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Key Documents

196871

Sigma-Aldrich

BAY 11-7082

InSolution, ≥95%, Selectively and irreversibly inhibits the TNFα-inducible phosphorylation of IκB-α

Synonym(s):

InSolution BAY 11-7082

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About This Item

Empirical Formula (Hill Notation):
C10H9NO2S
Molecular Weight:
207.25
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥95% (HPLC)

form

liquid

potency

10 μM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

shipped in

wet ice

storage temp.

2-8°C

General description

Potential anti-inflammatory agent. Selectively and irreversibly inhibits the TNFα-inducible phosphorylation of IκB-α (IC50 = 10 µM) without affecting the constitutive IκB-α phosphorylation. Decreases nuclear translocation of NFκB and inhibits TNFα-induced surface expression of the endothelial-leukocyte cell adhesion molecules E-selectin, VCAM-1, and ICAM-1. E-selectin inhibition was shown to be irreversible (IC50 ~10 µM). Also reversibly increased the activity of p38 kinase and JNK-1 and stimulated tyrosine phosphorylation of a 130-140 kDa protein.

Biochem/physiol Actions

Cell permeable: yes
Primary Target
TNF-α-inducible phosphorylation of IκBα
Product does not compete with ATP.
Reversible: no

Packaging

Packaged under inert gas

Warning

Toxicity: Irritant (B)

Physical form

Supplied as a 100 mM (10 mg/483 µl) solution of BAY 11-7082 (Cat. No. 196870) in DMSO.

Other Notes

Kamthong PJ. and Wu, M-C. 2001. Biochem. J. 356.
Izban, K.F., et al. 2000. Hum. Pathol.31, 1482.
Pierce, J.W., et al. 1997. J. Biol. Chem. 272, 21096.

Legal Information

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

Storage Class Code

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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Mariana Sponchiado et al.
Physiological reports, 9(3), e14749-e14749 (2021-02-14)
Substance P (SP) is a tachykinin that regulates airway mucous secretion in both health and disease. Our study aimed to determine whether overexpression of SP without pre-existing inflammation was sufficient to induce changes in mucin secretion and transport in small

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