TOPLINE
Deucravacitinib, an oral selective inhibitor of tyrosine kinase 2, resulted in a higher rate of American College of Rheumatology 20% improvement in response (ACR20) than placebo at week 16 in adults with active psoriatic arthritis (PsA), with sustained ACR20 responses, improvements across multiple disease domains, and a well-tolerated safety profile through week 52.
METHODOLOGY
- A phase 3 randomized controlled trial was conducted across 124 sites in 18 countries to evaluate the efficacy and safety of deucravacitinib in adults with active PsA over 52 weeks.
- A total of 729 adults (mean age, 49 years; 51.7% women) with active PsA were included. Eligible patients had a history of psoriasis or active psoriasis; C-reactive protein levels of ≥ 3 mg/L; an inadequate response or intolerance to conventional synthetic disease-modifying antirheumatic drugs or nonsteroidal anti-inflammatory drugs; and/or prior exposure to two or fewer TNF inhibitors.
- Participants were randomly assigned to receive deucravacitinib 6 mg once daily (n = 312), placebo (n = 312), or apremilast 30 mg twice daily (safety reference arm; n = 105) for 16 weeks. After the 16-week placebo-controlled period, patients receiving placebo switched to 6 mg deucravacitinib once daily and continued treatment through week 52, while those receiving deucravacitinib or apremilast continued their assigned treatment.
- The primary endpoint was achievement of an ACR20 response, defined as ≥ 20% improvement from baseline in tender and swollen joint counts and 20% improvement in three of five other key data measures, at week 16.
- Secondary endpoints included change in Health Assessment Questionnaire-Disability Index (HAQ-DI) from baseline, 75% improvement in Psoriasis Area and Severity Index (PASI75), minimal disease activity (MDA), enthesitis and dactylitis resolution, and other disease activity measures. Endpoints were also assessed at week 52, with safety assessments comprising all adverse events (AEs) and serious AEs.
TAKEAWAY
- At week 16, 54.2% of patients receiving deucravacitinib achieved an ACR20 response compared with 39.4% of patients receiving placebo (P = .0002). Responses were maintained through week 52 (62.2% in the deucravacitinib-deucravacitinib group and 67.3% in the placebo-deucravacitinib group), with similar improvements observed for ACR50 and ACR70 responses.
- At week 16, a higher proportion of patients in the deucravacitinib group achieved PASI75 (P < .0001) and MDA (P = .0007) than in the placebo group, with significantly greater improvements in HAQ-DI and physical health at week 16 (P < .05 for both).
- Clinical effectiveness measures and patient-reported outcomes continued to improve with deucravacitinib after week 16 and were sustained through week 52.
- During the placebo-controlled period (weeks 0-16), AEs occurred in 62.8%, 54.7%, and 73.3% of patients in the deucravacitinib, placebo, and apremilast groups, respectively. Most AEs were mild to moderate and resolved without intervention. At 52 weeks, the overall exposure-adjusted incidence rates of AEs per 100 person-years were 201.4, 238.9, and 366.5 for the placebo-deucravacitinib, deucravacitinib-deucravacitinib, and apremilast-apremilast arms, respectively. No deaths occurred.
IN PRACTICE
“Consistent efficacy in multiple subgroups supports the role of deucravacitinib as an oral treatment option for patients with PsA,” the authors wrote.
SOURCE
This study was led by Philip J. Mease, MD, from Providence Swedish Medical Center and the University of Washington School of Medicine in Seattle. It was published online on July 20, 2026, in Arthritis & Rheumatology.
LIMITATIONS
A small proportion of patients had prior TNF inhibitor exposure and had failed only one TNF inhibitor. The study population was mainly White and older than 45 years, which may limit generalizability. Physician-assessed rather than imaging-confirmed axial involvement in PsA may also affect interpretation of the findings.
DISCLOSURES
The study received support from Bristol Myers Squibb. Five authors declared being employed by and/or holding stocks in Bristol Myers Squibb. Several authors reported receiving grants, consulting fees, and/or honoraria or having other ties with multiple pharmaceutical companies, including Bristol Myers Squibb.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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