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Merck

420128

JNK Inhibitor II

InSolution, ≥98%

Synonym(s):

InSolution JNK Inhibitor II

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About This Item

Empirical Formula (Hill Notation):
C14H8N2O
Molecular Weight:
220.23
NACRES:
NA.77
UNSPSC Code:
12352200

Product Name

JNK Inhibitor II, InSolution, ≥98%

assay

≥98% (HPLC)

form

liquid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

color

yellow-brown

shipped in

wet ice

storage temp.

−20°C

Quality Level

Biochem/physiol Actions

Product competes with ATP.
Reversible: yes
Cell permeable: yes
Primary Target
JNK 1, JNK 2, JNK 3
Target IC50: 40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3

Disclaimer

Toxicity: Irritant (B)

General description

A potent, cell-permeable, selective, and reversible inhibitor of c-Jun N-terminal kinase (JNK) (IC50 = 40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3). The inhibition is competitive with respect to ATP. Exhibits over 300-fold greater selectivity for JNK as compared to ERK1 and p38-2 MAP kinases. Inhibits the phosphorylation of c-Jun and blocks the expression of IL-2, IFN-γ, TNF-α, and COX-2 in cells. Blocks IL-1-induced accumulation of phospho-Jun and induction of c-Jun transcription.

Other Notes

Bennett, B.L., et al. 2001. Proc. Natl. Acad. Sci. USA98, 13681.
Han, Z., et al. 2001. J. Clin. Invest.108, 73.

Packaging

Packaged under inert gas

Physical form

A 50 mM (5 mg/454 µl) solution of JNK Inhibitor II (Cat. No. 420119) in DMSO.

Preparation Note

Following initial use, aliquot and refrigerate (4°C) for short-term storage or freeze (-20°C) for long-term storage.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

10 - Combustible liquids

wgk

WGK 2

flash_point_f

188.6 °F - closed cup - (Dimethylsulfoxide)

flash_point_c

87 °C - closed cup - (Dimethylsulfoxide)


Certificates of Analysis (COA)

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Jia-Rong Fan et al.
iScience, 26(6), 106992-106992 (2023-06-28)
Nuclear deformation has been observed in some cancer cells for decades, but its underlying mechanism and biological significance remain elusive. To address these questions, we employed human lung cancer A549 cell line as a model in context with transforming growth

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