Doo Young Jung

• Employing a matched-pair strategy using inert payloads and non-binding antibodies, to systematically isolate and quantify the contributions of payload and target engagement to overall observed toxicity, providing a clear mechanistic attribution for dose-limiting adverse events
• Utilizing tissue microarrays with quantitative immunohistochemistry for target expression, to map the biodistribution of target antigens in critical normal organs,creating a preclinical risk assessment tool for on-target toxicity before candidate selection
• Developing computational toxicology models that partition free payload and intact ADC concentrations, to predict which component is driving clinical adverse events, informing linker design strategies to minimize systemic payload release

Join this interactive roundtable to explore how non-specific ADC uptake into healthy tissues contributes to dose-limiting toxicities and what the industry can do to predict better, characterize, and mitigate these mechanisms early in development.

Join this discussion to examine how emerging mechanistic insights can be translated into safer ADC design strategies and improved therapeutic window by:

• Investigating non-specific ADC uptake pathways beyond macropinocytosis by leveraging CRISPR-Cas9 screening and healthy cell models to identify the receptors and endocytic mechanisms driving off-target toxicities
• Understanding how ADC physicochemical properties such as surface charge, hydrophobicity, linker stability, and DAR influence non-specific uptake into healthy tissues, and debating which design parameters offer the greatest opportunity for toxicity mitigation
• Translating mechanistic insights from fluorescent imaging, spatial biology, and clinically validated ADC safety data into predictive screening strategies that enable earlier candidate prioritization and improved therapeutic windows