E3 Ligase Recruiters
To date most R&D in the protein degrader field has focussed on exploiting Cereblon (CRBN) and Von Hippel-Lindau tumour suppressor (VHL) E3 ligases. Where structural information is available, over half of the current clinical stage PROTACs utilise CRBN based ligase recruiters, where the beyond rule-of-5 (bRo5) molecular property space is more favourable for optimisation and delivery of oral bioavailable degraders.1
However, for CRBN ligase recruiters, selectivity for degradation of the protein of interest (POI) versus proteasomal degradation of neo-substrates, where the CRBN ligase recruiter acts as a molecular glue, remains a challenge. Several neo-substrates are known to play important physiological roles and their protein degradation can often lead to toxicological consequences. As an example, degradation of Spalt Like Transcription Factor 4 (SALL4) by thalidomide resulted in teratogenicity and the epidemic of severe birth defects in the late 50’s-early 60’s.
Given the interest in CRBN from a clinical perspective, our toolbox is biased towards CRBN-based recruiters, but with a significant subset designed to reduce potential neo-substrate protein degradation (Figure 1).