Rheumatoid arthritis (RA) is a chronic autoimmune disease leading to progressive joint damage and functional disability [1,2]. The treatment landscape for RA has evolved substantially over the last 30 years. Currently, a wide range of conventional synthetic (cs), biological (b), and targeted synthetic (ts) disease-modifying anti-rheumatic drugs (DMARDs) have been licensed, leading to considerable improvements in clinical outcomes [3,4]. Among bDMARDs, five different tumor necrosis factor-α inhibitors (TNFis), one B cell-depleting agent (rituximab), two interleukin (IL)-6 receptor inhibitors (tocilizumab, sarilumab), and the T cell co-stimulation blocker (abatacept) are routinely adopted, while tsDMARDs approved for RA include the four Janus kinase inhibitors (JAKis) tofacitinib, baricitinib, upadacitinib, and filgotinib [5–7].
