SP600125

SP600125 is an orally active, reversible, and ATP-competitive JNK inhibitor with IC50s of 40, 40 and 90 nM for JNK1, JNK2 and JNK3, respectively. SP600125 is a potent ferroptosis inhibitor. SP600125 induces the transformation of bladder cancer cells from autophagy to apoptosis[1][2][3].

Product Specifications

CAS Number

[129-56-6]

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

Apoptosis; Autophagy; Ferroptosis; JNK

Type

Reference compound

Related Pathways

Apoptosis; Autophagy; MAPK/ERK Pathway

Applications

Cancer-Kinase/protease

Field of Research

Cancer

Assay Protocol

https://www.medchemexpress.com/SP600125.html

Concentration

10mM

Purity

99.73

Solubility

DMSO : 11.67 mg/mL (ultrasonic; warming; heat to 60°C)

Smiles

O=C1C2=C3C(NN=C3C4=C1C=CC=C4)=CC=C2

Molecular Formula

C14H8N2O

Molecular Weight

220.23

Precautions

H302, H315, H319, H335

References & Citations

[1]Bennett BL, et al. SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase. Proc Natl Acad Sci U S A, 2001, 98 (24), 13681-13686.|[2]Vaishnav D, et al. SP600125, an inhibitor of c-jun N-terminal kinase, activates CREB by a p38 MAPK-mediated pathway. Biochem Biophys Res Commun, 2003, 307 (4), 855-860.|[3]Kim JA, et al. SP600125 suppresses Cdk1 and induces endoreplication directly from G2 phase, independent of JNK inhibition. Oncogene, 2010, 29 (11), 1702-1716.|[4]Zheng Y, et al. JNK inhibitor SP600125 protects against lipopolysaccharide-induced acute lung injury via upregulation ofclaudin-4. Exp Ther Med. 2014 Jul;8 (1) :153-158.|[5]Zhang H, et al. SP600125 Suppresses Keap1 Expression and Results in NRF2-mediated Prevention of Diabetic Nephropathy. J Mol Endocrinol. J Mol Endocrinol. 2018 Feb;60 (2) :145-157.|[6]Yatsushige H, et al. Role of c-Jun N-terminal kinase in cerebral vasospasm after experimental subarachnoid hemorrhage. Stroke. 2005 Jul;36 (7) :1538-43.