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Armstrong highlights several major takeaways from her portion of the AAD 2026 session titled 'IL-23 Innovation: New Data Addressing Plaque Psoriasis.'
At the 2026 American Academy of Dermatology (AAD) Annual Meeting in Denver, April W. Armstrong, MD, MPH, of UCLA’s David Geffen School of Medicine, gave the HCPLive team a comprehensive look at the evolving role of interleukin (IL)-23 inhibition in the management of plaque psoriasis.
The interview followed her session, ‘IL-23 Innovation: New Data Addressing Plaque Psoriasis.’1 Given the emergence of the IL-23 pathway as a central therapeutic target in recent years, Armstrong touched on the mechanistic rationale behind the pathway’s growing prominence and its role as a key regulator in inflammatory pathways driving not only psoriasis but also related comorbidities such as inflammatory bowel disease.
The following Q&A summary highlights Armstrong’s responses to questions about her session:
HCPLive: 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?
Armstrong: 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.
HCPLive: 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?
Armstrong: 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, 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?
HCPLive: 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?
Armstrong: 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.
The quotes used in this summary were edited for clarity.
Armstrong has 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.
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