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CC-930

现货
Catalog No.
A3288
JNK抑制剂
组合的产品项目
规格价格库存 数量
50mg
¥ 11,940.00
Ship with 10-15 days
5mg
¥ 2,340.00
Ship with 10-15 days
10mg
¥ 3,540.00
Ship with 10-15 days
25mg
¥ 7,020.00
Ship with 10-15 days

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Background

CC-930 is a potent and selective inhibitor of JNK1/JNK2/JNK3 with IC50 values of 61 nM, 7 nM and 6 nM respectively. [1]
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.[2]
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.[1] 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[3] 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.[3] 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[4].
References:
[1].    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.
[2].    Waetzig V, Herdegen T: Context-specific inhibition of JNKs: overcoming the dilemma of protection and damage. Trends Pharmacol Sci 2005, 26(9):455-461.
[3].    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.
[4].    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.

Chemical Properties

StorageStore at -20°C
M.Wt448.44
Cas No.899805-25-5
FormulaC21H23F3N6O2
SynonymsTanzisertib;CC930;CC 930
SolubilitySoluble in DMSO
Chemical Name4-[[9-[(3S)-oxolan-3-yl]-8-(2,4,6-trifluoroanilino)purin-2-yl]amino]cyclohexan-1-ol
SDFDownload SDF
Canonical SMILESC1CC(CCC1NC2=NC=C3C(=N2)N(C(=N3)NC4=C(C=C(C=C4F)F)F)C5CCOC5)O
运输条件试用装:蓝冰运输。 其他可选规格:常温运输或根据您的要求用蓝冰运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。

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化学结构

CC-930