Abstract
Spleen tyrosine kinase (Syk), through its capacity to promote the pathogenic activation of B lymphocytes, myeloid cells, osteoclasts, and stromal fibroblast-like synoviocytes, has been subject to intense translational and clinical scrutiny as a potential therapeutic target in rheumatoid arthritis (RA) (1). Initial phase II clinical trials with the Syk inhibitor fostamatinib showed promising effectivity in treating RA patients that had displayed inadequate responses to methotrexate (2,3). However, concerns were raised of drug-dependent adverse effects in these studies, and fostamatinib did not improve disease in RA patients failing other biologic agents (4). This article is protected by copyright. All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 1364-1365 |
| Number of pages | 2 |
| Journal | Arthritis & Rheumatology |
| Volume | 70 |
| Issue number | 9 |
| Early online date | 18 Apr 2018 |
| DOIs | |
| Publication status | Published - Sept 2018 |
Keywords
- Editorial
- Humans
- Proteomics
- Biomarkers
- Drug Development
- Arthritis, Rheumatoid