Cemdisiran monotherapy achieved a placebo-adjusted MG-ADL score improvement of -2.3 points at week 24, outperforming both placebo and the cemdi-poze combination numerically. How clinically meaningful is this improvement, and how does it compare to currently approved C5 inhibitors?

Both cemdisiran and cemdi-poze demonstrated significant reductions in QMG scores, but cemdisiran achieved these outcomes with only ~74% complement inhibition compared to nearly 99% for the combination. How might this partial inhibition approach influence safety and long-term tolerability for gMG patients?

The NIMBLE trial reported that 76.6% of patients on cemdisiran achieved a ≥3-point MG-ADL improvement compared with 44.1% on placebo. How do you interpret this responder rate in the context of current treatment options for gMG?

No meningococcal infections and no discontinuations due to adverse events were reported in the cemdisiran arm over the 24-week period. How significant are these safety findings when considering broader adoption of complement-targeted therapies?

Cemdisiran demonstrated quarterly subcutaneous dosing compared to more frequent administrations required for most existing complement inhibitors. How might this dosing convenience impact patient adherence and overall disease management strategies?

Regeneron is developing both cemdisiran monotherapy and the cemdi-poze combination across multiple complement-mediated diseases, including PNH and geographic atrophy. How do you see these results in gMG informing treatment strategies across related indications?

With a U.S. regulatory submission planned for early 2026, what factors do you expect the FDA to weigh most heavily given the efficacy, safety, and convenience advantages demonstrated by cemdisiran?

Given the expanding treatment landscape in gMG, including FcRn inhibitors, C5 antibodies, and siRNA therapeutics, where do you see cemdisiran monotherapy and cemdi-poze potentially fitting in terms of patient selection and sequencing of therapies?