-based assay with concentration of 1 to 5μM. The activation of JNK signaling is identified in many immune-mediated kidney disease models. Thus, as the JNK inhibitor, CC-401 is found to be effective in these renal injury models. In the acute anti-GBM disease, CC-401 inhibits JNK activation and causes 50%-70% reduction of proteinuria. In addition, CC-401 is also used in liver injury models [1, 2 and 3].
References:[1] Ma F Y, Flanc R S, Tesch G H, et al. A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. Journal of the American Society of Nephrology, 2007, 18(2): 472-484.[2] Flanc R S, Ma F Y, Tesch G H, et al. A pathogenic role for JNK signaling in experimental anti-GBM glomerulonephritis. Kidney international, 2007, 72(6): 698-708.[3] Bogoyevitch M A, Arthur P G. Inhibitors of c-Jun N-terminal kinases—JuNK no more Biochimica et Biophysica Acta (BBA)-Proteins and Proteomics, 2008, 1784(1): 76-93.