The study showed meaningful EASI score reductions within just a few doses. How clinically relevant is this early onset in terms of patient satisfaction and potential differentiation from current standard therapies?

Rezpegaldesleukin works through a Treg proliferation mechanism. Can you explain how this differs fundamentally from other biologics or JAK inhibitors in atopic dermatitis, and why this may offer a longer-term solution to immune imbalance?

All three dosing arms (q2w and q4w) achieved the primary endpoint, but vIGA-AD 0/1 and EASI-90 were more pronounced at higher doses. How do you interpret the dose-response relationship, and what dosing schedule would you expect to carry forward into Phase 3?

The high and mid-dose arms showed statistically significant improvements in Itch NRS. Given the central role of itch in AD burden, how compelling are these results from a patient quality-of-life perspective?

Robust reductions in Th2 biomarkers like IL-19 and CCL17 were observed alongside Treg expansion. How important are these biomarker shifts in validating rezpegaldesleukin’s mechanism, and could they serve as predictive indicators in future trials?

No increased rates of conjunctivitis, oral ulcers, or herpes were reported—side effects commonly seen with other AD therapies. Do you think this cleaner safety profile could be a deciding factor for certain patient populations?

The study reported comparable EASI-75 and EASI-90 rates in both moderate and severe baseline vIGA-AD subgroups. Does this suggest rezpegaldesleukin may offer a consistent effect across the AD severity spectrum, and how might that influence its positioning

With Phase 3 planning ahead and Fast Track designation granted, what are the key regulatory and clinical hurdles you anticipate, and how might rezpegaldesleukin fit into a treatment landscape that already includes dupilumab, tralokinumab, and JAK inhibitors?