CC-930

JNK inhibitor,potent and selective CAS# 899805-25-5

CC-930

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Catalog No. BCC1459----Order now to get a substantial discount!

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CC-930

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Chemical Properties of CC-930

Cas No. 899805-25-5 SDF Download SDF
PubChem ID 11597537 Appearance Powder
Formula C21H23F3N6O2 M.Wt 448.44
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Tanzisertib
Solubility DMSO : ≥ 33 mg/mL (73.59 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 4-[[9-[(3S)-oxolan-3-yl]-8-(2,4,6-trifluoroanilino)purin-2-yl]amino]cyclohexan-1-ol
SMILES C1CC(CCC1NC2=NC=C3C(=N2)N(C(=N3)NC4=C(C=C(C=C4F)F)F)C5CCOC5)O
Standard InChIKey IBGLGMOPHJQDJB-MOKVOYLWSA-N
Standard InChI InChI=1S/C21H23F3N6O2/c22-11-7-15(23)18(16(24)8-11)28-21-27-17-9-25-20(26-12-1-3-14(31)4-2-12)29-19(17)30(21)13-5-6-32-10-13/h7-9,12-14,31H,1-6,10H2,(H,27,28)(H,25,26,29)/t12?,13-,14?/m0/s1
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 CC-930

DescriptionCC-930 is a potent JNK1/JNK2/JNK3 inhibitor with IC50 values of 61/7/6 nM, respectively, and used for the treatment of fibrotic and infammatory indications.In Vitro:CC-930 inhibits the formation of phospho-cJun in human PBMC stimulated by phorbol-12-myristate-13-acetate and phytohemeagglutinin (IC50=1 μM)[1]. CC-930 (1-2 μM) substantially reduces hepatocyte apoptosis and necrosis, abrogates apoptosis and necrosis in FC-loaded WT hepatocytes[2]. CC-930 blocks the JNK pathway that is activated by pro-fibrotic cytokines in systemic sclerosis[3].In Vivo:CC-930 (10 and 30 mg/kg, p.o.) inhibits the production of TNFa by 23% and 77% in the acute rat LPS-induced TNFa production PK-PD model[1]. CC-930 (150 mg/kg) prevents the development of fibrosis in different models, but can also induce the regression of pre-existing fibrosis[3].

References:
[1]. Plantevin Krenitsky V, et al. Discovery of CC-930, an orally active anti-fibrotic JNK inhibitor. Bioorg Med Chem Lett. 2012 Feb 1;22(3):1433-8. [2]. Gan LT, et al. Hepatocyte free cholesterol lipotoxicity results from JNK1-mediated mitochondrial injury and is HMGB1 and TLR4-dependent. J Hepatol. 2014 Dec;61(6):1376-84. [3]. Reich N, et al. Jun N-terminal kinase as a potential molecular target for prevention and treatment of dermal fibrosis. Ann Rheum Dis. 2012 May;71(5):737-45. [4]. Tavernier SJ, et al. Regulated IRE1-dependent mRNA decay sets the threshold for dendritic cell survival. Nat Cell Biol. 2017 Jun;19(6):698-710.

Protocol

Cell Assay [3]
Systemic sclerosis (SSc) fibroblasts are incubated with 1 µM CC-930 in 96-well plates for 20 h. Then MTT is added at a final concentration of 1 mg/mL, and the cells are further incubated at 37°C for 4 h. Mock-treated fibroblasts are used as controls, and all other results are normalised to untreated cells.

Animal Administration [3]
To evaluate the regression of fibrosis on inhibition of JNK, a modified model of bleomycin-induced dermal fibrosis is used. In this model, treatment is initiated 3 weeks after the beginning of the challenge with bleomycin, when significant dermal fibrosis is already established. The outcome of six different groups with a total number of 40 mice is analysed. The first group of mice receive subcutaneous injections of NaCl for 6 weeks. The second group is injected for 3 weeks with bleomycin followed by injections of NaCl for another 3 weeks to analyse the degree of fibrosis before treatment, and to control the spontaneous regression of fibrosis. The third group of mice is killed after 6 weeks of injections with bleomycin. The fourth and the fifth group are treated with CC-930 at doses of 50 mg/kg and 150 mg/kg for the last 3 weeks of continuous challenge with bleomycin for 6 weeks. The sixth group is a positive control group consisting of mice challenged with bleomycin for 6 weeks and treated in parallel with imatinib at doses of 50 mg/kg for the last 3 weeks.

References:
[1]. Plantevin Krenitsky V, et al. Discovery of CC-930, an orally active anti-fibrotic JNK inhibitor. Bioorg Med Chem Lett. 2012 Feb 1;22(3):1433-8. [2]. Gan LT, et al. Hepatocyte free cholesterol lipotoxicity results from JNK1-mediated mitochondrial injury and is HMGB1 and TLR4-dependent. J Hepatol. 2014 Dec;61(6):1376-84. [3]. Reich N, et al. Jun N-terminal kinase as a potential molecular target for prevention and treatment of dermal fibrosis. Ann Rheum Dis. 2012 May;71(5):737-45. [4]. Tavernier SJ, et al. Regulated IRE1-dependent mRNA decay sets the threshold for dendritic cell survival. Nat Cell Biol. 2017 Jun;19(6):698-710.

CC-930 Dilution Calculator

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Preparing Stock Solutions of CC-930

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.23 mL 11.1498 mL 22.2995 mL 44.5991 mL 55.7488 mL
5 mM 0.446 mL 2.23 mL 4.4599 mL 8.9198 mL 11.1498 mL
10 mM 0.223 mL 1.115 mL 2.23 mL 4.4599 mL 5.5749 mL
50 mM 0.0446 mL 0.223 mL 0.446 mL 0.892 mL 1.115 mL
100 mM 0.0223 mL 0.1115 mL 0.223 mL 0.446 mL 0.5575 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 CC-930

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.

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References on CC-930

Discovery of CC-930, an orally active anti-fibrotic JNK inhibitor.[Pubmed:22244937]

Bioorg Med Chem Lett. 2012 Feb 1;22(3):1433-8.

In this Letter we describe the discovery of potent, selective, and orally active aminopurine JNK inhibitors. Improving the physico-chemical properties as well as increasing the potency and selectivity of a subseries with rat plasma exposure, led to the identification of four structurally diverse inhibitors. Differentiation based on PK profiles in multiple species as well as activity in a chronic efficacy model led to the identification of 1 (CC-930) as a development candidate, which is currently in Phase II clinical trial for IPF.

Description

Tanzisertib (CC-930) is a potent JNK1/2/3 inhibitor with IC50s of 61/7/6 nM, respectively.

Keywords:

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