Comparing JAK Inhibitor Mechanisms of Action in RA Treatment

In this episode, 'Comparing JAK Inhibitor Mechanisms of Action in RA Treatment,' the expert rheumatologist Dr. Julia Buchfuhrer explored the following questions:

Beyond tumor necrosis factor (TNF) inhibitors, which other biologics are being used in clinical practice for rheumatoid arthritis (RA), and in which patients are they most appropriate?

What are the available Janus kinase (JAK) inhibitors for RA, and how do their mechanisms of action differ from each other?

Dr. Buchfuhrer examined the importance of drawing on the full range of available RA therapies rather than defaulting to familiar options, since patient factors such as anti-cyclic citrullinated peptide (CCP) and rheumatoid factor (RF) status can influence which therapy is likely to work best. She reviewed the three FDA-approved JAK inhibitors for RA — tofacitinib, baricitinib, and upadacitinib — and discussed how their differing selectivity across JAK1, JAK2, and JAK3 affects both efficacy and safety, since JAK2/3 inhibition affects blood cell production while JAK1 inhibition more directly targets the inflammatory cascade.

Throughout the conversation, the experts provided a comprehensive reflection on the field and the factors that may shape how clinicians approach care moving forward.

The next episode in this series, 'Class Switching Outcomes in RA: Key Findings From the SELECT-SWITCH Trial,' features the panelists advancing their conversation on rheumatoid arthritis and focusing on head-to-head trial data comparing a JAK1 inhibitor against a TNF inhibitor in patients who had failed a prior TNF inhibitor, along with longer-term safety findings.