Exploration of the tunability of BRD4 degradation by DCAF16 trans-labelling covalent glues

Eur J Med Chem. 2024 Dec 5:279:116904. doi: 10.1016/j.ejmech.2024.116904. Epub 2024 Sep 24.

Abstract

Chemically induced proximity modalities such as targeted protein degradation (TPD) hold promise for expanding the number of proteins that can be manipulated pharmacologically. However, current TPD strategies are often limited to proteins with preexisting ligands. Molecular glues (e.g. glutarimide ligands for CUL4CRBN), offer the potential to target undruggable proteins. Yet, their rational design is largely unattainable due to the unpredictability of the 'gain-of-function' nature of the glue interaction upon chemical modification of ligands. We recently reported a covalent trans-labelling glue mechanism which we named 'Template-assisted covalent modification', where an electrophile decorated BRD4 inhibitor was effectively delivered to a cysteine residue on DCAF16 due to an electrophile-induced BRD4-DCAF16 interaction. Herein, we report our efforts to evaluate how various electrophilic modifications to the BRD4 binder, JQ1, affect DCAF16 recruitment and subsequent BRD4 degradation efficiency. We discovered a moderate correlation between the electrophile-induced BRD4-DCAF16 ternary complex formation and BRD4 degradation. Moreover, we show that a more solvent-exposed warhead presentation optimally recruits DCAF16 and promotes BRD4 degradation. The diversity of covalent attachments in this class of BRD4 degraders suggests a high tolerance and tunability for the BRD4-DCAF16 interaction. This offers a new avenue for rational glue design by introducing covalent warheads to known binders.

MeSH terms

  • Azepines / chemical synthesis
  • Azepines / chemistry
  • Azepines / pharmacology
  • Bromodomain Containing Proteins
  • Cell Cycle Proteins* / antagonists & inhibitors
  • Cell Cycle Proteins* / metabolism
  • Dose-Response Relationship, Drug
  • Humans
  • Molecular Structure
  • Proteolysis / drug effects
  • Structure-Activity Relationship
  • Transcription Factors* / antagonists & inhibitors
  • Transcription Factors* / metabolism
  • Triazoles / chemical synthesis
  • Triazoles / chemistry
  • Triazoles / pharmacology

Substances

  • BRD4 protein, human
  • Transcription Factors
  • Cell Cycle Proteins
  • Triazoles
  • Azepines
  • (+)-JQ1 compound
  • Bromodomain Containing Proteins