The VERITAC-2 trial met its primary endpoint, showing a statistically significant improvement in PFS for patients with ESR1 mutations. How meaningful is this finding in the context of current treatment options for ER+/HER2- metastatic breast cancer?

Vepdegestrant is the first PROTAC degrader to demonstrate clinical benefit in a Phase 3 trial. What makes PROTAC technology different from traditional endocrine therapies, and how could this approach reshape the future of breast cancer treatment?

Endocrine resistance is a major challenge in treating ER+ metastatic breast cancer, with ESR1 mutations playing a key role. How does vepdegestrant address this resistance compared to existing selective estrogen receptor degraders (SERDs) like fulvestrant?

The trial compared vepdegestrant to fulvestrant, a widely used SERD. How do the efficacy and safety data from VERITAC-2 compare, and could vepdegestrant become the preferred option for patients in this setting?

At the time of analysis, overall survival data were immature. Given the importance of OS in regulatory and clinical decision-making, what would you like to see in future analyses to confirm vepdegestrant’s long-term benefit?

With these results, Arvinas and Pfizer plan to share data with global regulatory agencies. What are the key considerations for regulatory approval, and could vepdegestrant receive an accelerated review based on its Fast Track designation?

Vepdegestrant is also being explored in combination with CDK4/6 inhibitors and other targeted agents. How might it fit into a broader treatment strategy for ER+/HER2- breast cancer, particularly in earlier-line settings?

This is the first Phase 3 success for a PROTAC degrader in oncology. Do you see this as a validation of the PROTAC platform, and could this technology be applied to other tumor types with challenging targets?