The tovecimig plus paclitaxel arm showed a 17.1% ORR versus 5.3% with paclitaxel alone (p=0.031). How clinically meaningful is this 11.8% improvement in a disease where second-line options are practically non-existent?

The rate of progressive disease was nearly three times lower in the combination arm (16.2%) than in paclitaxel alone (42.1%). In your view, how does this signal influence the interpretation of disease control in this population?

The study has yet to trigger analysis of PFS, OS, and DoR due to a lower-than-expected number of events. Could this delay signal a potentially positive trend for durability, or does it complicate interpretation of early efficacy?

What do you make of the study’s 2:1 randomization and its protocol allowing crossover after confirmed progression? How might this impact eventual OS readouts and real-world applicability?

Tovecimig has shown partial responses even as a monotherapy in VEGF-resistant patients. Why might the combination with paclitaxel still be needed for optimal effect in BTC, and what does this suggest about resistance mechanisms?

Statistical significance was achieved for ORR, but only one complete response was seen. How should clinicians balance statistical outcomes with real-world expectations in aggressive cancers like BTC?

Given that ~85% of BTC patients lack an actionable mutation and no FDA-approved second-line therapy exists, how might these findings shift clinical practice or regulatory thinking?

Tovecimig targets both DLL4 and VEGF-A. From a mechanistic perspective, how might this dual inhibition differ from conventional anti-angiogenic strategies in terms of tumor microenvironment modulation or resistance?