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Journal of Biomedicine and Biotechnology
Volume 2011, Article ID 569068, 21 pages
Review Article

Rodent Preclinical Models for Developing Novel Antiarthritic Molecules: Comparative Biology and Preferred Methods for Evaluating Efficacy

1Department of Pathology, Amgen Inc., Thousand Oaks, CA 91320, USA
2GEMpath Inc., 2867 Humboldt Cir, Longmont, CO 80503, USA
3Department of Metabolic Disorders, Amgen Inc., Thousand Oaks, CA 91320, USA
4Department of Inflammation, Amgen Inc., Thousand Oaks, CA 91320, USA
5Willamette Health Partners, Salem, OR 97301, USA
6HAMILTON Bonaduz AG, 7402 Bonaduz, Switzerland
7Department of Global Development, Amgen Inc., Thousand Oaks, CA 91320, USA
8EUROCBI GmbH, Benglen, 8121 Zurich, Switzerland

Received 10 September 2010; Accepted 20 October 2010

Academic Editor: Oreste Gualillo

Copyright © 2011 Brad Bolon et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Rodent models of immune-mediated arthritis (RMIA) are the conventional approach to evaluating mechanisms of inflammatory joint disease and the comparative efficacy of antiarthritic agents. Rat adjuvant-induced (AIA), collagen-induced (CIA), and streptococcal cell wall-induced (SCW) arthritides are preferred models of the joint pathology that occurs in human rheumatoid arthritis (RA). Lesions of AIA are most severe and consistent; structural and immunological changes of CIA best resemble RA. Lesion extent and severity in RMIA depends on experimental methodology (inciting agent, adjuvant, etc.) and individual physiologic parameters (age, genetics, hormonal status, etc.). The effectiveness of antiarthritic molecules varies with the agent, therapeutic regimen, and choice of RMIA. All RMIA are driven by overactivity of proinflammatory pathways, but the dominant molecules differ among the models. Hence, as with the human clinical experience, the efficacy of various antiarthritic molecules differs among RMIA, especially when the agent is a specific cytokine inhibitor.