News|Articles|September 19, 2025

Guttman-Yassky Showcases 2 Paths to Long-Term AD Control at EADV 2025

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Key Takeaways

  • Rocatinlimab targets OX40, offering potential long-term disease modification and durable responses, even after treatment cessation, despite a slower onset.
  • Upadacitinib demonstrates consistent long-term efficacy over 140 weeks, maintaining rapid response durability, beneficial for patients.
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At EADV 2025, she showcased how OX40 and JAK inhibition offer complementary approaches to long-term disease control.

At this year’s European Academy of Dermatology & Venereology (EADV) Congress 2025, Emma Guttman-Yassky, MD, PhD, professor of dermatology and immunology and the health system chair of the department of dermatology at the Icahn School of Medicine at Mount Sinai, presented new data on 2 therapies shaping the evolving treatment landscape for atopic dermatitis: rocatinlimab, an investigational OX40 inhibitor with potential for long-term disease modification, and upadacitinib, a JAK inhibitor with demonstrated durability of response over nearly 3 years of follow-up. In this conversation with Dermatology Times, Guttman-Yassky highlights the clinical takeaways, safety considerations, and practical insights for clinicians, while also exploring how these therapies may fit into treatment strategies for both younger and older patient populations.

Q&A

DT: What are the major takeaways for clinicians on rocatinlimab?

Guttman-Yassky: Rocatinlimab targets OX40, part of a new drug class that also includes agents against OX40 ligand. This mechanism is unique because it targets activated memory cells—the cells that repopulate lesions after clearance. By addressing these cells, the drug has the potential not only to clear disease but also to extend response durability. This opens the door to disease modification, meaning patients may remain clear longer, even after treatment stops. Clinicians should know this class of drugs may work more slowly than others because it acts indirectly. It takes time, but many patients achieve clearance. Importantly, the durability of response after stopping therapy may be a key differentiator.

DT: Did the trial analyze biologic-naïve patients compared with those who had prior biologic or systemic therapy?

Guttman-Yassky: Yes, both groups were included and responded well. Typically, biologic-naïve patients respond a little better, but even patients with prior biologic exposure saw significant improvement, which is very encouraging.

DT: How did the safety profile compare with other biologics and systemic therapies?

Guttman-Yassky: The safety profile was good over the 24-week primary endpoint. A longer study is ongoing to assess 48 weeks and beyond, but so far, there have been no new safety concerns compared with other biologics.

DT: What differentiates rocatinlimab from other biologics, JAK inhibitors, or systemic therapies?

Guttman-Yassky: First, it’s administered every 4 weeks, which is convenient. Second, in phase 2, most patients who stopped the drug maintained EASI-75 responses for another 20 weeks. Unlike other biologics, where efficacy peaks at 24 weeks, rocatinlimab continues to improve through week 48. That durability, even after stopping treatment, could be the most exciting aspect of this class. Most patients with lifelong disease won’t mind waiting a little longer for efficacy if it means long-term disease modification. That’s why the primary endpoint was set at 24 weeks instead of 16. The onset may be slower, but the longevity of response is very valuable.

DT: How do you see rocatinlimab fitting into current AD treatment goals, and how do you explain it to patients?

Guttman-Yassky: The number one question patients ask is, “When can I stop, or how can I space injections?” This class holds promise in answering that. Efficacy may take longer, but eventually patients may be able to space treatment—every 8, 12, or even 24 weeks.

DT: Do you see this becoming a first-line therapy?

Guttman-Yassky: Yes. Fewer injections per year is meaningful for both patients and insurers. Personally, I would prefer a therapy with fewer injections, even if it takes longer to achieve results, especially if it offers long-term benefits.

DT: As for your presentation on upadacitinib, did you see consistent durability of response over the 140-week follow-up?

Guttman-Yassky: Yes. JAK inhibitors like upadacitinib can achieve rapid efficacy—patients improve quickly. Some thought responses wouldn’t last since it’s not a biologic, but we’ve seen that long-term use maintains responses. This is very meaningful for patients.

DT: For older patients with comorbidities, how do you balance long-term systemic therapy?

Guttman-Yassky: JAK inhibitors do have safety baggage, and the risks increase in older individuals. While the patient numbers are smaller in AD compared with other conditions, caution is important. Still, JAK inhibitors remain an option, especially for patients who avoid injections. They’re also flexible. You can stop and restart when needed, which is helpful for moderate disease.

DT: How do you choose between JAK inhibitors and biologics in this age group?

Guttman-Yassky: I usually favor biologics for older patients because they have a safer profile in this population. JAK inhibitors are quite safe in younger patients, but risks rise with age. Still, for patients who absolutely refuse injections, JAK inhibitors are an option.

DT: What practical advice would you give clinicians managing older patients on JAK inhibitors or systemic therapies?

Guttman-Yassky: Discuss and document risks and benefits thoroughly. I bring older patients in more often, order bloodwork more frequently, and coordinate with their primary care physicians. We check lipids, adjust medications if needed, and provide holistic care. Counseling and close follow-up are essential.

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