FDA Updates Guselkumab Label to Add Joint Damage Inhibition for PsA

The United States Food and Drug Administration (US FDA) has approved a supplemental Biologics License Application (sBLA) for guselkumab (Tremfya) to include evidence of inhibition of structural joint damage progression in adults with active psoriatic arthritis (PsA), Johnson & Johnson announced May 28, 2026. The label update makes guselkumab the only IL-23 inhibitor with structural inhibition data in its US prescribing information — a distinction the company characterizes as a clinically meaningful differentiator in a competitive class.¹

"Joint damage associated with active psoriatic arthritis can happen as soon as 6 months after onset of disease, so it's important to have treatment solutions that can help provide daily symptom relief while also protecting joints from long-term structural damage," Philip J. Mease, MD, Director of Rheumatology Research at the Swedish Medical Center/Providence St. Joseph Health and Clinical Professor at the University of Washington School of Medicine in Seattle, Washington, said in a statement.¹ Mease served as a CHORD trial investigator and is a paid consultant for Johnson & Johnson. "With the inclusion of these findings in the label, we now have stronger clinical evidence that sets TREMFYA apart as a treatment option for patients with active PsA at risk for joint damage."¹

The update is supported by results from the phase 3b APEX trial (NCT04882098), a randomized, double-blind, placebo-controlled, multicenter study in biologic-naive adults with active PsA who had inadequate responses to standard therapies including csDMARDs, apremilast, and NSAIDs. APEX enrolled approximately 1,020 patients, randomizing them in a 5:7:7 ratio to guselkumab 100 mg subcutaneously every 4 weeks (Q4W), guselkumab 100 mg at weeks 0 and 4 then every 8 weeks (Q8W), or placebo every 4 weeks. Key eligibility criteria required at least 3 tender joints, at least 3 swollen joints, C-reactive protein ≥0.3 mg/dL, and at least 2 erosive joints at baseline — an entry criterion that enriched the study population for patients with established structural disease burden.²

At week 24, both guselkumab regimens met the trial's primary endpoint of ACR20 response, with rates of 66.6% (Q4W) and 68.3% (Q8W) versus 47.0% with placebo (P <.001 for both).² The major secondary endpoint — change from baseline in total PsA-modified van der Heijde-Sharp (vdH-S) score, a composite measure of joint erosion and joint space narrowing — was also met. The least-squares mean change from baseline to week 24 was 0.55 for guselkumab Q4W and 0.54 for guselkumab Q8W, compared with 1.35 for placebo (P = .002 and P <.001, respectively) — representing approximately 2.5-fold greater inhibition of radiographic progression versus placebo.² The vdH-S scores in the APEX analysis were derived from week 48 radiograph reads, as noted in the press release.¹

Structural inhibition was sustained through week 48, with the radiographic benefit maintained across both dose groups in biologic-naive patients. In an additional analysis of patients who crossed over from placebo to guselkumab at week 24, the rate of radiographic progression was reduced by 57% from week 24 to week 48, compared with the rate observed during the placebo-controlled period — suggesting benefit from IL-23 inhibition even after initial damage accrual, though the crossover design limits causal interpretation.¹

The label claim that guselkumab is the only IL-23 inhibitor with structural inhibition data reflects a regulatory and trial design reality rather than a demonstrated superiority over other agents in the class: risankizumab's pivotal PsA trials (KEEPsAKE-1 and -2) were not designed to assess radiographic progression as a primary or ranked secondary endpoint and therefore did not generate label-qualifying structural data.

Guselkumab is a fully human monoclonal antibody that selectively inhibits the IL-23p19 subunit. The agent is also described by J&J as dual-acting, based on in vitro data showing binding to CD64, a receptor expressed on IL-23–producing myeloid cells; the clinical significance of CD64 binding has not been established.¹

Safety in APEX was consistent with guselkumab's established profile across its approved indications. No new safety signals were identified. The most common adverse events in PsA clinical trials include upper respiratory tract infections, oral candidiasis, headache, diarrhea, and urinary tract infections. Guselkumab carries no boxed warning but requires tuberculosis screening prior to initiation and monitoring for serious infections during treatment.¹

Guselkumab is currently approved in the US for adults and pediatric patients (≥6 years, ≥40 kg) with moderate-to-severe plaque psoriasis; adults and pediatric patients (≥6 years, ≥40 kg) with active PsA; adults with moderately to severely active ulcerative colitis; and adults with moderately to severely active Crohn's disease.¹

References

1. Johnson & Johnson. FDA approves label expansion, cementing Tremfya as the only IL-23 inhibitor proven to help stop further joint damage. Press release. May 28, 2026. https://www.prnewswire.com/news-releases/fda-approves-label-expansion-cementing-tremfya-as-the-only-il23-inhibitor-proven-to-help-stop-further-joint-damage-302785103.html

2. Mease PJ, Ritchlin CT, Coates LC, et al. Inhibition of structural damage progression with the selective interleukin-23 inhibitor guselkumab in participants with active PsA: results through week 24 of the phase 3b, randomised, double-blind, placebo-controlled APEX study. Ann Rheum Dis. 2025;84(12):1983–1994. doi:10.1016/j.ard.2025.08.006