CC 401 dihydrochloride

Pricing Availability   Qty
Description: High affinity JNK inhibitor; also inhibits HCMV replication
Chemical Name: 3-[3-[2-(1-Piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole dihydrochloride
Purity: ≥98% (HPLC)
Literature (1)
Pathways (1)

Biological Activity for CC 401 dihydrochloride

CC 401 dihydrochloride is a high affinity JNK inhibitor (Ki values are 25-50 nM). Inhibits JNK via competitive binding of the ATP-binding site of active, phosphorylated JNK. Exhibits > 40-fold selectivity for JNK over p38, ERK, IKK2, protein kinase C, Lck and ZAP70. Hepatoprotective. Also inhibits HCMV replication.

Compound Libraries for CC 401 dihydrochloride

CC 401 dihydrochloride is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.

Technical Data for CC 401 dihydrochloride

M. Wt 461.39
Formula C22H24N6O.2HCl
Storage Store at -20°C
Purity ≥98% (HPLC)
CAS Number 2250025-96-6
PubChem ID 66576998
Smiles N1(CCCCC1)CCOC2=CC=CC(C3=NNC4=CC=C(C5=NN=CN5)C=C34)=C2.Cl.Cl

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

Tocris products are intended for laboratory research use only, unless stated otherwise.

Solubility Data for CC 401 dihydrochloride

Solvent Max Conc. mg/mL Max Conc. mM
water 46.14 100
DMSO 46.14 100

Preparing Stock Solutions for CC 401 dihydrochloride

The following data is based on the product molecular weight 461.39. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Select a batch to recalculate based on the batch molecular weight:
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 2.17 mL 10.84 mL 21.67 mL
5 mM 0.43 mL 2.17 mL 4.33 mL
10 mM 0.22 mL 1.08 mL 2.17 mL
50 mM 0.04 mL 0.22 mL 0.43 mL

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Product Datasheets for CC 401 dihydrochloride

References for CC 401 dihydrochloride

References are publications that support the biological activity of the product.

Uehara et al (2004) c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation. 78 324 PMID: 15316358

Uehara et al (2005) JNK mediates hepatic ischemia reperfusion injury. J.Hepatol. 42 850 PMID: 15885356

Ma et al (2007) A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J.Am.Soc.Nephrol. 18 472 PMID: 17202416

Ma et al (2009) Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab.Invest. 89 470 PMID: 19188913

Zhang et al (2015) The c-Jun N-terminal kinase inhibitor SP600125 inhibits human cytomegalovirus replication. J.Med.Virol. 87 2135 PMID: 26058558

Vasilevskaya et al (2015) Inhibition of JNK sensitizes hypoxic colon cancer cells to DNA-damaging agents. Clin.Cancer.Res. 21 4143 PMID: 26023085

If you know of a relevant reference for CC 401 dihydrochloride, please let us know.

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Citations for CC 401 dihydrochloride

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Literature in this Area

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!

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MAPK Signaling Scientific Review

MAPK Signaling Scientific Review

MAP kinase signaling is integral to the regulation of numerous cellular processes such as proliferation and differentiation, and as a result is an important focus of cancer and immunology research. Updated for 2016, this review discusses the regulation of the MAPK pathway and properties of MAPK cascades. Compounds available from Tocris are listed.

Pathways for CC 401 dihydrochloride

MAPK Signaling Pathway

MAPK Signaling Pathway

The mitogen-activated protein kinase pathway evokes an intracellular signaling cascade in response to extracellular stimuli such as heat and stress. It can influence cell division, metabolism and survival.