129-56-6
129-56-6
Chemical Structure
SP600125
- CAS No.: 129-56-6
- Formula:C14H8N2O
- Molecular Weight:220.23
IUPAC Name: dibenzo[cd,g]indazol-6(2H)-one
InChIKey: ACPOUJIDANTYHO-UHFFFAOYSA-N
SMILES: O=C1C2=C3C(NN=C3C4=C1C=CC=C4)=CC=C2
Biological Activity: 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].
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SP600125 | 99.46% | 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. | ||||||||||||||||||||
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SP600125 (GMP) | SP600125 (GMP) is SP600125 (HY-12041) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. 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. | |||||||||||||||||||||
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SP600125 (Standard) | 99.65% | SP600125 (Standard) is the analytical standard of SP600125. This product is intended for research and analytical applications. 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. | ||||||||||||||||||||
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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. [Content Brief]
- [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. [Content Brief]
- [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. [Content Brief]
