Amelie Renaud

TL;DR: This study shows that PARP inhibitors trap the PARP1 and PARP2 enzymes at damaged DNA, providing a new mechanistic foundation for the rational application ofPARP inhibitors in cancer therapy.

TL;DR: BMN 673 is the most potent clinical PARP inhibitor tested to date with the highest efficiency at trapping PARP–DNA complexes and is also approximately 100-fold more cytotoxic than olaparib and rucaparIB in combination with the DNA alkylating agents methyl methane sulfonate and temozolomide.

TL;DR: The design, synthesis, and evaluation of new indenoisoquinolines that are dual inhibitors of both Tdp1 and Top1 are documents, which places the more active compounds among the most potent known inhibitors of this target.

TL;DR: Through structure-activity relationship (SAR) studies, it is demonstrated that arylidene thioxothiazolidinones inhibit Tdp1 and compound 50 is identified as a submicromolar inhibitor of TDP1 (IC₅₀ = 0.87 μM).

TL;DR: It is demonstrated that BMN 673 is the most potent clinical PARP inhibitor to date with the highest efficiency at trapping PARP-DNA complexes and more cytotoxic as a single agent than olaparib.