Janus kinase inhibitors (i.e. tofacitinib) selectively suppress Janus kinase/signal transduction and activator of transcription (JAK–STAT) signaling pathway that is implicated in the pathogenesis of rheumatoid arthritis (RA). Inlike biologic agents, JAK inhibitors are oral, nonimmunogenic, small molecules and represent a new family of targeted synthetic disease modifying antirheumatic drugs (DMARDs). The institution of tofacitinib is recommended in patients with moderately severe to severe RA who do not achieve an adequate response with conventional synthetic DMARDs, particularly in those who have unfavorable prognostic factors (i.e. high ESR and C-reactive protein, high swollen joints count, rheumatoid factor and/or ACCP, early erosions). Monotherapy with JAKinhibitors had certain advantages over monotherapy with biologic DMARDs. However, in clinical practice is recommended to use tofacitinib in combination with methotrexated or other conventional synthetic DMARDs.
Rheumatoid arthritis, JAK-inhibitors, tofacitinib.