EADV 2026 Atopic Dermatitis Highlights: Tilrekimig, RAC2 Inhibition, and Level Up Data

At Fall Clinical 2026, Christopher Bunick, MD, PhD, associate professor of dermatology at the Yale School of Medicine and editor in chief of Dermatology Times, presented updates on JAK inhibitor safety and how to choose oral antibiotics and retinoids for acne management. Outside of his Fall Clinical sessions, Bunick reviewed atopic dermatitis late-breaking data from EADV 2026, as well as biomarker analysis from the Level Up trial, which he presented in Vienna.

Late-Breakers in the Atopic Dermatitis

Bunick attended EADV at the end of September and described the gathering as a meeting of dermatologists from across the world. He said several late-breakers were of interest, with a number of important presentations in the atopic dermatitis session. Tilrekimig, a tri-specific biologic targeting TSLP, IL-4, and IL-13, showed skin efficacy as well as itch efficacy, he said.

Bunick also highlighted a new molecule, ENV-294, an inhibitor of RAC2. He described RAC2 as a protein not yet discussed in atopic dermatitis. The late-breaker study data included only 9 patients, but has potential for future growth.

“The late-breaker only involved nine patients, but what a dramatic response in EASI score was seen in those 9 patients,” Bunick said.

“It’s going to be really interesting to watch how the RAC2 program develops over time,” he said.

Future trials will need to bear out the response. “We’ll see if future trials can bear out, but RAC2 is a molecule to watch,” Bunick said.

Level Up Biomarker and Histology Analysis

Level Up was a randomized controlled trial comparing upadacitinib and dupilumab head-to-head. At EADV, Bunick presented Level Up biomarker data and histology from patient biopsies, examining inflammatory biomarkers and skin barrier gene upregulation in each arm.

Inflammatory pathway improvement was more extensive with upadacitinib than with dupilumab. Barrier genes such as filaggrin and loricrin also improved earlier and more significantly with the JAK inhibitor.

“What was really fascinating was to actually see in action from this trial, the improvement in the inflammatory pathways of the JAK inhibitor, which was much more extensive than dupilumab,” Bunick said.

Mono-Targeted Biologic Versus JAK1 Inhibition

Bunick said the Level-Up findings speak to the difference between a mono-targeted biologic and a JAK inhibitor. Dupilumab targets IL-4 receptor alpha and controls IL-4 and IL-13 signaling, which he said limits what it can accomplish. Upadacitinib selectively targets JAK1 and affects multiple pathways, including IL-4, IL-13, IL-31, TSLP, IL-22, and interferon gamma.

Bunick said the comprehensive targeting of those cytokines was reflected in the biomarker and histology analyses of the skin barrier. He described presenting the findings at EADV as a privilege.

For more coverage from Fall Clinical, click here