MG IKK Inhibitor III; BMS-34554 1PC x 1M

Biochem/physiol Actions

Reversible: no

Product does not compete with ATP.

Target IC₅₀: ~300 nM against IKK-2; 4 µM against cellular IκBα phosphorylation in THP-1 cells; 1-5 µM LPS-induced cytokine production in THP-1 cells

Cell permeable: yes

General description

A cell-permeable, potent, selective, and allosteric site-binding inhibitor of IKK-2 (IC₅₀ ~300 nM) that displays anti-inflammatory properties. Exhibits ~10-fold greater selectivity for IKK-2 over IKK-1 (IC₅₀ ~4.0 µM) and does not inhibit IKKε and a panel of more than 15 unrelated protein kinases even at concentrations as high as 100 µM. Inhibits cellular IκBα phosphorylation (IC₅₀ = 4 µM in THP-1 cells) and LPS-induced cytokine production both in vitro (IC₅₀ = 1-5 µM in THP-1 cells) and in vivo (IC₅₀ = 10 mg/kg in mice). Effectively blocks inflammation and joint destruction in a murine arthritis model.

A cell-permeable quinoxaline compound that displays anti-inflammatory properties. Acts as a potent, selective, and allosteric site-binding inhibitor of IKK-2 (IC₅₀ = ~ 300 nM). Exhibits ~10-fold greater selectivity over IKK-1 (IC₅₀ = ~ 4 µM) and no activity towards IKKε and a panel of more than 15 unrelated protein kinases even at concentrations as high as 100 µM. Inhibits cellular IκBα phosphorylation (IC₅₀ = 4 µM in THP-1 cells) and LPS-induced cytokine production both in vitro (IC₅₀ = 1-5 µM in THP-1 cells) and in vivo (IC₅₀ = 10 mg/kg in mice). Effectively blocks inflammation and joint destruction in a murine arthritis model.

Legal Information

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

Other Notes

Townsend, R.M., et al. 2004. Transplantation77, 1090.MacMaster, J.F., et al. 2003. Inflamm. Res.52, 508.McIntyre, K.W., et al. 2003. Arthritis Rheum.48, 2652.Burke, J. R., et al. 2003. J. Biol. Chem.278, 1450.

Packaging

1 mg in Plastic ampoule

Packaged under inert gas

Physical form

Supplied as bis-TFA salt.

Warning

Toxicity: Standard Handling (A)