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CC-401 HCl
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
CC-401 HCl图片
CAS NO:1438391-30-0
规格:≥98%
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW) 424.93
Formula C22H25ClN6O
CAS No. 1438391-30-0 (HCl);
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 10 mM in DMSO
Water: <1 mg/mL
Ethanol: <1 mg/mL
SMILES CodeC1(C2=CC=CC(OCCN3CCCCC3)=C2)=NNC4=C1C=C(C=C4)C5=NC=NN5.Cl
SynonymsCC401 HCl; CC 401; CC-401
实验参考方法
In Vitro

In vitro activity: CC-401, a small molecule that is a specific inhibitor of all three JNK isoforms. CC-401 competitively binds the ATP binding site in JNK, resulting in inhibition of the phosphorylation of the N-terminal activation domain of the transcription factor c-Jun. The specificity of this inhibitor is tested in vitro using osmotic stress of the HK-2 human tubular epithelial cell line.


Kinase Assay: CC-401 is a potent, specific, second generation and ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor with potential antineoplastic activity. It is a potent inhibitor of all three forms of JNK with Ki of ranging from 25 to 50 nM. It inhibits sorbitol-induced phosphorylation of c-Jun in a dosage-dependent manner. However, CC-401 does not prevent sorbitol-induced phosphorylation of JNK, p38, or ERK. The specific JNK inhibitor, CC-401, was synthesized by Celgene Corporation as a competitive inhibitor of the ATP binding site in the active, phosphorylated form of JNK. CC-401 has at least 40-fold selectivity for JNK compared with other related kinases.


Cell Assay:Human HK-2 proximal tubular epithelial cells are cultured in DMEM/F12 media supplemented with 10% FCS, 10 ng/mL EGF, and 10 μg/mL bovine pituitary extract. For Western blot studies, cells are seeded into six-well plates and allowed to adhere overnight, and medium is changed to DMEM/F12 supplemented with only 0.5% FCS for 24 h, by which time cells are confluent. CC-401 is prepared in citric acid (pH 5.5) and added to the confluent cells 1 h before the addition of 300 mM sorbitol, and cells are harvested 30 min later using urea-RIPA buffer. Three experiments are performed, each with two replicates per condition. For ELISA experiments, HK-2 cells are seeded into 24-well plates, allowed to adhere overnight, cultured in DMEM/F12 with 0.5% FCS for 24 h, and then incubated with CC-401 or vehicle for 60 min before stimulation with 1 μM Angiotensin II (AngII).

In VivoCC-401 treatment from days 7 to 24 slows the progression of proteinuria, which is significantly reduced compared to the no-treatment and vehicle groups at days 14 and 21. However, there is still an increase in the degree of proteinuria at day 21 in CC-401-treated rats compared to proteinuria at day 5. The vehicle and no-treatment groups developed renal impairment at day 24 as shown by an increase in serum creatinine. This is prevented by CC-401 treatment. The staining of p-JNK is moderately induced in bevazicumab and Oxaliplatin treatments as compared to control, and in the CC-401-treated samples p-cJun content is significantly lower, consistent with effective JNK inhibition. DNA damage is modestly elevated in combined treatments with CC-401.
Animal modelFemale severe combined immunodeficient mice (C.B.17 SCID) and female WKY rats
Formulation & DosageMice: 5, 25 mg/kg, i.p.; Rats: 200 mg/kg/b.i.d. by oral gavage
References J Am Soc Nephrol. 2007 Feb;18(2):472-84. Clin Cancer Res. 2015 Sep 15;21(18):4143-52.Lab Invest. 2009 Apr;89(4):470-84.