Gollins et al. reported that within this cohort, the Psoriatic arthritis response criteria (PsARC) response to 4th+ lines of b/tsDMARD was not significantly reduced compared with 2nd/3rd line in participants who had failed at least 3 b/tsDMARDs. Authors evaluated the primary clinical response to sequential lines of b/tsDMARD therapy in PsA, focusing on the effectiveness of later line treatments.

Data by Flouri et al. support greater drug persistence with secukinumab than with TNF inhibitors in patients with axSpA and peripheral spondyloarthritis, both with respect to efficacy- and safety-related discontinuations, while the achievement of 6-month treatment targets was comparable. Flouri et al. compared long term treatment persistence, efficacy and safety between secukinumab and TNF inhibitors in a cohort of patients with SpA treated in real life.

October 2025

Nozaki et al. showed that JAK inhibitor treatment provided sustained disease control (especially in high-risk RA patients) and promoted GC reduction, although TNF inhibitors remain a standard option. Nozaki et al. evaluated the clinical efficacy and continuation rates of JAK inhibitors and TNF inhibitors in RA patients with poor-prognosis factors (PPFs).

In this first global clinical study of a nanobody in inflammatory arthritis, sonelokimab, an
IL-17A- and IL-17F-inhibiting nanobody demonstrated strong efficacy across multiple domains including high-hurdle composite joint and skin responses. McInnes et al. reported on the Phase 2, randomized, double-blind, PBO-controlled ARGO trial which evaluated the efficacy and safety of sonelokimab in patients with active PsA.

September 2025

Gold et al. showed that icotrokinra showed superior clinical response rates versus PBO and deucravacitinib in Phase 3 moderate-to-severe plaque PsO trials. Authors evaluated the efficacy and safety of icotrokinra, a targeted oral peptide that selectively binds the IL-23 receptor, compared with both PBO and deucravacitinib in adults with moderate-to-severe plaque PsO.

Mease et al. showed that guselkumab provided significantly higher rates of clinical improvement and significant inhibition of structural damage progression versus PBO, with no new safety signals, at Week 24 in biologic-naïve participants with active and erosive PsA. Mease et al. report primary efficacy and safety results for the double-blind PBO-controlled phase (Weeks 0-24) of the 3-year APEX study.

Marzo-Ortega et al. report that dactylitis and enthesitis are associated with a greater disease burden and worse prognosis, highlighting the importance for physicians to identify these conditions and provide adequate treatment. Authors evaluated guselkumab’s efficacy on dactylitis resolution (DR) and enthesitis resolution (ER), and their impact on subsequent disease control, in patients with active PsA and prior inadequate response to tumour necrosis factor inhibitors (TNFi-IR).

August 2025

Results from the Phase 3 GRAVTI study by Hart et al. showed that SC induction followed by SC maintenance treatment with guselkumab resulted in superior clinical and endoscopic improvements in participants with moderately to severely active CD through 48 weeks compared with placebo. Hart et al. evaluated efficacy and safety of guselkumab SC induction followed by SC maintenance in participants with moderately to severely active CD in a    treat-through design.

This study by Sobotkova et al. confirmed the similar efficacy and overall safety of biological treatment for psoriasis in older and younger adult patients. Authors compared a large cohort of older adults during the first year of biological treatment for psoriasis to younger adult patients with similar characteristics to advance knowledge about the biologic treatment of psoriasis in older patients.

Baraliakos et al. compared real-world effectiveness of upadacitinib, TNF inhibitors, or IL-17 inhibitors following inadequate response to an initial TNF inhibitor in patients with axSpA. Upadacitinib was associated with greater reductions in pain and fewer affected joints compared with switching to a second TNF inhibitor or IL-17 inhibitor.