c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis.

By Zuoning Han, David L. Boyle, Lufen Chang, B. Bennett, M. Karin, Li Yang, Anthony M. Manning, Gary S. Firestein. Journal of Clinical Investigation, 2001

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MAPK signalling pathways as molecular targets for anti-inflammatory therapy--from molecular mechanisms to therapeutic benefits. (2005, background): “SP600125, developed by Celgene, is an inhibitor of JNK2 that does not interfere with the ERK or p38 MAP kinase pathways and reduces paw swelling in a rat model of inflammatory arthritis [93].”
Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis (2010, background): “The critical role of JNK was confirmed using small molecule inhibitors and JNK knockout synoviocytes where MMP3 expression is significantly decreased compared to control FLS (59).”
Evolving concepts of rheumatoid arthritis (2003, background): “A selective JNK inhibitor, SP600125, is mildly anti-inflammatory in the rat adjuvant-induced arthritis, but provides striking protection against bone and cartilage destructio”