CC-401 dihydrochloride
Based on 6 publication(s) in Google Scholar
CC-401 dihydrochloride is a potent inhibitor of all three forms of JNK with Ki of 25 to 50 nM.
For research use only. We do not sell to patients.
- CAS No.: 2319601-04-0
- Formula: C22H26Cl2N6O
- Molecular Weight:461.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) CC-401 dihydrochloride
More- Science. 2017 Dec 1;358(6367):eaan4368. [Abstract]
- Cell Syst. 2018 Apr 25;6(4):424-443.e7. [Abstract]
- J Med Chem. 2023 Mar 23;66(6):4106-4130. [Abstract]
- Mol Cancer Res. 2016 Aug;14(8):753-63. [Abstract]
- Int Immunopharmacol. 2025 Jan 3:145:113781. [Abstract]
- Cell Signal. 2026 Mar:139:112333. [Abstract]
Biological Activity
Description
IC50 & Target
Ki: 25 to 50 nM (JNK)[1].
In Vitro
CC-401 dihydrochloride has at least 40-fold selectivity for JNK compared with other related kinases, including p38, extracellular signal-regulated kinase (ERK), inhibitor of κB kinase (IKK2), protein kinase C, Lck, zeta-associated protein of 70 kDa (ZAP70). In cell-based assays, 1 to 5 μM CC-401 dihydrochloride provides specific JNK inhibition. CC-401 dihydrochloride, a small molecule that is a specific inhibitor of all three JNK isoforms. CC-401 dihydrochloride 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. CC-401 dihydrochloride inhibits sorbitol-induced phosphorylation of c-Jun in a dosage-dependent manner. However, CC-401 dihydrochloride does not prevent sorbitol-induced phosphorylation of JNK, p38, or ERK[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. .
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 2319601-04-0
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Molecular Weight 461.39
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Formula C22H26Cl2N6O
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SMILES
C1(C2=CC=CC(OCCN3CCCCC3)=C2)=NNC4=C1C=C(C=C4)C5=NC=NN5.Cl.Cl
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (6)
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Journal Impact Factor
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Most Recent
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Science
2017 Dec 1;358(6367):eaan4368. PMID: 29191878 -
Cell Syst
A Library of Phosphoproteomic and Chromatin Signatures for Characterizing Cellular Responses to Drug Perturbations. [Abstract]2018 Apr 25;6(4):424-443.e7. PMID: 29655704 -
J Med Chem
Comparative Efficacy and Selectivity of Pharmacological Inhibitors of DYRK and CLK Protein Kinases. [Abstract]2023 Mar 23;66(6):4106-4130. PMID: 36876904 -
Mol Cancer Res
2016 Aug;14(8):753-63. PMID: 27216154 -
Int Immunopharmacol
Genome-wide screen based on 2DG activated NLRP3 inflammasome reveals the priming signal of TLR2/4 to IKKβ but not IKKα. [Abstract]2025 Jan 3:145:113781. PMID: 39657538 -
Cell Signal
PERK-eIF2alpha-mediated translational inhibition of MCL-1 contributes to potential 2-deoxy-D-glucose and BAD mimetic combinatorial cancer therapy. [Abstract]2026 Mar:139:112333. PMID: 41423011
Purity & Documentation
References
[1]. Vasilevskaya IA, et al. Inhibition of JNK Sensitizes Hypoxic Colon Cancer Cells to DNA-Damaging Agents. Clin Cancer Res. 2015 Sep 15;21(18):4143-52. [Content Brief]
[2]. Ma FY, et al. Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab Invest. 2009 Apr;89(4):470-84. [Content Brief]
[3]. Ma FY, et al. A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J Am Soc Nephrol. 2007 Feb;18(2):472-84. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)