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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • BAF/PBAF chromatin remodeling complexes are implicated in cancer.
  • Targeting ATPase subunits of these complexes presents a potential therapeutic strategy.

Purpose of the Study:

  • To develop proteolysis targeting chimera (PROTAC) degraders for SMARCA2 and SMARCA4.
  • To investigate the efficacy of these degraders in cancer models.

Main Methods:

  • Design and synthesis of PROTAC molecules utilizing a bromodomain ligand and VHL E3 ligase recruitment.
  • Structure-based drug design and biophysical characterization.
  • Assessment of anti-proliferative effects and cell death induction in cancer cell lines.

Main Results:

  • Developed ACBI1, a potent and cooperative degrader of SMARCA2, SMARCA4, and PBRM1.
  • ACBI1 induced anti-proliferative effects and cell death via SMARCA2 depletion in SMARCA4 mutant cancer cells.
  • Demonstrated efficacy in acute myeloid leukemia cells dependent on SMARCA4 ATPase activity.

Conclusions:

  • Biophysics- and structure-based PROTAC design is effective for degrading challenging targets like BAF/PBAF subunits.
  • ACBI1 represents a promising therapeutic candidate for tumors sensitive to BAF complex ATPase loss.
  • This work paves the way for novel therapeutics targeting chromatin remodeling complexes in cancer.