Meet the Expert Interview with Dr Andrew Blauvelt

Dr Andrew Blauvelt

Department of Dermatology, University of Maryland School of Medicine, MD, USA

Meet the expert:

Dr Blauvelt on the most exciting news from this year’s AAD.

At this year’s American Academy of Dermatology Annual Meeting 2026, Dr Blauvelt highlighted a clear shift towards highly effective oral therapies in psoriasis, particularly next-generation tyrosine kinase 2 (TYK2) inhibitors demonstrating biologic-like efficacy. In atopic dermatitis (AD), he emphasised the growing and increasingly diverse pipeline, including agents such as amlitelimab with potential disease-modifying effects and long-acting interleukin-13 (IL-13) inhibitors. He also pointed to the expansion of treatment options in high-unmet-need areas, such as hidradenitis suppurativa (HS) and vitiligo, where oral Janus kinase (JAK) inhibitors are expected to play an important role.

Dr Blauvelt, what was the most exciting psoriasis news for you at this year’s AAD?

“We have seen a slowing of novel therapies for psoriasis in recent years after the tremendous uptick in biologic therapies that we had continuously over the last 20 years, and we’ve seen a slowing in the biologic area.

In recent years, the latest advances have been coming in the oral space. That started with deucravacitinib a couple of years ago, the first TYK2 inhibitor. At this meeting’s late-breaker session, we saw 2 first-look phase 3 data presentations on novel second-generation TYK2 inhibitors. I presented on envudeucitinib, and Dr Melinda Gooderham (SKiN Centre for Dermatology at Queen’s University, ON, Canada) on zasocitinib.”

Could you elaborate further on the envudeucitinib results?

“Envudeucitinib is a novel, next-generation TYK2 inhibitor. Both envudeucitinib and zasocitinib were specifically designed to be superior to deucravacitinib. We have very good examples with every mechanism of action, that not all drugs work the same. Just because they have the same target doesn’t mean we’ll have the same efficacy or safety. We’ve seen that, over and over again, with tumour necrosis factor (TNF) blockers, interleukin-17 (IL-17) blockers, and interleukin-23 (IL-23) blockers: a wide variety of efficacies and some differences in safety. There are good ones and bad ones, and these were designed to be superior, to hit their target better, and to hit their target longer. In my view, we saw dramatically different efficacy results with both drugs compared with deucravacitinib, the first TYK2 inhibitor.

Specifically, I reported that about 75% of patients met the primary endpoint of the Psoriasis Area and Severity Index (PASI) 75. Compared with deucravacitinib at the same time point, PASI 75 was about 55%. So, 55% versus 75%, very different. Then, another feature of both drugs is that efficacy continues to improve beyond the week 16 endpoint. We saw increasing efficacy through week 24, with PASI 100 reaching 40%, which is impressive. It’s been pretty consistent with other IL-23 blockers and with deucravacitinib: they tend to peak in efficacy around week 24, not at the primary endpoint or at week 16, and we saw the same with envudeucitinib. In fact, I can’t even say it’s a peak because we only have data for week 24. Of course, numbers may continue to go up.

To differentiate similar drugs, I personally like to compare by PASI 100, which is the highest bar of achievement, a complete skin clearance. That’s when you start to see differences in drug A versus drug B, so to speak.”

What about the safety of envudeucitinib?

“Very interesting also, kind of a little bit surprising in terms of its safety profile, which turned out, at least in the short run, in the first 24 weeks, to be very safe. In fact, we didn’t see signals with this drug that we saw with deucravacitinib. There are some theories about that.

Deucravacitinib has a metabolite that may contribute to off-TYK2 activity on other JAKs, and although the drug itself doesn’t act on JAK1, 2, or 3, the metabolite may be active. That may be why we see a little bit of lipid elevation and a little bit of herpes simplex reactivation signal with deucravacitinib, small numbers that we didn’t really see with envudeucitinib. We might start seeing a few safety issues with more time and with more patients, or maybe, since it doesn’t have the same metabolite, this drug may not only be more efficacious, but it actually may be safer than deucravacitinib.”

Moving on to AD, were there any interesting data for you at the congress?

“Actually, there were more late-breaker talks on AD than there were on psoriasis. The AD pipeline has really exploded in recent years.

A paper presented by Prof. Eric Simpson (Oregon Health & Science University, OR, USA) was also a prominent phase 3 reveal of amlitelimab. The OX40 ligand antibody is being studied in moderate-to-severe AD, and we knew from the phase 2 data that it tends to have slightly lower short-term efficacy than our IL-13 blockers but improves over time. We also learned in phase 2 that a significant number of patients can remain in remission off the drug. So, we say that this drug has a remitting effect, which makes it very interesting. So, even though the short-term efficacy is lower than that of our standard drugs, there will likely be a place for amlitelimab in patients seeking greater long-term efficacy and the possibility of remission. The phase 3 result was consistent with the phase 2 data, as the Investigator’s Global Assessment of 0 or 1 (IGA 0/1) rate at week 24 was in the 30% range, which is lower than that seen with dupilumab and lebrikizumab. But Prof. Simpson showed that, over time, that number rose into the 50% range for IGA 0/1, which is high.

Safety-wise, he addressed that there have been 2 reports of Kaposi’s sarcoma (KS) in patients treated with amlitelimab. KS is the dreaded cancer of AIDS patients, but it is not HIV-associated; it’s associated with human herpesvirus 8. That virus tends to be pocketed in certain populations: in AIDS patients, in men who have sex with men, in the eastern Mediterranean region of southern Italy, Greece, and in the Sub-Saharan region. So, it’s a virus that’s not widespread in the population, and to get KS, you need the virus and a hit to the immune system. Both cases were in the higher-risk population of men who have sex with men, and perhaps amlitelimab made the expression of human herpesvirus 8 appear in terms of KS. Many people are talking about those 2 cases and whether they will have a big impact on the drug, be too much of a barrier, or if there will be pre-treatment mitigation strategies. But I want to emphasise that if you don’t have herpesvirus 8, you won’t develop KS. It is a possible side effect that may occur in a subset of patients.

Were there other notable AD developments?

“Yes, there were several studies by Chinese investigators on interleukin-4 (IL-4) receptor alpha antibody drugs developed by Chinese companies. They showed very dramatic results with their dupilumab-like drugs in Chinese populations. So good that many in the audience found them a little hard to believe. Looking into these trials more intensely will be interesting.”

Any final highlights?

“The last late-breaker on AD that should be highlighted was given by Dr Emma Guttman (Mount Sinai Hospital, NY, USA). She presented additional long-term phase 2 data for a drug called zumilokibart, a long-acting, lebrikizumab-like anti–interleukin-13 (IL-13) antibody with a half-life of 77 days. It was exciting for me to see the possibility of a new AD drug that could be given twice a year instead of twice a month.

HS is also a hot area, and vitiligo. A lot is being done in both diseases. What we’ll see soon are approvals for oral JAK inhibitors. So, upadacitinib has been studied in HS, as well as in vitiligo and alopecia areata. We’re likely to see upadacitinib approved for these other diseases. Then there’s povorcitinib. It’s also an oral JAK inhibitor, and we’re also likely to see povorcitinib approved for HS and for vitiligo.

In recent years, we have seen the drug icotrokinra approved for the treatment of psoriasis. This novel interleukin-23 (IL-23)–like peptide binds the IL-23 receptor and blocks normal IL-23 binding. It’s a completely new mechanism of action and, in my view, the best new oral drug for psoriasis. The phase 3 data were presented at last year’s AAD, and a year later, the drug was approved. This year, we heard about additional long-term data on icotrokinra presented as posters, showing continued strong efficacy over time.

In chronic spontaneous urticaria, our good old friend dupilumab and the oral Bruton tyrosine kinase (BTK) inhibitor remibrutinib have been newly approved, with more supportive data on these 2 drugs presented at this year’s AAD. Dupilumab also gained approval for bullous pemphigoid, representing a significant shift from traditional corticosteroid-based management towards a targeted therapy option.”

Medical writing support was provided by Dr Susanne Kammerer and Karin Drooff, MPH.