SP600125 is a selective, ATP-competitive JNK inhibitor. SP600125 reversibly inhibits JNK1, 2 and 3 (IC50 = 40 - 90 nM) with negligible activity at ERK2, p38β and a range of enzymes (IC50 > 10 μM). SP600125 potently decreased renal epithelial tubular cell apoptosis induced by renal ischemia/reperfusion via suppression of the extrinsic pathway. In cells, SP600125 dose dependently inhibited the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-gamma, TNF-alpha, and prevented the activation and differentiation of primary human CD4 cell cultures. In mice, SP600125 (15 mg/kg or 30 mg/kg) blocked lipopolysaccharide (LPS)-induced TNF-α expression and anti-CD3-induced apoptosis of CD4(+) CD8(+) thymocytes.
|Cell lines||A549 cells|
|Preparation method||Cell viability assay.
Cell viability was evaluated using the Cell Counting kit (CCK)-8 assay (AbMole). In brief, the cells were seeded into 96-well plates at a density of 3×103 cells/well and left to adhere overnight. The cells were then incubated with or without 0–40 nM SP600125. Then, 100 μl CCK-8 was added and incubated in the dark at 37°C for 3 h. The absorbance was determined using the MRX II microplate reader (Dynex, Chantilly, VA, USA) at a wavelength of 450 nm.
|Incubation time||24 h|
|Animal models||Female CD-1 mice|
|Formulation||30% PEG-400/20% polypropylene glycol/15% Cremophor EL/5% ethanol/30% saline|
|Dosages||0, 12, 24, and 36 h, 15 mg/kg|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||DMSO 40 mg/mL|
|Source||Molecules and Cells (2017). Figure 5. SP600125 (Abmole Bioscience, USA)|
|Method||Wound healing assay|
|Cell Lines||EGI-1 cells|
|Results||The JNK inhibitor significantly decreased cell migration and invasion, as well as JNK phosphorylation (Figs. 5A-5C), but not cell proliferation (Fig. 5D).|
Mol Cells 2017 May 31;40(5):363-370.
JNK inhibitor SP600125 protects against lipopolysaccharide-induced acute lung injury via upregulation of claudin-4.
Zheng Y, et al. Exp Ther Med. 2014 Jul;8(1):153-158. PMID: 24944614.
SP600125, a selective JNK inhibitor, protects ischemic renal injury via suppressing the extrinsic pathways of apoptosis.
Wang Y, et al. Life Sci. 2007 May 8;80(22):2067-75. PMID: 17459422.
SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase.
Bennett BL, et al. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13681-6. PMID: 11717429.
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