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Avoid the trap: Targeting PARP1 beyond human malignancy.

Chiho Kim1, Chuo Chen1, Yonghao Yu1

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Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors are used in cancer, but can cause toxicity. New PARP1 degraders offer a promising approach for treating non-oncological diseases linked to aberrant PARP1 activation.

Keywords:
BRCANAD(+)PARPbreast cancercell deathischemia reperfusion injuryneurodegenerationovarian cancerphase transitionpoly(ADP-ribose)stroke

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Poly(ADP-ribose) polymerase 1 (PARP1) is crucial for DNA damage response via poly(ADP-ribosyl)ation (PARylation).
  • PARP1 inhibitors are effective in homologous recombination-deficient cancers.
  • Aberrant PARP1 activation in non-oncological diseases causes NAD+ depletion, PAR formation, cell death, and tissue damage.

Purpose of the Study:

  • To review the biology and implications of PARP1 trapping.
  • To discuss novel PARP1 PROTAC compounds as non-trapping degraders.
  • To explore the potential of these compounds in non-oncological diseases.

Main Methods:

  • Literature review of PARP1 biology, inhibitors, and trapping mechanisms.
  • Analysis of recent developments in PARP1 PROTAC technology.
  • Discussion of disease models and therapeutic potential.

Main Results:

  • PARP1 trapping by current inhibitors leads to DNA damage, immune response, and cytotoxicity.
  • PARP1 deletion shows protective effects in animal models.
  • PARP1 PROTACs offer a "non-trapping" degradation strategy.

Conclusions:

  • PARP1 trapping is a significant concern with existing PARP1 inhibitors.
  • PARP1 PROTACs represent a promising therapeutic strategy for non-oncological diseases.
  • Targeted degradation of PARP1 may overcome limitations of current inhibitors.