Publications

Bennett et al, showed that tofacitinib treatment in adults with rheumatoid arthritis led to a significant increase in lower limb and thigh muscle volume, accompanied by rises in serum creatinine without evidence of renal impairment.

Hernández-Hernández et al. showed that in a real-world clinical settings, UPA persistence is lower among RA patients who have received prior IL-6i treatment; and that treatment strategies to avoid UPA in patients with cardiovascular risk (CVR) appear to be primarily driven by pivotal safety studies rather than regulatory guidance.

In patients with UC and refractory spondyloarthritis (SpA)—many of whom had previously failed multiple biologic therapies—TOF demonstrated effectiveness, particularly in those with peripheral SpA. Macaluso et al. assessed the effectiveness of TOF in UC-associated SpA. Articular responses were evaluated using rheumatologic scores.

Schaefer et al. showed that treatment with JAKis (predominantly BARI and TOF) was associated with an increased HR of malignancies compared to treatment with bDMARDs in the overall study cohort, consistent with results from the ORAL surveillance trial. To better understand the complex role of JAKis in cancer development in RA patients, Schaefer et al. estimated the effects of JAKis compared to bDMARDs on the risk of malignancy (excluding NMSC) in patients with RA.

Wollenhaupt et al. undertook a post-hoc analysis of data from eight Phase 3 and 3b/4 clinical trials to assess change from baseline (Δ) weight and BMI in patients with moderate to severe RA receiving TOF through 12 months. Additionally, Wollenhaupt et al. evaluated correlations between baseline/changes in disease activity, baseline CRP, and changes in lipids with Δweight and BMI. Wollenhaupt et al. showed that mean Δweight and BMI increased over time and were greater with TOF (all doses) versus placebo at Months 3 and 6, and with TOF monotherapy versus combination therapy, at Months 3, 6, and 12. The correlation and sensitivity analyses showed weak correlation between Δweight or BMI with TOF and DAS28-4(ESR), baseline CRP or lipid changes.

Phase 2 study data show that zimlovisertib + tofacitinib was more effective than tofacitinib alone, in patients with moderate-to-severe RA and an inadequate response to MTX.

Zavoriti and Miossec explored the impact of tofacitinib on inflammation and coagulation in RA. Tofacitinib reduced synovial and vascular inflammation by inhibiting IFNɣ, IL-17A, and IL-6 production but failed to prevent the prothrombotic effects of inflammatory cytokines on endothelial cells. These findings suggest that while tofacitinib reduces inflammation, it does not mitigate associated thrombotic risk.

Baraliakos et al. evaluated the long-term safety and efficacy of bimekizumab in axSpA through a 2-year analysis of the BE MOBILE 1 and BE MOBILE 2 studies. Bimekizumab was well tolerated, with a consistent safety profile and no new safety signals. Clinical improvements, including ASAS40 response and MRI remission, were sustained through Wk104.

Gossec et al. demonstrated that tofacitinib significantly reduced fatigue in patients with ankylosing spondylitis, with median times to clinically meaningful improvements of 8 and 12 weeks for initial and stable improvement events, respectively. These changes were observed as early as two weeks and were more pronounced compared to placebo.

Deodhar et al. conducted a pooled analysis of Phase 2 and 3 RCT data to assess the safety of tofacitinib in AS. The results showed that tofacitinib 5 mg BID had a tolerable safety profile over 48 weeks, consistent with its use in other inflammatory conditions such as RA and PsA.