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
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
Quality Level
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
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.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
JNK 1, JNK 2, JNK 3
JNK 1, JNK 2, JNK 3
Product competes with ATP.
Reversible: yes
Target IC50: 40 nM for JNK-1 and JNK-2 and 90 nM for JNK-3
Packaging
Packaged under inert gas
Warning
Toxicity: Irritant (B)
Physical form
A 50 mM (5 mg/454 µl) solution of JNK Inhibitor II (Cat. No. 420119) in DMSO.
Reconstitution
Following initial use, aliquot and refrigerate (4°C) for short-term storage or freeze (-20°C) for long-term storage.
Other Notes
Bennett, B.L., et al. 2001. Proc. Natl. Acad. Sci. USA98, 13681.
Han, Z., et al. 2001. J. Clin. Invest.108, 73.
Han, Z., et al. 2001. J. Clin. Invest.108, 73.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class
10 - Combustible liquids
wgk_germany
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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