Day Two

• Understanding European VC expectations to enable biotechs to tailor fundraising strategies and secure investment in a competitive climate
• Identifying how recent deals signal which emerging modalities – like novel ligases, non-oncology therapeutics, and going beyond the proteosome – investors are looking for as priorities evolve in the TPD space
• Examining how early-stage proof-of-concept studies help validate platforms and increase commitment from pharma and VC partners
• Exploring how early-stage collaborations between academic founders, biotechs, investors and university tech-transfer offices influence IP strategy, company creation, and translational readiness in Europe

• Engineering bispecific antibody degraders to enable selective, lysosomal degradation of target membrane proteins
• Pairing therapeutic targets with membrane E3 ligases to achieve tissue-specific degradation while sparing healthy tissues
• Expanding therapeutic reach to hard-to-drug and challenging membrane targets

New Data

• Leveraging proteomics to identify compatible target–internalisation driver pairs that support tissue-specific degradation and therapeutic precision
• Exploring non-proteasomal degradation pathways to expand modality options and reduce toxicity associated with intracellular accumulation
• Integrating sweeping mechanisms to recycle biologics while degrading targets to improve durability and reduce off-target degradation

• EPI-326 is a bispecific EGFR EpiTAC that drives targeted degradation of mutant and wild type EGFR specifically within tumours
• Highlighting deep and durable efficacy, favourable safety and PK, and path to IND and clinic for EPI-326
• Demonstrating preclinical advancements with in vivo data on additional programs, emphasising catalytic degrader mechanisms and tissue-specific delivery
• Exploring the transformative potential of bispecific antibody degraders for oncology and inflammatory diseases

•  A systematic exploration of the chemical space of CRBN-binding scaffolds (300 compounds synthesized and tested)
• SAR insights and highlighting representative, structurally novel, and effective binders.
• An overview of HitChem’s CRBN molecular glue library design strategy and HTS case studies on multiple targets

• Leveraging Sibylla’s platform to design folding-interfering molecules that disrupt protein folding pathways for targeted degradation
• Optimising compounds for potent Cyclin D1 degradation and favourable ADME profiles to enable therapeutic development
• Sharing in vitro and in vivo validation data to support translational development of folding interfering molecules targeting Cyclin D1

• Leveraging predictive modelling and ML-driven tools to accelerate degrader design and optimisation
• Evaluating opportunities and limitations of 3D structural modelling to understand ternary complex formation and degradation mechanisms
• Integrating in silico strategies to enhance PK prediction, inform rational design decisions, and streamline development of degraders with improved pharmacokinetic profiles

• Identifying ligands for a chromatin regulatory protein with limited prior tractability and validating functional degrader activity
• Optimising degrader architecture through iterative design to enhance potency, selectivity and degradation efficiency
• Outlining challenges and solutions in progressing an advanced preclinical degrader toward development candidate nomination

• Exploring induced proximity mechanisms that stabilise protein–protein interactions to restore proteostasis in neurodegeneration and cancer
• Applying structure-guided chemistry and biophysical characterisation to optimise cooperativity and target engagement in molecular glue design
• Discussing how Ambagon’s platform expands induced proximity beyond degradation to address disease-agnostic biological pathways

• Showcasing TRAP-1, a novel small molecule that facilitates ternary complex formation between mutant p53 and BRD4, enabling transcriptional reactivation of p53 in oncogenic contexts.
• Demonstrating robust induction of p53 target genes and selective growth inhibition in p53Y220C pancreatic cancer models, underscoring the mechanistic requirement for chemically induced proximity.
• Establishing TCIPs as a promising therapeutic modality to restore tumour suppressor function and address historically intractable transcription factor targets.

Non-Degrader

• Reviewing the current preclinical, clinical, and commercial TPD landscape to guide pipeline prioritisation
• Identifying key trends from 2025 to shape competitive positioning and investment strategies
• Defining future directions for TPD in 2026 and beyond to enable smarter resource allocation and innovation planning