Cohort 3 patients receiving 200 mg BID soquelitinib showed a 71.1% mean reduction in EASI at day 28, compared to 54.6% in cohorts 1–2. How compelling is this dose-response relationship in shaping dose selection for future trials?

The data indicated that cohort 3 began separating from placebo by day 8, considerably earlier than cohorts 1 and 2. How clinically significant is this early response in the context of current atopic dermatitis therapies, and could it affect patient adherence or satisfaction?

Placebo patients in all three cohorts failed to reach IGA 0/1 or EASI 75 at day 28. Given the notoriously high placebo response in dermatology trials, what do you make of this finding, and does it speak to the strength of the active arm or something else?

The company highlights durable effects after just 28 days of treatment. What biological or clinical markers would you prioritize to validate these claims of durability in a longer follow-up or future Phase 2 study?

The trial reported reductions in cytokines like IL-5, IL-9, IL-17, and IL-31, along with an increase in circulating T regulatory cells. How do these biomarker trends support ITK inhibition as a disease-modifying approach in atopic dermatitis?

Cohort 3 included patients with more severe disease and prior systemic therapy failure, yet still achieved better results. How might this influence how soquelitinib is positioned relative to JAK inhibitors or biologics like dupilumab?

Soquelitinib demonstrated a clean safety profile with no DLTs and minimal AEs, even at the 200 mg BID dose. What aspects of this safety data would you watch closely in longer treatment durations or larger patient populations?

The amended protocol extends treatment to 8 weeks in the next cohort using the same 200 mg BID dose. What key efficacy or mechanistic endpoints would you want to see in that cohort to confirm the promise shown in cohort 3 and support Phase 2 advancement?