Philip Mease, MD: The Biggest PsA Readouts From EULAR 2026

Four psoriatic arthritis (PsA) readouts from the 2026 EULAR Congress moved the field on distinct fronts: structural protection, durability, head-to-head efficacy, and metabolic comorbidity management. Guselkumab became the first IL-23 inhibitor with an FDA label claim for inhibiting structural joint damage, based on 24-week APEX data showing roughly 2.5-fold greater inhibition of radiographic progression versus placebo.¹

Izokibep, a small-protein IL-17A inhibitor, produced 52-week data showing sustained ACR50/70, PASI90/100, and minimal disease activity responses.² The head-to-head BE BOLD trial delivered the first joint-focused superiority result between 2 biologic mechanisms in PsA, with bimekizumab besting risankizumab on ACR50 at week 16.³ And TOGETHER-PsA tested whether treating obesity alongside inflammation changes outcomes, pairing ixekizumab with the GLP-1/GIP agonist tirzepatide.⁴

“Many of the medicines we use for treating PsA will eventually wear out in effect,” said Philip Mease, MD, Director of Rheumatology Research at Providence Swedish Medical Center and Clinical Professor of Medicine at the University of Washington School of Medicine, Seattle. “They may work very well for the initial period, and even for several years, but then eventually lose effect.” That durability problem runs through all 4 studies: each adds either a new mechanism, a new dosing profile, or a new comorbidity-focused strategy to counter it.

Mease, a co-investigator or presenter on several of these trials, walked RheumatologyLive through what each readout means in practice. In the following interview, he revisits the structural-damage case for guselkumab, the durability profile of izokibep, the head-to-head result for bimekizumab, and the mechanistic rationale behind combining GLP-1 therapy with a biologic in PsA.

HCPLive: How does the new guselkumab label for inhibiting structural joint damage shape its place in your treatment algorithm?

Philip Mease, MD: There are several pillars of treatment that are important when we think about the overall well-being of a patient. Improvement of symptoms and signs is one pillar, having a drug that's relatively safe is another, and demonstrating the ability of a drug to inhibit or halt the progression of structural damage in the joints is yet another. As you look at x-rays over time in patients with a destructive inflammatory arthritis, the joints gradually crumble and are no longer functional, and are quite painful. With the newer medications we've been using over the last several decades, especially the biologics and targeted synthetic DMARDs, virtually all of them have shown an ability to inhibit structural damage.

Now we have evidence with guselkumab, one of the interleukin-23 inhibitors, that it can inhibit structural damage progression. This was shown in a study called APEX, in which patients received either monthly guselkumab or guselkumab every 2 months, which is the approved label dosing, versus placebo. There was clear efficacy in terms of non-progression in patients treated with both doses, and it was essentially equivalent whether they received it monthly or every 2 months. This solidified the drug's ability to inhibit structural damage, and the FDA recognized this and added it to the drug's label. Now, when we're speaking with a patient about efficacy, we can say not only that your symptoms and signs of pain and stiffness and fatigue will improve, and your function will improve, but also that it inhibits structural damage. This sets it apart; we don't have that evidence yet for other IL-23 inhibitors, so it's a welcome addition to the label. This study also required that all patients have evidence of joint damage at baseline, so anyone without existing damage was excluded going in. We wanted to focus on the most severe patients to demonstrate this ability.

What is your clinical read on the new izokibep late-breaking data, and how might it fit into your treatment algorithm pending approval?

Mease: Izokibep is a uniquely structured IL-17A inhibitor; it's a small molecule biologic, and 1 of the potential advantages of a small molecular entity is that it may have a better capability of penetrating difficult-to-penetrate tissues. We had previously shown izokibep's ability to be effective at shorter time points, and this is now 52-week data showing durability of effect over time. This was shown not only in ACR20, 50, and 70 responses compared to placebo, which were quite strong and durable, but also in other important disease measures, such as improvement of skin psoriasis, dactylitis, function, and quality of life. This gives us evidence that it can be not only a quickly acting but also a quite durable IL-17A inhibitor. One of the things we find is that with time, many of the medicines we use for treating psoriatic arthritis will eventually wear out in effect; they may work very well for the initial period, even for several years, but then eventually lose effect. That's why it's valuable to have additional medicines, and the IL-17 class is a good part of that. Because of the relative safety of the medication, we don't see a high infection signal, a malignancy signal, or a cardiovascular or thrombosis signal, so it's a relatively safe medicine, and it's welcome to have an additional treatment option.

Why is the TOGETHER-PsA data on combining a GLP-1 receptor agonist with a biologic such an important topic right now?

Mease: I've gotten really swept up into this topic. There's a background here: GRAPPA, the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, which I help lead, is very involved in teaching and educating people around the world about psoriasis and psoriatic arthritis. I'm leading a working group within GRAPPA to develop teaching slides and give lectures globally, both virtually and in person, on the importance of obesity as a problem in psoriatic arthritis and psoriasis. There's a genetic proclivity to having obesity, and being obese is in and of itself a pro-inflammatory problem: adipocytes from obese fatty tissue produce adipokines, which contribute to inflammation in the body. One of the things we've been seeing more and more, with the addition of GLP-1 receptor agonists, is that patients come back and say they're feeling better overall, their disease process is better. They not only feel better about losing weight, but their inflammation feels less. This was a study to try to demonstrate the additive ability of using a GLP-1 receptor agonist, tirzepatide, which is a dual GIP and GLP-1 receptor agonist. We're getting a hint, which will be proven with further studies, that the GLP-1 receptor agonist group, particularly tirzepatide, can be immunomodulatory in and of themselves, in addition to the other treatments we're giving these patients.

What did the BE BOLD head-to-head data between bimekizumab and risankizumab show, and were there any safety findings that stood out?

Mease: BE BOLD was a head-to-head study between the IL-17A/F inhibitor bimekizumab and the IL-23 inhibitor risankizumab in PsA. We hadn't had a previous head-to-head trial to really get a feeling for how these 2 mechanisms of action compare. We know both can be very effective in psoriatic arthritis from their development programs, so this was a chance to see how they compared directly. What was reported at this meeting was the week 16 data, which showed a superiority of bimekizumab compared to risankizumab in several key endpoints, including ACR50, the primary endpoint, as well as ACR20 and ACR70, and other key endpoints including improvement in function and quality of life.

In terms of other measures in PsA, both agents worked very well, and we're excited to see the effectiveness of IL-17A and F, as well as IL-23, in these studies. Both are safer medicines than some of the other medicines we've historically used, including the anti-TNF group, so it's good to have this quality of evidence showing the ability of IL-17A and F to improve PsA. On safety, one of the things we can see with the IL-17A or A and F inhibitor class is candida infections, and that was seen here; it was not a high proportion of patients, and it tended to be mild to moderate and easily treatable. There was also a very rare instance of inflammatory bowel disease with bimekizumab, which is a known potential side effect. Other than that, there were no major issues, such as problems with serious infection or malignancy, between the two. Overall, both medicines are relatively safe.

Editor's Note: This transcript has been edited for grammar and clarity using artificial intelligence tools.

Mease’s disclosures include AbbVie, Amgen, BMS, Eli Lilly, Johnson & Johnson, Novartis, Pfizer, and others.

References

1. Mease PJ, Ritchlin CT, Coates LC, et al. Inhibition of structural damage progression with guselkumab, a selective IL-23i, in participants with active PsA: results through week 24 of the phase 3b, randomized, double-blind, placebo-controlled APEX study. Abstract presented at: EULAR 2025 Congress; June 11-14, 2025; Barcelona, Spain.

2. Mease PJ, Behrens F, Kivitz A, et al. Efficacy and safety of izokibep, a novel IL-17A inhibitor, in patients with active psoriatic arthritis: week 52 results from a randomised, double-blind, placebo-controlled, multicentre, phase 2b/3 study. Abstract OP073. EULAR Congress 2026; June 3-6, 2026; London, England.

3. McInnes IB, et al. Bimekizumab efficacy and safety versus risankizumab in active PsA: 16-week results from the head-to-head BE BOLD study. Abstract LB0001. EULAR Congress 2026; June 3-6, 2026; London, England.

4. Merola JF, Mease P, Kivitz A, et al. Ixekizumab With Tirzepatide Achieved Greater Disease Control Than Ixekizumab Alone in Adults With Psoriatic Arthritis and Overweight or Obesity: Results From a Randomized Clinical Trial. Arthritis Rheumatol. 2026. doi:10.1002/art.70134