In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
CC-930 is a potent and selective inhibitor of JNK1/JNK2/JNK3 with IC50 values of 61 nM, 7 nM and 6 nM respectively. 
JNKs (c-Jun N-terminal kinases) belong to kinases which were originally indentified. They bind to c-Jun then phosphorylate it on Ser-63 and Ser-73 which located in its transcriptional activation domain. JNKs belong to MAPK family. They contain ten isforms encoded by three genes: JNK1, JNK2 and JNK3. They are 46 KD or 55 KD protein. They play an important role in stress stimuli, such as heat shock, cytokines, and osmotic shock. They are also responsive to the cellular apoptosis pathway and T cell differentiation. They are activated through a dual phosphorylation of Thr and Tyr residues within a Thr-Pro-Tyr motif which located in kinase subdomain. JNKs modify the activity of many proteins that act in the nucleus reside or at the mitochondria. JNKs activate the downstream molecules which include p53, c-Jun, ELK1, SMAD4 and HSF1. JNKs regulate several important cellular functions, such as cell growth, survival, differentiation and apoptosis.
CC-930 kinetically competitive with ATP in the phosphorylation of the substrate c-Jun against all isoforms of JNK with Ki values of 44 ± 3 nM (JNK1), 6.2 ± 0.6 nM and IC50 value of 5 nm for JNK3. EGFR is the only non-MAP kinase which inhibited more than 50% at 3 M. It did not inhibit greater than 50% against 22 diverse non-kinase enzymes at 10 M. CC-930 reduced the phosphorylation of c-Jun the stimulated by TGF β at 1 μM which is a clinically relevant concentration in fi broblasts CC-930 also was showed the potent antifibrotic founctions in the TSK1 model. CC-930 reduced hypodermal thickening with a dose-dependent manner by up to 85±4% in TSK1 mice. CC-930 has no effect on kidney hypertrophy, blood pressur, podocyte loss, glomerular fibrosis in diabetic spontaneously hypertensive rats (SHR). However, CC-930 reduced the levels of ccl2 mRNA in diabetic kidneys.
. Plantevin Krenitsky V, Nadolny L, Delgado M, Ayala L, Clareen SS, Hilgraf R, Albers R, Hegde S, D'Sidocky N, Sapienza J et al: Discovery of CC-930, an orally active anti-fibrotic JNK inhibitor. Bioorg Med Chem Lett, 22(3):1433-1438.
. Waetzig V, Herdegen T: Context-specific inhibition of JNKs: overcoming the dilemma of protection and damage. Trends Pharmacol Sci 2005, 26(9):455-461.
. Reich N, Tomcik M, Zerr P, Lang V, Dees C, Avouac J, Palumbo K, Horn A, Akhmetshina A, Beyer C et al: Jun N-terminal kinase as a potential molecular target for prevention and treatment of dermal fibrosis. Ann Rheum Dis, 71(5):737-745.
. Lim AK, Ma FY, Nikolic-Paterson DJ, Ozols E, Young MJ, Bennett BL, Friedman GC, Tesch GH: Evaluation of JNK blockade as an early intervention treatment for type 1 diabetic nephropathy in hypertensive rats. Am J Nephrol, 34(4):337-346.
|Storage||Store at -20°C|
|Solubility||Soluble in DMSO|