PROTAC PARP2 degrader-1 is an orally active PARP2 PROTAC degrader with a DC50 of 2 μM. PROTAC PARP2 degrader-1 potently inhibits the enzymatic activities of PARP1 ( IC50 = 2.74 nM) and PARP2 ( IC50 = 0.32 nM), with approximately 10-fold higher selectivity for PARP2. PROTAC PARP2 degrader-1 induces cell cycle arrest and apoptosis, and exhibits significant anti-tumor efficacy in mouse models. PROTAC PARP2 degrader-1 can be used for the research of triple-negative breast cancer [1]. (Pink: PARP-2 ligand; Blue: Cereblon ligand; Black: linker ).
In Vivo, PROTAC PARP2 degrader-1 (Compound C8) (12.5-100 mg/kg; ig, ip; 21 days) dose-dependently suppresses MDA-MB-231 TNBC xenograft growth[1].
In Vitro, PROTAC PARP2 degrader-1 (Compound C8) (5-10 days) potently inhibits the proliferation of MDA-MB-436, Capan-1, MDA-MB-468 and MDA-MB-231 cells, with IC50 values of 0.026 μM, 0.061 μM, 0.69 μM and 0.53 μM, respectively. Moreover, its activity in non-BRCA-mutant TNBC cells is significantly higher than that of Olaparib[1]. PROTAC PARP2 degrader-1 (C8) (0.5 μM; 24 h) selectively degrades nuclear PARP2 in MDA-MB-231 cells without affecting the level of cytoplasmic PARP2[1]. PROTAC PARP2 degrader-1 (0.312-5 μM; 14 days) potently and dose-dependently inhibits colony formation of MDA-MB-231 cells[1]. PROTAC PARP2 degrader-1 (0.156-2.5 μM; 24-48 h) induces dose-dependent G2/M cell cycle arrest in MDA-MB-436 and MDA-MB-231 cells[1]. PROTAC PARP2 degrader-1 (C8) (0.312-5 μM; 48-72 h) induces dose-dependent apoptosis in MDA-MB-436 and MDA-MB-231 cells, and [the sentence is incomplete in the source text, maintained as is] compared with Olaparib[1].
References:
[1]. Pu C, et al. Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer. Eur J Med Chem. 2022;236:114321.
In Vivo, PROTAC PARP2 degrader-1 (Compound C8) (12.5-100 mg/kg; ig, ip; 21 days) dose-dependently suppresses MDA-MB-231 TNBC xenograft growth[1].
In Vitro, PROTAC PARP2 degrader-1 (Compound C8) (5-10 days) potently inhibits the proliferation of MDA-MB-436, Capan-1, MDA-MB-468 and MDA-MB-231 cells, with IC50 values of 0.026 μM, 0.061 μM, 0.69 μM and 0.53 μM, respectively. Moreover, its activity in non-BRCA-mutant TNBC cells is significantly higher than that of Olaparib[1]. PROTAC PARP2 degrader-1 (C8) (0.5 μM; 24 h) selectively degrades nuclear PARP2 in MDA-MB-231 cells without affecting the level of cytoplasmic PARP2[1]. PROTAC PARP2 degrader-1 (0.312-5 μM; 14 days) potently and dose-dependently inhibits colony formation of MDA-MB-231 cells[1]. PROTAC PARP2 degrader-1 (0.156-2.5 μM; 24-48 h) induces dose-dependent G2/M cell cycle arrest in MDA-MB-436 and MDA-MB-231 cells[1]. PROTAC PARP2 degrader-1 (C8) (0.312-5 μM; 48-72 h) induces dose-dependent apoptosis in MDA-MB-436 and MDA-MB-231 cells, and [the sentence is incomplete in the source text, maintained as is] compared with Olaparib[1].
References:
[1]. Pu C, et al. Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer. Eur J Med Chem. 2022;236:114321.
















