Product Description: 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].
Applications: Cancer-Kinase/protease
Formula: C14H8N2O
References: [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.
CAS Number: 129-56-6
Molecular Weight: 220.23
Compound Purity: 99.73
Research Area: Cancer
Solubility: DMSO : 12.5 mg/mL (ultrasonic)
Target: Apoptosis;Autophagy;Ferroptosis;JNK