Uncontrolled inflammation in psoriatic arthritis (PsA) contributes to structural joint damage, which is associated with long-term disability, impaired physical function, and reduced health-related quality of life.¹ Guselkumab, a fully human, dual-acting monoclonal antibody that selectively inhibits the interleukin (IL)-23p19 subunit, demonstrated efficacy across PsA domains and significantly inhibited structural damage progression vs. placebo at week 24 in the phase 3b APEX study in patients with active and erosive PsA.¹ At the EULAR 2026 Congress, Professor Christopher Ritchlin from the University of Rochester Medical Center, United States, presented the post hoc analysis of the phase 3b APEX study evaluating the relationship between clinical response and structural damage progression at week 24 among guselkumab-randomized patients.¹

APEX enrolled biologic-naïve adults aged ≥18 years with active PsA for at least 6 months despite prior conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), apremilast, or nonsteroidal anti-inflammatory drugs (NSAIDs).¹ Patients were required to meet the Classification Criteria for Psoriatic Arthritis (CASPAR), have ≥3 swollen and ≥3 tender joints, C-reactive protein (CRP) ≥0.3mg/dL, and ≥2 joints with erosions on baseline radiographs of the hands and feet.¹ Active plaque psoriasis, defined as ≥1 plaque measuring ≥2cm, and/or nail psoriasis was also required.¹

Patients were randomized to receive guselkumab every 4 weeks (Q4W), guselkumab every 8 weeks (Q8W), or placebo through week 24, after which placebo-treated patients switched to guselkumab Q4W.¹ The current post hoc analysis assessed the least squares mean (LSM) change from baseline in the PsA-modified van der Heijde-Sharp (vdH-S) score according to clinical response across joint efficacy, composite disease activity, physical function, and pain measures at week 24.¹ Baseline demographic, PsA, and radiographic characteristics were well balanced across treatment groups.¹

Among guselkumab-randomized patients receiving either Q4W or Q8W dosing, those who achieved clinical responses across joint efficacy measures had numerically lower levels of structural damage progression at week 24.¹ A graded relationship was observed across American College of Rheumatology (ACR) response levels, with ACR20, ACR50, and ACR70 responders showing progressively lower LSM changes in the PsA-modified vdH-S score compared with clinical nonresponders.¹

A similar relationship was observed across composite disease activity measures.¹ Patients who achieved low disease activity (LDA) or minimal disease activity (MDA), as assessed by Disease Activity Index for Psoriatic Arthritis (DAPSA), clinical DAPSA (cDAPSA), and MDA criteria, had numerically lower levels of structural damage progression than clinical nonresponders at week 24.¹ These findings indicated that greater clinical disease control was associated with less radiographic progression across multiple composite measures.¹

Patient-reported outcomes showed a consistent pattern.¹ Among patients assessed for physical function and pain, those who achieved normalized physical function, defined by Health Assessment Questionnaire-Disability Index (HAQ-DI) ≤0.5, or minimal pain, defined as patient-reported pain visual analog scale (VAS) ≤15, had numerically lower levels of structural damage progression than clinical nonresponders at week 24.¹

In conclusion, this post-hoc analysis of the phase 3b APEX study showed that among patients with active and erosive PsA receiving guselkumab Q4W or Q8W, achievement of clinical response was associated with less structural damage progression at week 24.¹ The association was observed across joint efficacy, composite disease measures, and patient-reported outcomes, including ACR20/50/70, DAPSA and cDAPSA LDA, MDA, normalized physical function, and minimal pain.¹ Further analyses beyond week 24 will provide additional insights into the maintenance of structural damage inhibition among clinical responders and the longer-term outcomes of clinical nonresponders.¹