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.

Articles

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.

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

Eingun James Song, MD, is the director of clinical research for Frontier Dermatology. 

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

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David Kass, MD, is the Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine.

Severe Obesity Linked to Distinct Myocardial Dysfunction in HFpEF

 with preserved ejection fraction (HFpEF) includes two biologically distinct subgroups defined by body mass index (BMI).

Given the known disproportionate impact of obesity on HFpEF, a National Institutes of Health-funded study identified reduced cardiomyocyte contraction despite preserved ejection fraction in patients with 

Understanding HFpEF: Clinical Burden and Remaining Gaps

Approximately 75 million people worldwide live with heart failure, including about 7 million in the United States. HFpEF accounts for more than 50% of these cases.

“Some hearts in heart failure are very big and dilated, like a giant measuring cup. I could pour out just a little of what’s inside, but that could still fill a glass,” study investigator David Kass, MD, the Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine, said. “The percent coming out is not very much because it’s a very large volume to start with—that’s what we call ejection fraction.”

Obesity has been identified as a major driver of HFpEF, with excess adipose tissue contributing to systemic inflammation, metabolic dysfunction, and mechanical cardiac strain, ultimately leading to increased ventricular stiffness, elevated filling pressures, and reduced functional capacity.

Many therapies effective in heart failure with reduced ejection fraction (HFrEF) have not shown consistent benefit in HFpEF, with multiple large clinical trials yielding neutral or modest results, Kass explained. One of the first therapies to demonstrate clear outcome benefits in HFpEF was sodium-glucose cotransporter-2 (SGLT2) inhibitors, originally developed for diabetes before showing cardiovascular benefit.

How Did Kass and Colleagues Conduct Their Research?

Researchers at Johns Hopkins conducted a biopsy-based investigation of myocardial tissue from patients with HFpEF, using millimeter-scale samples obtained through an established clinical research program.

From these samples, investigators isolated individual cardiomyocytes and conducted approximately 30 functional measurements assessing key aspects of myocardial performance, including calcium responsiveness, cellular stiffness, and structural properties.

To analyze patterns across the dataset, researchers applied a machine learning–based clustering approach to identify potential subgroups within HFpEF based on cellular characteristics.

The algorithm identified two clearly distinct groups within the HFpEF population divided by BMI

One group demonstrated severe obesity, while the comparison group had an average BMI of approximately 30 kg/m².

Notably, traditional clinical measures commonly used to characterize heart failure—including blood pressure, cardiac output, and filling pressures—did not differ between the groups.

Impaired Cardiomyocyte Function in Severe Obesity–Associated HFpEF

In patients with HFpEF and severe obesity, cardiomyocyte contraction was significantly reduced compared with less obese patients, despite similar clinical hemodynamic profiles.

These cells demonstrated reduced calcium responsiveness and diminished force generation, both of which are essential for increasing cardiac output during physical activity.

“In the very obese group, contraction… was not preserved… it was actually quite reduced,” Kass said.

These cellular abnormalities were also reflected in clinical performance. Patients whose cardiomyocytes showed worse function had reduced exercise capacity and higher intracardiac pressures during physiological stress testing.

The findings challenge the traditional view of HFpEF as a single disease defined primarily by impaired relaxation and preserved systolic function.

Instead, HFpEF appears to include biologically distinct subgroups that are not captured by standard clinical metrics such as ejection fraction.

“Even though all these patients look like HFpEF clinically, at the cellular level they are quite different,” the investigator said.

The results raise questions about whether current HFpEF treatment strategies adequately reflect underlying biological differences between patient subgroups.

Many existing and investigational therapies assume preserved or even enhanced myocardial contraction in HFpEF. However, these assumptions may not apply uniformly, particularly in patients with severe obesity–associated disease.

The findings suggest a potential mismatch between therapeutic mechanisms and disease biology in certain HFpEF phenotypes, highlighting the need for more stratified approaches to treatment.

Editor’s Note: Kass reports no relevant disclosures. 

Scientists find people with severe obesity and heart failure have weakened heart muscle contractions. Weight loss may reverse this condition. EurekAlert! Published April 23, 2026. Accessed April 24, 2026. 

https://www.eurekalert.org/news-releases/1124709?

Borlaug BA, Jensen MC, Kitzman DW, Carolyn S.P. Lam, Masaru Obokata, Rider OJ. Obesity and heart failure with preserved ejection fraction: new insights and pathophysiological targets. 

Kass explains 2 distinct biological subgroups discovered in HFpEF and how they relate to a paradigm shift. 

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The HCPLive heart failure page is a resource for medical news and expert insights on HF. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for heart disease, reduced and preserved ejection fraction, and more.

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Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Elizabeth Bauer, MD, is the chair of the Obesity and Nutrition Disease State Network at the American Association of Clinical Endocrinology (AACE) and associate professor of medicine at Uniformed Services University.

Diabetes Dialogue: Technology, Therapeutics, & Real-World Perspectives!

Diabetes Dialogue: Nutrition, Medication, and Treatment in Obesity With Elizabeth Bauer, MD

In this episode of Diabetes Dialogue, recorded on-site at the American Association of Clinical Endocrinology (AACE) Annual Meeting 2026 in Las Vegas, Nevada, cohosts Diana Isaacs, PharmD, and Natalie Bellini, DNP, welcome Elizabeth Bauer, MD, a clinical endocrinologist and obesity specialist, to discuss key updates in obesity management presented during her “Year in Review” session at the AACE Annual Meeting. Bauer opens by highlighting AACE’s updated obesity algorithm, released in late 2024, which builds on the organization’s prior adiposity-based chronic disease framework and shifts obesity care further away from BMI-centered diagnosis toward a more comprehensive, disease-centric model. She explains the algorithm’s emphasis on anthropometric assessment, adiposity distribution, and obesity staging, noting that clinicians must move beyond weight alone to better identify obesity-related complications and personalize treatment decisions.

The discussion focuses on the algorithm’s practical value, particularly its structured staging system and medication tables that help clinicians match pharmacotherapy to obesity-related comorbidities such as diabetes, MASLD, and obstructive sleep apnea. Bauer emphasizes that treatment goals should be complication-specific—for example, modest weight loss may improve glycemia, while greater total body weight reduction is needed for meaningful improvement in MASH. She and the hosts stress that obesity management should prioritize whole-person health rather than weight alone, drawing parallels to the evolution of diabetes treatment toward complication-driven care.

The group then turns to emerging pharmacotherapies, with Bauer reviewing several phase 2 and 3 obesity trials involving newer incretin-based agents. She highlights mazdutide, a once-weekly GLP-1–based therapy studied in Chinese populations using lower BMI thresholds more reflective of Asian obesity risk, as well as combination therapies such as semaglutide plus cagrilintide, which demonstrated greater efficacy than semaglutide alone but with substantially higher gastrointestinal adverse effects. Bauer notes that while these agents show impressive weight loss potential, tolerability remains a major clinical challenge, particularly with nausea and dose escalation.

A significant portion of the conversation centers on management of GI side effects from GLP-1 receptor agonists. Bauer explains her clinical philosophy of treating obesity like any other chronic disease—avoiding the routine practice of prescribing one medication to manage side effects caused by another whenever possible. While she may prescribe small, limited quantities of ondansetron during titration, she emphasizes that persistent nausea should prompt dose adjustment or medication changes rather than indefinite antiemetic use. The hosts discuss how slower titration strategies in real-world practice often improve tolerability compared with rigid clinical trial protocols and may help optimize long-acting monthly GLP-1 agents currently in development.

The episode also reviews bariatric surgery data, including randomized trials comparing laparoscopic banding, sleeve gastrectomy, and Roux-en-Y gastric bypass. Bauer notes that both sleeve gastrectomy and Roux-en-Y demonstrated superior efficacy and fewer complications compared with lap band procedures, while long-term comparisons between sleeve and bypass showed strong outcomes for both, with Roux-en-Y numerically favoring weight loss but often without statistically significant superiority. She also discusses higher reoperation rates among patients initially undergoing sleeve gastrectomy, often due to inadequate weight loss or significant reflux requiring conversion to bypass.

The conversation concludes with an important discussion on post-bariatric surgery weight regain and the growing use of GLP-1–based therapies after surgery. Bauer challenges the misconception that surgery “cures” obesity, emphasizing that obesity remains a chronic disease driven by persistent biology, inflammation, and environmental factors even after anatomical intervention. She notes emerging evidence suggesting that GLP-1 therapies used before or after bariatric surgery may improve long-term outcomes and reduce weight regain. She closes by reinforcing the need for clinicians to approach obesity with the same chronic disease mindset applied to diabetes—recognizing that durable management requires ongoing treatment, not a one-time intervention.

Editors’ Note: Isaacs reports disclosures with Dexcom, Abbott, Lilly, Novo Nordisk, Medtronic, Insulet, and others. Bellini reports disclosures with Abbott Diabetes Care, MannKind, Povention Bio, and others. Bauer reports no relevant disclosures.

Bauer E. DSN Year in Review: Nutrition & Obesity. Presented at the American Association of Clinical Endocrinology, Las Vegas, NV. April 22-24, 2026.

Podcasts

Elizabeth Bauer, MD, joins the show to discuss her AACE 2026 presentation on key updates in obesity management and nutrition.

Endocrinology

The HCPLive endocrinology page is a comprehensive resource for clinical news and insights on endocrine system conditions. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for diabetes, hormonal disease, and more.

Type 1 Diabetes

Type 2 Diabetes

Strategic Alliance Partnership

Crinecerfont Reduces Glucocorticoid Doses in CAH, With Richard Auchus, MD, PhD

Crinecerfont (Crenessity) has demonstrated substantial and sustained reductions in glucocorticoid doses among adults with 

classic congenital adrenal hyperplasia (CAH)

, according to 2-year data from the CAHtalyst Adult study.

American Association of Clinical Endocrinology (AACE) Annual Meeting 2026

 in Las Vegas, Nevada, by Richard Auchus, MD, PhD, professor of pharmacology and internal medicine at the University of Michigan.

“Glucocorticoids are not a good thing to be taking chronically – yes, you need them to survive, but you don’t really need them overnight,” Auchus told 

 in an exclusive interview. “What crinecerfont did was allow us to reduce the dose and put it in a more physiological regime, front-loading it in the morning, allowing them to have a circadian rhythm, and maintaining disease control at a level that the endocrinologist in the trial felt was appropriate for that patient.”

Crinecerfont, a selective oral corticotropin-releasing factor type 1 receptor (CRF1) antagonist, functions by reducing and controlling excess adrenocorticotropic hormone and adrenal antigens. It was first approved by the US Food and Drug Administration (FDA) in December of 2024 for the treatment of CAH in conjunction with glucocorticoids among adults and children ≥4 years.

CAHtalyst Adult was a randomized, double-blind, placebo-controlled phase 3 study evaluating crinecerfont in adults with classic CAH. It consisted of a 24-week randomized period during which patients were assigned to either crinecerfont or placebo, followed by 1 year of active treatment with crinecerfont. Patients were then given the option to participate in an open-label extension period, which is projected to last for roughly 3 years.

Patients were eligible for the study if they had a medically confirmed CAH diagnosis due to 21-hydroxylase deficiency and were on a stable steroid regimen. Patients with a diagnosis of any other known form of classic CAH, a history of bilateral adrenalectomy, hypopituitarism, or other conditions requiring chronic glucocorticoid therapy, or a clinically significant unstable medical condition or chronic disease aside from CAH, among other criteria, were excluded from the trial.

The present data highlights 2-year data from the open-label extension – by month 24, 69% of the participants (103/149) had achieved a physiologic glucocorticoid dose of ≤11 mg/m2/day of hydrocortisone equivalents. Additionally, many participants had eliminated nonphysiologic glucocorticoid types altogether. Among the patients initially taking dexamethasone (n = 20), 75% shifted to a dexamethasone-free regimen, while 62% (37/60) taking >2 doses of hydrocortisone per day were able to eliminate a dose.

Auchus also highlighted the significant retention throughout the open-label extension: >80% of patients were still taking crinecerfont at 2 years with no new safety signals detected.

“CAH is a chronic disease, and there’s a lot of disease burden for these patients,” Auchus said. “We want them to be able to just take their medicine and get on with their lives and not worry about things. I think that high retention rate tells you that people are on board with this system.”

Editors’ Note: Auchus reports disclosures with Adrenas Therapeutics, Corcept, Crinetics, Neurocrine Biosciences, Recordati, Astellas, and others.

Bancos I, Hamidi O, Kiefer F, et al. Adults With Classic Congenital Adrenal Hyperplasia Taking Crinecerfont Demonstrated Sustained Decreases in Glucocorticoid Doses: 2-Year Results from the CAHtalyst Adult Study. Presented at the American Association of Clinical Endocrinology Annual Meeting 2026, Las Vegas, NV. April 22-24, 2026.

Neurocrine Biosciences, Inc. Neurocrine Biosciences Presents New Two-Year CRENESSITY (crinecerfont) Data Showing Sustained Glucocorticoid Dose Reductions While Maintaining Androgen Control in Adults with Classic Congenital Adrenal Hyperplasia. 

. April 22, 2026. Accessed April 24, 2026. 

https://www.prnewswire.com/news-releases/neurocrine-biosciences-presents-new-two-year-crenessity-crinecerfont-data-showing-sustained-glucocorticoid-dose-reductions-while-maintaining-androgen-control-in-adults-with-classic-congenital-adrenal-hyperplasia-302749451.html

Iapoce C. FDA Approves Crinecerfont for Congenital Adrenal Hyperplasia. 

. December 13, 2024. Accessed April 24, 2026. 

https://www.hcplive.com/view/fda-approves-crinecerfont-for-congenital-adrenal-hyperplasia

Neurocrine Biosciences. Global Safety and Efficacy Registration Study of Crinecerfont for Congenital Adrenal Hyperplasia (CAHtalyst). ClinicalTrials.gov Identifier: NCT04490915. Updated February 5, 2025. Accessed April 24, 2026. 

https://clinicaltrials.gov/study/NCT04490915

Auchus discusses the 2-year results from CAHtalyst Adult, highlighting the substantial retention rates over the open-label extension period.

Jagbir Gill, MD, MPH, is an Associate Professor of Medicine in the Division of Nephrology at the University of British Columbia and Medical Director of the Kidney Transplant Program at St. Paul’s Hospital in Vancouver. He also serves as Medical Director of Data and Quality for BC Transplant, President of the Canadian Organ Replacement Register Board of Directors, and as Treasurer for the Canadian Society of Transplantation.

Gill describes how storytelling and patient representation can build trust and education in Indigenous populations regarding transplantation. 


Nephrology

The HCPLive nephrology page is a resource for medical news and expert insights on kidney disease. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments in nephrology, and more.

Chronic Kidney Disease

Transplant Care Strategies to Target Mistrust, Close Gaps in Indigenous Communities

Scott Isaacs, MD, is an Adjunct Assistant Professor of Medicine at Emory University. He currently serves as Immediate Past President of the American Association of Clinical Endocrinology (AACE).

Isaacs explains how prediabetes care is shifting toward early intervention, risk stratification, and prevention of cardiometabolic disease, not just progression to diabetes.

Breaking the ‘Watch and Wait’ Model in Prediabetes Care, With Scott Isaacs, MD

Oksana Hamidi, DO, is an associate professor in the division of endocrinology and metabolism at the University of Texas Southwestern Medical Center.

Hamidi reviews 2-year CAHtalyst data showing crinecerfont enabled sustained glucocorticoid reductions to physiologic range in adults with classic congenital adrenal hyperplasia.

CAHtalyst Adult: Sustained GC Reduction With Crinecerfont in CAH, With Oksana Hamidi, DO

Chelsie Derman is an associate editor for 

who covers allergy and  psychiatry. She joined MJH Life Sciences in September 2023 after graduating from The College of New Jersey with a bachelor’s degree in journalism and professional writing. In her free time, she enjoys creative writing and reading.

Twin phase 3 trials show triple therapy with budesonide–glycopyrronium–formoterol improves FEV1 and lowers severe exacerbation rates in patients with uncontrolled asthma on ICS–LABA


Pulmonology

Infectious Disease condition center page is a comprehensive resource for clinical news and insights on respiratory health. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for asthma, COPD, interstitial lung disease, COVID-19, and more.

Asthma

The HCPLive asthma page is a comprehensive resource for clinical news and insights on asthmatic disease. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for allergic and severe asthma, and more.

BGF Triple Therapy Improves Lung Function in Phase 3 Uncontrolled Asthma Controls

Christopher G. Bunick, MD, PhD, is an associate professor of dermatology at Yale University School of Medicine.

Christopher Bunick, MD, PhD, and colleagues conducted a review bispecific and trispecific antibodies in atopic dermatitis.

Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD

Linda DiMeglio, MD, MPH, joins the show to discuss the growing movement towards screening and testing for T1D at an early stage.

podcasts page features a feed of medical news and interview podcast series, including DocTalk, Lungcast, Derm Discussions, and Heart Trials.

Diabetes Dialogue

Diabetes Dialogue: Technology, Therapeutics, & Real-World Perspectives is a monthly podcast hosted by Diana Isaacs, PharmD, and Natalie Bellini, DNP, aimed at providing a regular roundup of the latest clinically applicable insights across diabetes and metabolic diseases, with a focus on leveraging technology to improve care.

Diabetes Dialogue: The Push for Early-Stage T1D Screening and Treatment, With Linda DiMeglio, MD, MPH

Abigail Brooks is an assistant managing editor for 

She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

New real world data suggest GLP-1 RAs do not drive DKA or pancreatitis risk in adult patients with type 1 diabetes and may reduce hospital admissions.

GLP-1 RAs Do Not Raise Diabetic Ketoacidosis, Pancreatitis Risk in Type 1 Diabetes

Shah discusses the potential of GLP-1 receptor agonists as adjunctive therapy in type 1 diabetes, from glycemic control to cardiometabolic risk.

Beyond Insulin: Evaluating GLP-1 RAs as Adjunctive Therapy in Type 1 Diabetes, With Viral Shah, MD

Jeffrey Mechanick, MD, is the medical director of the Marie-Josee and Henry R. Kravis Center for Cardiovascular Health at Mount Sinai Fuster Heart Hospital and a professor of medicine at the Icahn School of Medicine at Mount Sinai.

Mechanick discusses the importance of dietary interventions in endocrinology and highlights the need for further education and awareness of metabolic function.

Latest News

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

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Severe Obesity Linked to Distinct Myocardial Dysfunction in HFpEF

Diabetes Dialogue: Nutrition, Medication, and Treatment in Obesity With Elizabeth Bauer, MD

Crinecerfont Reduces Glucocorticoid Doses in CAH, With Richard Auchus, MD, PhD