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K112

Sigma-Aldrich

KN-92

≥90%, solid

Synonym(s):

2-[N-(4′-Methoxybenzenesulfonyl)]amino-N-(4′-chlorophenyl)-2-propenyl-N-methylbenzylamine phosphate

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About This Item

Empirical Formula (Hill Notation):
C24H25ClN2O3S · H3O4P
Molecular Weight:
554.98
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:

assay

≥90%

form

solid

color

white

solubility

DMSO: 6 mg/mL

storage temp.

2-8°C

SMILES string

OP(O)(O)=O.COc1ccc(cc1)S(=O)(=O)Nc2ccccc2CN(C)C\C=C\c3ccc(Cl)cc3

Biochem/physiol Actions

Does not inhibit Ca2+/calmodulin-dependent protein kinase II; negative control for KN-93.

Caution

Photosensitive

Storage Class

13 - Non Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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I Niki et al.
Biochemical and biophysical research communications, 191(1), 255-261 (1993-02-26)
Roles of Ca/calmodulin-dependent protein kinase II (Ca/CaM kinase II) and myosin light chain kinase (MLCK) in insulin release from rat pancreatic islets were investigated. Western blotting using polyclonal antibody to Ca/CaM kinase II suggested the presence of this kinase in
M Sumi et al.
Biochemical and biophysical research communications, 181(3), 968-975 (1991-12-31)
We reported that one of the isoquinolinesulfonamide derivatives, KN-62, is a potent and specific inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMKII) (Tokumitsu, H., Chijiwa, T., Hagiwara, M., Mizutani, A., Terasawa, M. and Hidaka, H. (1990) J. Biol. Chem. 265, 4315-4320).
N Mamiya et al.
Biochemical and biophysical research communications, 195(2), 608-615 (1993-09-15)
A novel Ca2+/calmodulin-dependent protein kinase II (CaM Kinase II) inhibitor, KN-93 potently inhibits gastric acid secretion from parietal cells. As previously reported (1), treatment of parietal cells with a selective inhibitor of CaM kinase II, KN-62 resulted in the inhibition
Chenghai Dong et al.
Neuroscience letters, 583, 199-204 (2014-09-30)
The ubiquitin-proteasome pathway is essential for long-term synaptic plasticity, but its exact roles remain unclear. Previously we established that proteasome inhibition increased the early, induction part of late-phase long-term potentiation (L-LTP) but blocks the late, maintenance part. Our prior work
Chiung-Chun Huang et al.
The international journal of neuropsychopharmacology, 17(8), 1233-1242 (2014-02-22)
The intercalated cell masses (ITCs) of the amygdala are clusters of GABAergic interneurons that surround the basolateral complex of the amygdala. ITCs have been increasingly implicated in the acquisition and extinction of conditioned fear responses, but the underlying cellular mechanisms

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