Unlocking the Mechanisms and Kinetics of Targeted Protein Degradation

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Date: 21 July 2021 (Wednesday)
Time: New York 10:00 | London 15:00 | Paris 16:00 | Singapore 22:00 | Tokyo 23:00 | Sydney 00:00 (22 July) ]
Duration: 1 hour 45 minutes
Event structure: 3×15 minute presentations + 45 min panel discussion + 15 min Q&A
Registration fee: Complimentary access
Webinar on-demand: Available to view until midnight 6th Aug 2021 (registration is required)

The field of targeted protein degradation (TPD) continues to expand rapidly beyond the study of PROTACs and molecular glues, to now include a variety of induced proximity mechanisms to target proteins that were previously considered undruggable. Regardless of the mechanism utilized to achieve target degradation, characterization and optimization of these molecules presents a significant challenge. In this webinar, our panel of experts will discuss luminescence-based and energy transfer technologies that allow for the kinetic and high throughput measurement of target degradation, as well as the measurement of key cellular mechanisms affecting PROTAC functionality, including permeability, binding affinity, ternary complex formation and target ubiquitination. Considerations for establishing high throughput assays to screen for promising drug candidates will be presented. Additionally, we will explore the utility of Biograders, which can be engineered with exquisite specificity. Here we will highlight this specificity to inform on the cellular prevalence of nucleotide loaded states across various KRAS mutants. Our webinar will be followed by a panel discussion and Q&A session.

Panel Discussion Topics:

• What does the future hold for PROTACs, Molecular Glues, biodegraders, and other induced degradation strategies? Are there specific challenges associated with each and how might these be overcome?
• What does the screening pipeline for chemical degraders look like, and does this depend on the strategies used or the information available in the context of med chem design? Does this differ for biodegraders, and if so, how?
• Similar to PROTACs, will biodegraders show efficacy dependence on E3 ligase choice? Is there more flexibility in this space due to the lack of a requirement for a chemical E3 ligase binder?
• How critical are disease-relevant cell lines for primary screening?