April W. Armstrong, MD, MPH

Most adolescents with moderate to severe 

 reported controlled disease within 2 weeks of starting dupilumab (Dupixent), according to 1-year interim results from the RELIEVE-AD-PEDs study presented at the 

2026 European Academy of Dermatology and Venereology (EADV) Congress

The prospective survey study enrolled patients aged 12 - 17 years through the DUPIXENT MyWay support program, measuring control with the Atopic Dermatitis Control Tool (ADCT), a validated 6-item instrument on which scores of 7 or higher signal uncontrolled disease.¹˒² Among 126 subjects completing the month 12 survey, 88.1% (111/126) remained on dupilumab, and mean ADCT scores fell from 13.3 at baseline to 4.9 (

Controlled disease rose from 12.1% of patients at baseline to 57.9% at 2 weeks and 73.8% at Month 12 (both 

 < .001), and reports of more than 2 flares in the prior 4 weeks fell from 51.3% to 15.1%.¹ April Armstrong, MD, MPH, professor and chief of dermatology at the University of California Los Angeles, is first author of the analysis. In the following Q&A interview, Armstrong spoke with 

 at EADV 2026 in Vienna about the findings and their implications:

: At the 12-month mark, 73.8% of adolescents reported "controlled disease" on the ADCT, up from just 12.1% at baseline. What did you find most notable about how quickly and how durably that control was achieved?

 It’s notable that a majority of adolescents 12-17 years old reported disease control at two weeks after starting dupilumab treatment and control was sustained through one year. This prospective real-world study reinforces what we’ve seen in the dupilumab clinical trials, early and sustained benefit, so this was not surprising to see in clinical practice as well.

: Disease control jumped to 57.9% as early as 2 weeks after starting dupilumab. What does that early separation tell you about the real-world treatment experience for adolescent patients and their families?

These data show that dupilumab can work quickly on improving six domains measured with the Atopic Dermatitis Control Tool (ADCT): overall severity of atopic dermatitis symptoms, frequency of intense episodes of itching, extent of atopic dermatitis-related bother, frequency of sleep impact, impact of atopic dermatitis on daily activities, and impact of atopic dermatitis on mood or emotions. For adolescents struggling with moderate or severe disease, improving these aspects soon after initiating dupilumab can provide much needed relief.

: With flare frequency dropping from 51.3% to 15.1% of patients reporting more than 2 flares a month, how should clinicians weigh that reduction when counseling teenage patients and parents on what to expect from treatment?

With the real-world data showing dupilumab reduced the frequency of flares as early as two weeks and through one year, it gives me confidence when I discuss potential outcomes with my patients and their caregivers that dupilumab may improve this aspect of the disease quickly and durably. Fewer flares mean less scratching and perpetuation of the itch-scratch cycle.

: This is a real-world, patient-reported cohort rather than a controlled trial, and only 126 of the original 314 enrollees had reached the 12-month survey at this interim analysis. How do you think about the strength of these conclusions given that design, and what would you want to see in the full dataset?

At the time of this interim analysis, not all 314 patients had reached one year of treatment, so future analyses will include data for all enrolled patients at one year. Given the strength of the results at the interim analysis, I expect to see similar results once the full patient population reaches 12 months of study.

: Treatment satisfaction stayed high through a year of follow-up. What questions does this data leave open for the field, whether around long-term durability, adherence, or how these findings should shape dupilumab use in adolescents going forward?

 High treatment satisfaction suggests that patients are feeling benefit and are more likely to continue taking a medicine. Dupilumab targets two key drivers of the type 2 inflammation underlying atopic dermatitis, so treatment persistence is important to maintain these results because it continuously works even between flares.

Editor’s note: This summary has been edited for grammar and clarity using artificial intelligence tools. Armstrong has previously disclosed serving as an investigator and/or consultant for AbbVie, BMS, Dermavant, Dermira, Janssen, Eli Lilly, LEO Pharma, Modernizing Medicine, Ortho Dermatologics, Regeneron Pharmaceuticals, Inc., Sanofi Genzyme, Science 37, and UCB.

Armstrong A, Paller AS, Yang M, et al. Sustained disease control among adolescents with moderate-to-severe atopic dermatitis treated with dupilumab in clinical practice: 1-year results from the RELIEVE-AD-PEDs study. Presented at: 2026 European Academy of Dermatology and Venereology Congress; September 30-October 3, 2026; Vienna, Austria.

Pariser DM, Simpson EL, Gadkari A, et al. Evaluating patient-perceived control of atopic dermatitis: design, validation, and scoring of the Atopic Dermatitis Control Tool (ADCT). Curr Med Res Opin. 2020;36(3):367-376. doi:10.1080/03007995.2019.1699516.

Articles

April Armstrong, MD, MPH, discusses 1-year RELIEVE-AD-PEDs data on rapid, sustained dupilumab disease control in adolescents with atopic dermatitis.

RELIEVE-AD-PEDs: Dupilumab Sustains Adolescent Atopic Dermatitis Control at 1 Year

2026 American Academy of Dermatology (AAD) Annual Meeting

, leading experts highlighted the rapid pace of innovation reshaping the management of chronic inflammatory skin diseases.

Among them, April W. Armstrong, MD, MPH, of the David Geffen School of Medicine at UCLA, spoke about several insights spanning psoriasis, atopic dermatitis, and emerging therapeutic strategies, drawing from multiple sessions in which she participated. In this discussion, Armstrong underscored both the remarkable progress made with the therapeutic landscape, emphasizing the rising importance of mechanism-driven treatment selection, long-term safety data, and individualized patient care.

The following Q&A interview summarizes her responses to inquiries during her 

The IL-23 pathway has become a central target in psoriasis over the past few years. How would you characterize what makes IL-23 inhibition mechanistically different, and why has it emerged as a therapeutic target?

There are a few things to consider about IL-23 inhibition. We know that IL-23 inhibition is really central in terms of being this master regulator for diseases such as plaque psoriasis. We actually also know it's really important for conditions such as Crohn's disease or ulcerative colitis, oftentimes comorbidities that are important to our dermatology patients who may have inflammatory skin diseases and have an increased risk of those other conditions. Now, when we're thinking about IL-23, why it's important is that it's very key in terms of making sure that in the process of naive T-cell differentiation, these T cells are differentiated into certain types of cells, such as Th17 cells and so forth.

Because of that, it has a tremendous influence in terms of the pathological states, with regard to potentially directing some of the inappropriately elevated levels of differentiation into Th17 cells that can be pathologic in states such as psoriasis. Now, when we have therapies that target the IL-23 pathway, for example, it can be very specifically targeting that of of diseases that are affected by this, namely psoriasis in this case. Also, what we see is that for therapies that are particularly targeting IL-23, oftentimes, there are very high rates of complete and near-complete skin response with some of the biologics that we've had for a long period of time. One of the distinct advantages of IL-23 modulation or inhibition in psoriasis is that it can get that durable response with extended dosing intervals.

Typically, we're thinking about dosing intervals of every 2 months or every 3 months with our injectable biologics. Now, we do have another class, which is IL-17 inhibitors in psoriasis, that are also extremely highly effective. With the newer IL-17 inhibitors, the dosing intervals are getting closer to those of the IL-23 inhibitors. Getting back to IL-23 inhibition, what we see is that a quite distinctive advantage is the favorable long-term safety profile. What we are seeing is that with patients who have been on IL-23 inhibitors for a while, for example, we have now over 6 or 7 years of long-term extension data. What we see is that it continues to be very safe in our patients who've been taking it for a long period of time, and we don't see signals with regard to serious infections or cancer in those patients who have taken it for a very long time.

We know your session also touches on unmet needs across patient populations. Which patient profiles or clinical scenarios still represent the biggest gaps in the management of psoriasis?

 We have come a long way in terms of managing our patients who have psoriasis and psoriatic arthritis, and caring for them has really been a pleasure as a dermatologist, along with our rheumatology colleagues, for the past two decades now. That being said, we also still have a number of areas where we have unmet needs. Number one is thinking about patients who may have limited body surface area involvement, but high-impact site involvement, for example, the treatment of patients with palmoplanter diseases. That's still one area that we are trying to figure out how to better manage that particular disease phenotype. We know that patients with palmoplantar psoriasis have one of the most difficult-to-treat phenotypes, and that is something that we're consistently trying to work on. This includes not only the hyperkeratotic type of palmoplantar psoriasis, but also palmoplantar pustulosis.

Another area is thinking about managing comorbidities in our patients with psoriasis. Namely, looking at obesity a little bit closer. We know that many patients with psoriasis, epidemiologically, there are higher rates of obesity in patients with psoriasis, and newer and newer data show that managing their obesity and getting patients to decrease their weight when they are in the obese category can not only improve their cardiovascular health. That intervention may actually have an independent effect, a positive effect, in terms of reducing their psoriasis or psoriatic arthritis disease activity. This is really interesting data. It's newer data, and something that we as a field are continuing to try to understand.

Then, finally, we may have patients who have severe psoriasis or psoriatic arthritis and who also have various complex comorbidities, and we’re thinking about how to care for those patients and ensure that the therapies that we have for them can potentially address these other comorbidities. But also, even if we have a therapy that's specifically for psoriasis and psoriatic arthritis, in the context of the other complex comorbidities, how can we make sure that these patients are safely managed by our pharmacological or other interventions?

Speaking of interventions, there's a growing number of IL-23 inhibitors now available. How are you thinking about selection and differentiation within your own practice?

We have a number of different IL-23 inhibitors that are available. We have the biologics…and we have a newly-approved IL-23 receptor inhibitor. That's an oral peptide, and that's icotrokinra. So, now we have oral therapies for targeting the IL-23 pathway in patients with plaque psoriasis, as well as biologics. Having all these different options, I think, is really great for our patients, because even within the IL-23 class, we have known from the real-world studies that sometimes failing one IL-23 therapy doesn't necessarily mean that they will fail another IL-23 therapy.

A few things when we're considering these different medications: For example, for patients who have moderate to severe plaque psoriasis, when our dermatologists and dermatology and NPs and PAs are thinking oral therapies could benefit that patient population in terms of targeting the il 23 pathway, we can now, we now have FDA-approved therapy for that, and can consider icotrkinra. When we are looking at icotrokinra, the efficacy rates are at the level of biologics. So that's very exciting and really great news for our patients who especially those who have been wanting an oral therapy for a long time.

When we're looking at our patients who may benefit more potentially in terms of biologic therapies, we have tildrakizumab, which I think is really wonderful for patients who have, for example, Medicare coverage. This is because this tildrakizumab is the only medication within the IL-23 class that's covered under Medicare Part B benefits. So for our patients who are our Medicare age, who may not have good supplemental coverage, for example, that's definitely a good choice. Then we also have, for example, guselkumab and risankizumab, which I think as a field we have known for a very long time to have high efficacy in treating our patients with plaque psoriasis. Also, [they have] very good safety data as well. I think those continue to be excellent choices for patients.

 To dermatologists who are in the audience, who may be looking to translate some of these tips into their everyday practice, what would you say are the most immediately actionable takeaways?

I will say when we're thinking about our various options that we have for patients with plaque psoriasis. Now, I think number one, evaluating whether they have psoriatic arthritis is important because there is some differentiation among the various therapies with regard to PsA. That gap, I think, between IL-17s and IL-23s is closing. Newer data also show, for example, that guselkumab can decrease the radiographic progression of patients with psoriatic arthritis. So that's encouraging for our patient, for our patients. The other aspect is, when we're thinking about patients, it's very important to also understand what comorbidities they may have, and some of our therapies have multiple indications.

If they have a certain set of comorbidities where they can use essentially one medication to treat not only psoriasis and psoriatic arthritis, but also, for example, inflammatory bowel disease. Then think about, really thinking about the IL-23 class would be, would be most appropriate for those patients. Also, when we look at our biologics, for example, there are differences, although I would say the differences are pretty small these days, as we're very fortunate to have highly efficacious medications. But there are small differences among the biologics. For example, our newer biologic bimekizumab, which is an IL-17 inhibitor, has very robust, high response rates that we've seen in clinical trials, as well as in the long-term extension studies. That's also something to be aware of.

Finally, as I talked about earlier, we now have oral options. Our IL-23 receptor inhibitor, icotrokinra, has biologic-level efficacy at the level we're seeing. I think the expectation for our oral therapies has increased even more. Also, with two emerging…TYK2 inhibitors coming up through the pipeline, I think we will have better therapies in the future for our patients who desire oral therapies for the management of moderate to severe plaque psoriasis.

Concerning your portion of the ‘What's New in Dermatology’ session you presented on atopic dermatitis, what were some of the treatments that you chose to highlight?

When we are looking at what's new in atopic dermatitis, I feel that the field is ‘drinking from a fire hydrant.’ We have continual innovations in that area, and also at a speed that we really haven't seen before in dermatology. Some of the things that I highlighted in my session included long-term data for the FDA-approved therapies, both in the biologic realm as well as oral JAK inhibitors. Specifically, when we're thinking about safety data, one of the key reassuring messages we've seen with regards to the long term safety for the oral JAK inhibitors is that in the atopic dermatitis population, for example, the rates of serious infections or the rates of MACE events…seem to be quite similar to the background [atopic dermatitis] patients who have moderate to severe disease severity. So that's very important.

Now that being said, it's still very important to make sure that your patients start an oral JAK inhibitor, to make sure that they get their vaccination, especially their Zoster vaccination, because the use of oral JAK inhibitors can be associated with higher rates of zoster. So I want to make sure that all my patients get their Zoster vaccination before or as the second shot, as they started their oral JAK inhibitors. The other aspect that I highlighted in my study is really thinking about emerging therapies and new MOAs for patients with atopic dermatitis. I will say when we're looking at emerging therapies, there are some that are still relying on the existing, proven pathways. But there are also explorations for neural pathways.

For example, now we have more data on the OX40-ligand pathway, and we have longer-term data with regard to that particular pathway. In addition to that, we also see newer innovations in inhibitors that target il four receptor alpha, which we know is a known mechanism, but looking newer innovations, looking at, can we target that even more specifically, potentially leading to greater, greater efficacy, we're also seeing oral therapies that are developed for atopic dermatitis, and not necessarily inhibiting jak Janus kinase molecules, but inhibiting stat six, for example. That's notable as well.

Finally, there are a number of different innovations that are looking at bi-specific or tri-specific molecules that really take advantage of different targets in atopic dermatitis and try to inhibit either two or sometimes even three targets in order to help address the heterogeneity in the patient presentations. And so hopefully, with one therapy, you're able to reach the greatest number of patients possible and have it be effective in the largest number of patients possible. So those are some of the things that I highlighted in my talk at the AAD.

You also discussed oral therapies during AAD. To which oral medications did you refer in this session?

 In this particular session, I refer to both the FDA-approved advanced oral therapies that we've been using for a while, things such as deucravacitinib, as well as apremilast, and our newly FDA-approved oral therapy, icotrokinra. I also highlighted two therapies that are TYK2 inhibitors that are emerging, and that just had their phase three readout at the AAD meeting. So, that's all of this, I think, is very exciting, and really shows how oral therapies are the next frontier in terms of development for patients with moderate to severe plaque psoriasis. A few things regarding deucravacitinib that I highlighted are that deucravacitinib is now FDA approved, for example, for the treatment of psoriatic arthritis. That's a very exciting mile marker, I think, for deucravacitinib. We've been using it for plaque psoriasis, and we've also known about the phase three data for a while, so now seeing it being available for patients with PsA, I think that's very exciting.

With regards to icotrokinra, just newly FDA-approved, really thinking about once a day oral therapy that have the level of efficacy that are essentially that's rivaling our biologics and and then thinking about the potential for our patients in the real world now, then that, now that we have a oral therapy that that have a really good safety profile and also high efficacy that we can recommend to our patients. And then finally, when we're looking at newer TYK2 inhibitors and their development, we have zasitnib and mbudocitinib, both of them targeting the tick two inhibitor, but in ways that are even more specific and therefore more potent as well, in terms of their MoA. And so I think what you're seeing is that the really the second generation of TYK2 inhibitors in plaque psoriasis, and their performance is one such that we're seeing higher and higher levels of performance with the second generation of TYK2 inhibitors.

Are there any other notable takeaways that you hope clinicians walk away with from this session?

I think that in addition to the oral therapy session that I covered, the psoriasis symposium, also covered a number of other areas, and I think they will hopefully have learned a lot with regards to some advances in the biologic era and and then also thinking about comorbidities, not just in terms of obesity comorbidities, which We've hasn't gained a lot of press lately, but also thinking about dermatologists role in terms of what that might be, in terms of managing these various comorbidities alongside of our primary care colleagues or other specialties. So there was a debate on whether dermatologists should take on some of the roles, or should we leave that to our primary care or other specialty colleagues?

We're also looking at psoriatic arthritis and understanding how early treatment of not just psoriasis but also psoriatic arthritis can potentially alter the trajectory of both of those conditions, and therefore, the selection of therapy initially is very important in our patient population. And then finally, let's not forget about our pediatric and adolescent patient population. Thankfully, most of our data now that we're seeing in that patient population is that our existing therapies that is approved for adults tend to also work very well in the pediatric patient population, and sometimes even better than what we see in adult population, which speaks to number one, potentially treating psoriasis earlier in that patient population can change the severity of their disease, the natural history of their disease. Also, we know that patients, when they are treated earlier in their disease course, tend to respond better than if they've had the condition for many years and haven't gotten it treated.

The quotes in this Q&A summary were edited for clarity.

Armstrong served as a consultant for and received honoraria from AbbVie, Almirall, Arcutis, ASLAN, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Dermira, EPI, Incyte, Janssen, LEO Pharma, Eli Lilly, Nimbus, Novartis, Ortho Dermatologics, Pfizer, Regeneron, Sanofi, Sun, and UCB and has participated in advisory boards for Boehringer Ingelheim and Parexel.

Armstrong A, et al. S065 What's New in Dermatology. Session presented at: 2026 American Academy of Dermatology Annual Meeting; March 27–31, 2026; Denver, CO.

Armstrong A, et al. S043 Psoriasis. Session presented at: 2026 American Academy of Dermatology Annual Meeting; March 27–31, 2026; Denver, CO.

Armstrong A, Strober B, Hawkes J, et al. INC01 IL-23 Innovation: New Data Addressing Plaque Psoriasis. Session presented at: 2026 American Academy of Dermatology Annual Meeting; March 27–31, 2026; Denver, CO.

Innovation in chronic inflammatory dermatoses is accelerating, with IL‑23 blockade positioned as a master-regulator approach in psoriasis offering durable clearance, extended dosing, and reassuring 6–7‑year safety without infection or malignancy signals. Unmet needs persist in palmoplantar phenotypes, complex comorbidity management, and obesity as a modifiable driver of psoriasis/PsA activity. Therapeutic selection is increasingly mechanism- and patient-profile–driven, incorporating PsA, IBD, and payer considerations. Oral options are expanding, including an IL‑23 receptor peptide (icotrokinra) with biologic-level efficacy and next‑generation TYK2 agents, and evolving atopic dermatitis MOAs beyond JAKs.

Armstrong spoke in an interview regarding several different sessions presented at the 2026 AAD meeting.

Q&A: IL-23, Oral Therapies, and Inflammatory Disease Management, With April W. Armstrong, MD, MPH

OX40 for Atopic Dermatitis: A Target at a Crossroads

 is a heterogeneous inflammatory skin disease driven by immune dysregulation across multiple T cell axes — Th2, Th17, Th22, and others — making it notoriously difficult to treat consistently across patient populations. Current approved biologics and small molecules largely intervene downstream, targeting individual cytokines or intracellular signaling cascades. Effective as these agents are, disease recurrence upon treatment discontinuation remains a significant limitation for many patients.

The OX40 pathway represented a potential workaround. By intervening upstream — at the interface between antigen-presenting cells and T cells — OX40-targeted therapies theoretically offered not just symptom control but the prospect of durable remission, including suppression of effector memory T cells long thought responsible for disease persistence after treatment withdrawal. Two agents advanced into late-phase development targeting this pathway: rocatinlimab, an anti-OX40 receptor monoclonal antibody developed by Kyowa Kirin with Amgen, and amlitelimab, an anti-OX40 ligand monoclonal antibody developed by Sanofi.

Rocatinlimab demonstrated clinically meaningful efficacy in the pivotal ROCKET-IGNITE and ROCKET-HORIZON Phase 3 trials, results of which were published in 

 in November 2025.¹ IGNITE enrolled 769 adults with moderate-to-severe atopic dermatitis, including patients previously treated with a biologic or systemic JAK inhibitor. At week 24, EASI-75 was achieved by 42% of patients receiving the 300 mg dose and 36% receiving 150 mg, compared with 13% on placebo (

 < .001 for both). vIGA-AD 0/1 was achieved by 24% and 19% of the respective dose groups versus 9% on placebo (

 = .002, respectively). In the HORIZON monotherapy trial, 33% of patients on rocatinlimab 300 mg achieved EASI-75 versus 14% on placebo (difference 19.1%; 95% CI, 12.4–25.2), with vIGA-AD 0/1 reached by 19% versus 7%.¹ 

However, rocatinlimab was associated with adverse events including pyrexia, chills, and aphthous ulcers, and its efficacy was not demonstrated to be superior to dupilumab in head-to-head data. In March 2026, Kyowa Kirin and Amgen announced the discontinuation of all rocatinlimab clinical trials following a planned safety review that identified 1 newly confirmed and 1 suspected case of Kaposi sarcoma across the global program, in addition to a previously confirmed case — findings the companies concluded suggested a potential mechanistic link to OX40 pathway modulation.²

The key mechanistic distinction separating rocatinlimab from amlitelimab is not simply target specificity but the downstream consequence of that distinction. Rocatinlimab binds the OX40 receptor on activated T cells and, critically, depletes those cells via antibody-dependent cellular cytotoxicity. Amlitelimab targets the OX40 ligand on dendritic cells and is explicitly non-depleting, blocking signaling through steric hindrance rather than cellular elimination. Sanofi has continued to advance its program despite disclosing 1 case of Kaposi's sarcoma in the ATLANTIS long-term safety study — occurring in a patient with known risk factors — and presented 3-trial Phase 3 data from COAST 1, COAST 2, and SHORE as late-breaking research at the 

2026 American Academy of Dermatology Annual Meeting

Across all 3 trials, amlitelimab was evaluated at dosing intervals of every 4 weeks (Q4W) and every 12 weeks (Q12W). In COAST 1 (n = 601), vIGA-AD 0/1 was achieved by 21.1% of patients in the Q4W arm and 22.5% in the Q12W arm, versus 9.2% on placebo (

 ≤ .01 for both). EASI-75 rates were 35.9% (Q4W) and 39.1% (Q12W) versus 19.1% on placebo (

 < .001 for both). In COAST 2, vIGA-AD 0/1 rates were 25.3% and 25.7% for Q4W and Q12W, respectively, compared with 14.8% on placebo (

 ≤ .025 for both); EASI-75 and peak pruritus numerical rating scale response reached nominal significance, though the more stringent vIGA-AD 0/1 with barely perceptible erythema endpoint did not. The combination therapy SHORE trial produced the highest response rates across the program, with vIGA-AD 0/1 achieved by 28.7% (Q4W) and 32.3% (Q12W) versus 16.8% on placebo, and EASI-75 rates approaching 47–48% in treated arms versus 32.3% for placebo.⁵ A key feature across all 3 datasets was progressive efficacy with no evidence of plateau at week 24, suggesting continued improvement beyond the primary endpoint window. In the ATLANTIS long-term safety analysis, vIGA-AD 0/1 rates increased from 35.4% at week 24 to 50.3% at week 52, with EASI-75 rising from 62.9% to 76.5% over the same period.³ COAST 2 did not meet its European co-primary estimand endpoints, a distinction with potential regulatory implications outside the United States.

Whether amlitelimab's mechanistic and safety profile is sufficiently differentiated from rocatinlimab's to overcome the shadow cast by the class-level Kaposi's sarcoma signal is an active point of debate among clinicians. 

 spoke with 3 leading dermatologists to explore both sides of this question, what the Phase 3 data show, and what comes next for OX40 targeting in atopic dermatitis.

 — Co-Chief Medical Officer and Director of Clinical Research, Frontier Dermatology

— Professor and Chief of Dermatology, University of California, Los Angeles

 — Director of Clinical Research, Southern California Dermatology and faculty at Harbor-UCLA Medical Center

Armstrong’s disclosures include AbbVie, Almirall, Arcutis, ASLAN, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Dermira, EPI, Incyte, Janssen, LEO Pharma, Eli Lilly, Nimbus, Novartis, Ortho Dermatologics, Parexel, Pfizer, Regeneron, Sanofi, Sun, and UCB. Soung’s disclosures include AbbVie, Amgen, Arcutis, Aslan, Bristol Myers Squibb, Coval Biopharma, Dermavant, Eli Lilly, Johnson & Johnson, KoBio Labs, National Psoriasis Foundation, Novartis, Ortho Dermatologic, Oruka, Pfizer, Regeneron/Sanofi, and UCB. Song’s disclosures include AbbVie, Alphyn Biologics, Amgen, Apogee, Arcutis, Bristol Myers Squibb, Boehringer Ingelheim, Dermavant, DermBiont, Galderma, Incyte, Janssen, LEO Pharma, MoonLake, Novartis, Ortho, Pfizer, Regeneron, Sanofi, Sun Pharmaceutical Industries, Timber Pharmaceuticals, and UCB.

Guttman-Yassky E, et al. Efficacy and safety of rocatinlimab for the treatment of moderate-to-severe atopic dermatitis in ROCKET-IGNITE and ROCKET-HORIZON: two global, double-blind, placebo-controlled, randomised phase 3 clinical trials. 

 2025;406(10510):1424-1442. doi:10.1016/S0140-6736(25)01865-3

Kyowa Kirin Co., Ltd. Kyowa Kirin announces discontinuation of rocatinlimab clinical trials. GlobeNewswire. Published March 3, 2026. 

https://www.globenewswire.com/news-release/2026/03/03/3248303/0/en/Kyowa-Kirin-Announces-Discontinuation-of-Rocatinlimab-Clinical-Trials.html

Sanofi. Sanofi's amlitelimab met all primary and key secondary endpoints in the COAST 1 phase 3 study in adults and adolescents with atopic dermatitis. Press release. Published September 4, 2025. 

https://www.sanofi.com/en/media-room/press-releases/2025/2025-09-04-05-00-00-3144170

Sanofi. Sanofi's amlitelimab confirms its potential in atopic dermatitis. Press release. Published January 23, 2026. 

https://www.sanofi.com/en/media-room/press-releases/2026/2026-01-23-06-00-00-3224400

Sanofi. AAD: new results from Sanofi's amlitelimab phase 3 studies in atopic dermatitis presented in late-breaking research session. Press release. Published March 28, 2026. 

https://www.sanofi.com/en/media-room/press-releases/2026/2026-03-28-15-00-00-3264184

Videos

Recent Oral Therapy Developments in Psoriasis, With April W. Armstrong, MD, MPH

 therapies has expanded in recent years, and new data has emerged in recent dermatology meetings expanding upon these drugs’ use among those with inflammatory diseases.

American Academy of Dermatology (AAD) Annual Meeting

 in Denvrer, April W. Armstrong, MD, MPH, of UCLA, spoke about several key highlights from her session on psoriasis, emphasizing the rapidly expanding role of oral medications for individuals with moderate-to-severe plaque psoriasis.

“In this particular session, I refer to both the FDA-approved advanced oral therapies that we've been using for a while, things such as deucravacitinib, as well as apremilast annd our newly FDA-approved oral therapy, icotrokinra,” Armstrong explained.

Armstrong touched on an array of emerging agents known to be reshaping clinical decision-making in the field, including established oral options such as deucravacitinib and apremilast. She also noted icotrokinra’s recent findings regarding its efficacy, pointing to its comparable efficacy to biologics. She noted that these advancements signal a shift toward oral agents as a “next frontier,” providing patients effective, convenient alternative options with favorable safety profiles.

One key aim of her AAD session was to explore the increasing role of TYK2 inhibition. During her discussion of the session, she highlighted the recent milestone of deucravacitinib’s US Food and Drug Administration (FDA) approval for psoriatic arthritis, in addition to its established role in psoriasis. The data, she noted, underscore its growing utility across disease manifestations.

Armstrong further pointed to next-generation TYK2 inhibitors currently in development, which may offer increased specificity and potency, with early results indicating improved clinical performance. Beyond therapeutics, she noted broader themes discussed during the talk, including the value of early intervention, particularly in psoriatic arthritis, to potentially alter long-term disease trajectories for patients.

Additionally, she discussed the ongoing debate the dermatologist’s role in managing comorbidities such as obesity in collaboration with other specialties. Later, she highlighted encouraging data in pediatric and adolescent populations, noting that many medications with FDA approvals for adults appear to be equally, if not more, effective in younger individuals. Taken together, Armstrong framed the current moment in psoriasis care as one of significant progress, marked by expanding options.

The quotes in this video summary were edited for clarity.

Johnson and Johnson. FDA approves ICOTYDE (icotrokinra), the first and only targeted oral peptide IL-23 receptor antagonist, for the treatment of moderate-to-severe plaque psoriasis. Press release. Published March 18, 2026. Accessed April 21, 2026. 

https://www.jnj.com/media-center/press-releases

Armstrong’s interview highlights oral therapies in the psoriasis treatment space highlighted in her session at the 2026 AAD meeting.