The SUMMIT trial demonstrated a placebo-adjusted symptom score reduction of 8.91 points at Week 24, with bezuclastinib achieving a -24.3 point change. How do you interpret this level of improvement in the context of NonAdvSM disease burden and previous treatment options?

Nearly 90% of patients on bezuclastinib achieved at least a 50% reduction in serum tryptase. What does this indicate about mast cell stabilization, and how predictive is it for long-term disease control?

With a statistically significant reduction in KIT D816V variant allele frequency, how might bezuclastinib be modifying disease at the molecular level, and does this suggest potential for broader impact across systemic mastocytosis subtypes?

How do you weigh improvements in subjective symptom scores like MS2D2 against objective lab markers such as serum tryptase or KIT VAF when evaluating treatment success in clinical practice?

Bezuclastinib showed a favorable safety profile, with most AEs being low grade. Given that this treatment may be used chronically, how critical is tolerability in encouraging patient adherence and regulatory approval?

Some unique adverse events like hair color change (69.5%) and mild liver enzyme elevations were noted. Do these types of side effects raise any red flags for you, or are they manageable in a long-term treatment setting?

Given the consistent achievement across all primary and secondary endpoints, what elements of the SUMMIT trial data make bezuclastinib a strong candidate for becoming the new standard of care for NonAdvSM?

Cogent plans to file an NDA by the end of 2025 and report data from PEAK and APEX trials in the second half of the year. What will you be watching for in those trials to confirm bezuclastinib’s role in both non-advanced and advanced SM?