Vesna Kramar
Senior Scientist, Cancer Immunotherapy & Discovery Roche
Seminars
This workshop offers a uniquely data-driven and translational perspective on co-stimulation. Drawing on clinical-stage learnings from haematologic indications, unpack how co-stimulation behaves in real patients, how early preclinical signals map to later clinical outcomes, and how these insights can critically inform the strategic design and next steps for T-cell engagers targeting solid tumors.
This workshop will cover:
- What Clinical Data Tells Us: Key findings from Roche’s haematology programs: how co-stimulatory domains improved efficacy, durability, and T-cell fitness in the clinic
- Bridging Preclinical → Clinical: How different domains signal in preclinical models, which readouts most reliably predict clinical behaviour, and which don’t
- Co-Stimulation in Solid Tumours: Why success in the haem space hasn’t yet translated to solid tumours, and what biological & microenvironmental barriers must be engineered around
- Domain & Biology Optimization: Comparative assessment of co-stimulatory signals (e.g., CD28 vs CD137) and how their biology may inform domain prioritisation specifically for solid tumour contexts
- Strategic Design Framework: Leveraging clinical learnings and key assumptions to define the strategic and next-step approaches for solid tumour co-stimulation design.
This expert-led discussion will unpack the unique translational challenges and opportunities for T-cell engagers across oncology and autoimmune indications. Panelists will explore how emerging scientific insights, target biology, and mechanistic understanding can inform smarter therapeutic design, combination strategies, and clinical development pathways for both cytotoxic and tolerability-driven indications.
- How does target biology influence format selection, CD3 affinity tuning, and tissue-selective delivery approaches in solid tumours vs autoimmune tissues?
- What translational tools (e.g., biomarkers, PD readouts, in vitro/in vivo models) are proving most predictive for efficacy and safety in both therapeutic areas?
- What combination strategies are most promising e.g., with checkpoint inhibitors, cytokines, or tolerance inducing agents and how do we time them?
- Where are current translational models falling short, and how can we better model immune engagement, off-tumour effects, and chronic exposure?
- How do we de-risk multi-targeting and immune activation in non-lethal diseases where tolerance, durability, and safety thresholds differ from oncology?
