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An iguratimod prodrug reduces RA-FLS invasiveness by disrupting STAT1–C3–TNFα-mediated crosstalk between fibroblast-like synoviocytes and macrophages
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DOI：10.1016/j.jot.2026.101187.png)
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Abstract
En 中文
Rheumatoid arthritis (RA) is driven in part by hyperactivated fibroblast-like synoviocytes (FLS) that invade articular structures. Iguratimod (IGU), a conventional synthetic DMARD, is clinically effective, but its direct molecular target and impact on synovial cell-cell crosstalk remain unclear. We aimed to elucidate how IGU regulates FLS invasiveness and inflammatory signaling, identify its upstream target within the JAK-STAT pathway, and develop a prodrug with improved pharmacokinetics while preserving disease-modifying activity.
Keywords:
Iguratimod
Rheumatoid arthritis
STAT1
Tyrosine kinase 2
Fibroblast-like synoviocytes
Prodrug
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