129075-73-6

The poly(ADP-ribose) polymerases (PARPs) form a family of enzymes with roles in DNA repair and apoptosis, particularly in response to reactive oxygen and nitrogen species. DPQ is a potent inhibitor of PARPs, inhibiting PARP1 with an IC₅₀ value of 40 nM. It is approximately 10-fold less potent against PARP2. DPQ can be used in either cells or in animals.

3,4-Dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone is a potent inhibitor of poly(ADP-ribose) polymerases, a family of enzymes that plays a crucial role in DNA repair and apoptosis in respons e to reactive oxygen and nitrogen species.

DPQ has been used as a PARP1 (poly(ADP-ribose) polymerase 1) inhibitor in in vivo studies to determine the loss of γ-H2AX (H2A histone family member X) upon irradiation.

Reagent for inhibition of PARP.

3,4-Dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone (DPQ) is known to decrease the PARP 1 (poly(ADP-ribose) polymerase 1) mediated apoptosis under the influence of ischemia. It is considered as more effective inhibitor than the traditionally used PARP1 inhibitor 3-aminobenzamide.

PARP-1

+4°C

[1] D DAVAR. Role of PARP inhibitors in cancer biology and therapy.[J]. Current medicinal chemistry, 2012, 19 23: 3907-3921. DOI: 10.2174/092986712802002464
[2] MARLENE T MATHEWS  Bradford C B. PARP-1 inhibition prevents oxidative and nitrosative stress-induced endothelial cell death via transactivation of the VEGF receptor 2.[J]. Arteriosclerosis, Thrombosis, and Vascular Biology, 2008, 28 4: 711-717. DOI: 10.1161/atvbaha.107.156406
[3] GABRIELE COSTANTINO. Modeling of Poly(ADP-ribose)polymerase (PARP) Inhibitors. Docking of Ligands and Quantitative Structure?Activity Relationship Analysis[J]. Journal of Medicinal Chemistry, 2001, 44 23: 3786-3794. DOI: 10.1021/jm010116l
[4] TOBIAS ELTZE. Imidazoquinolinone, imidazopyridine, and isoquinolindione derivatives as novel and potent inhibitors of the poly(ADP-ribose) polymerase (PARP): a comparison with standard PARP inhibitors.[J]. ACS Applied Electronic Materials, 2008: 1587-1598. DOI: 10.1124/mol.108.048751
[5] ELENA FONFRIA. TRPM2 channel opening in response to oxidative stress is dependent on activation of poly(ADP-ribose) polymerase[J]. British Journal of Pharmacology, 2009, 143 1: 186-192. DOI: 10.1038/sj.bjp.0705914
[6] L. GIOVANNELLI. Comet Assay as a Novel Approach for Studying DNA Damage in Focal Cerebral Ischemia: Differential Effects of NMDA Receptor Antagonists and Poly(ADP-Ribose) Polymerase Inhibitors[J]. Journal of Cerebral Blood Flow & Metabolism, 2002, 39 1 1: 697-704. DOI: 10.1097/00004647-200206000-00008