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PNAS | November 20, 2001 | vol. 98 | no. 24 | 13681-13686
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Cell Biology
 SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase

Brydon L. Bennett*, Dennis T. Sasaki, Brion W. Murray, Eoin C. O'Leary, Steve T. Sakata, Weiming Xu, Jim C. Leisten, Aparna Motiwala, Steve Pierce, Yoshitaka Satoh, Shripad S. Bhagwat, Anthony M. Manning, and David W. Anderson

Signal Research Division, Celgene Corporation, 5555 Oberlin Drive, San Diego, CA 92121

Edited by Joseph Schlessinger, Yale University School of Medicine, New Haven, CT, and approved October 1, 2001 (received for review April 19, 2001)

Jun N-terminal kinase (JNK) is a stress-activated protein kinase that can be induced by inflammatory cytokines, bacterial endotoxin, osmotic shock, UV radiation, and hypoxia. We report the identification of an anthrapyrazolone series with significant inhibition of JNK1, -2, and -3 (Ki = 0.19 µM). SP600125 is a reversible ATP-competitive inhibitor with >20-fold selectivity vs. a range of kinases and enzymes tested. 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 animal studies, SP600125 blocked (bacterial) lipopolysaccharide-induced expression of tumor necrosis factor-alpha and inhibited anti-CD3-induced apoptosis of CD4+ CD8+ thymocytes. Our study supports targeting JNK as an important strategy in inflammatory disease, apoptotic cell death, and cancer.

* To whom reprint requests should be addressed. E-mail: bbennett{at}signalpharm.com.

www.pnas.org/cgi/doi/10.1073/pnas.251194298
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