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Rheumatology (Oxford). 2019 Feb 1;58(2):197-205. doi: 10.1093/rheumatology/key070.

The rationale for Janus kinase inhibitors for the treatment of spondyloarthritis.

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The Centre for Arthritis and Rheumatic Diseases, St Vincent's University Hospital, Dublin, Ireland.
University College, Dublin, Ireland.
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, UK.
NIHR Leeds Musculoskeletal Biomedical Research Unit, Chapel Allerton Hospital, Leeds, UK.
Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Laboratory of Investigative Dermatology, The Rockefeller University, New York, USA.
Allergy, Immunology & Rheumatology Division, University of Rochester Medical Center, Rochester, NY, USA.
Unit for Molecular Immunology and Inflammation, VIB Inflammation Research Center, Ghent University and Department of Rheumatology, Ghent University Hospital, Ghent, Belgium.
Pfizer Inc, Groton, CT, USA.
Pfizer Inc, Collegeville, PA, USA.
Pfizer Inc, Cambridge, MA, USA.
Pfizer Inc, New York, NY, USA.


The pathogenesis of SpA is multifactorial and involves a range of immune cell types and cytokines, many of which utilize Janus kinase (JAK) pathways for signaling. In this review, we summarize the animal and pre-clinical data that have demonstrated the effects of JAK blockade on the underlying molecular mechanisms of SpA and provide a rationale for JAK inhibition for the treatment of SpA. We also review the available clinical trial data evaluating JAK inhibitors tofacitinib, baricitinib, peficitinib, filgotinib and upadacitinib in PsA, AS and related inflammatory diseases, which have demonstrated the efficacy of these agents across a range of SpA-associated disease manifestations. The available clinical trial data, supported by pre-clinical animal model studies demonstrate that JAK inhibition is a promising therapeutic strategy for the treatment of SpA and may offer the potential for improvements in multiple articular and extra-articular disease manifestations of PsA and AS.

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