SP600125 (JNK Inhibitor II) is a JNK inhibitor that inhibits JNK1, JNK2, and JNK3 (IC50=40/40/90 nM) with oral potency, reversibility, and ATP-competitive properties. SP600125 inhibits autophagy and induces apoptosis.

>98 %

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

SP 600125；SP-600125；Nsc75890

Yellow powder

DMSO : 65 mg/mL (295.15 mM)

JNK1；JNK2；Aurora A；TrkA ；JNK3

SP600125 is originally characterized as a selective ATP-competitive inhibitor of c-Jun N-terminal kinase JNK. In Jurkat T cells, SP600125 inhibits the phosphorylation of c-Jun with IC50 of 5 μM to 10 μM. In CD4+ cells, such as Th0 cells isolated from either human cord or peripheral blood, SP600125 blocks cell activation and differentiation and inhibits the expression of inflammatory genes COX-2, IL-2, IL-10, IFN-γ, and TNF-α, with IC50 of 5 μM to 12 μM. However, later studies reveal that SP600125 also suppresses aryl hydrocarbon receptor (AhR) , Mps1 , and a panel of other serine/threonine kinases, including Aurora kinase A, FLT3, MELK, and TRKA .In a mouse beta cells MIN6, SP600125 (20 μM) induces the phosphorylation of p38 MAPK and its downstream CREB-dependent promoter activation. In HCT116 cells, SP600125 (20 μM) blocks the G2 phase to mitosis transition and induces endoreplication. This ability of SP600125 is independent of JNK inhibition, but due to its inhibition of CDK1-cyclin B activation upstream of Aurora A and Polo-like kinase 1.

In mice, SP600125 (15 mg/kg or 30 mg/kg) significantly inhibits lipopolysaccharide (LPS)-induced TNF-α expression and anti-CD3-induced apoptosis of CD4+ CD8+ thymocytes.

[1] Bennett BL, et al. Proc Natl Acad Sci U S A, 2001, 98(24), 13681-13686.
[2] Joiakim A, et al. Drug Metab Dispos, 2003, 31(11), 1279-1282.
[3] Schmidt M, et al. EMBO Rep, 2005, 6(9), 866-872.