| Identification | Back Directory | [Name]
DPQ | [CAS]
129075-73-6 | [Synonyms]
DPQ
DMEM(Low Glucose)
PARP Inhibitor III, DPQ
PARP Inhibitor III, DPQ - CAS 129075-73-6 - Calbiochem
3,4-DIHYDRO-5[4-(1-PIPERIDINYL)BUTOXYL]-1(2H)-ISOQUINOLINE
3,4-DIHYDRO-5[4-(1-PIPERINDINYL)BUTOXY]-1(2H)-ISOQUINOLINE
5-(4-piperidin-1-ylbutoxy)-3,4-dihydro-2H-isoquinolin-1-one
3,4-DIHYDRO-5-[4-(1-PIPERIDINYL)BUTOXY]-1(2H)-ISOQUINOLINONE
3,4-DIHYDRO-5-[4-(1-PIPERIDINYL)BUTOXYL]-1(2H)-ISOQUINOLINONE
1(2H)-Isoquinolinone, 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-
5-[4-(1-PIPERIDINYL)-BUTYLOXY]-1,2,3,4-TETRAHYDROISOQUINOLIN-1-ONE | [Molecular Formula]
C18H26N2O2 | [MDL Number]
MFCD02258932 | [MOL File]
129075-73-6.mol | [Molecular Weight]
302.41 |
| Chemical Properties | Back Directory | [Melting point ]
107-109° | [Boiling point ]
528.8±50.0 °C(Predicted) | [density ]
1.096±0.06 g/cm3(Predicted) | [storage temp. ]
2-8°C | [solubility ]
DMSO: Soluble | [form ]
solid | [pka]
14.54±0.20(Predicted) | [color ]
White to off-white | [biological source]
synthetic (organic) |
| Hazard Information | Back Directory | [Description]
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. | [Uses]
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. | [Uses]
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. | [Uses]
Reagent for inhibition of PARP. | [Biochem/physiol Actions]
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. | [in vivo]
DPQ (10 mg/kg; intraperitoneal injection; single dose; 6 h) significantly attenuates lung inflammation, neutrophil infiltration, and vascular leakage in LPS-induced acute lung injury model of C57BL/6 mice, inhibiting NF-κB pathway activation[2].
DPQ (10 mg/kg; intraperitoneal injection; single dose; 4 weeks) improves cardiac function and reduced apoptosis and oxidative stress in myocardial infarction model of Wistar rats[3].
| Animal Model: | LPS-Induced Acute Lung Injury Model in C57BL/6 mice (male, 8-10 weeks old) | | Dosage: | 10 μg/kg (dissolved in 0.01% DMSO (PBS) | | Administration: | Intraperitoneal injection, 30 min after LPS chanllenge (7.5 mg/kg; ip; single dose)
| | Result: | Reduced neutrophil infiltration (50% decrease), MPO activity (40% decrease), and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in lungs.
Restored vascular permeability (Evans blue extravasation reduced by 35%), and inhibited apoptotic cell death (TUNEL-positive cells decreased by 45%).
Suppressed NF-κB activation with reduced IkB-α degradation and p65 phosphorylation. |
| Animal Model: |
Myocardial Infarction model in Wistar rats (male, 4 months old) via coronary artery ligation[3] | | Dosage: | 10 mg/kg (dissolved in DMSO)
| | Administration: | Intraperitoneal injection, single dose immediately after MI induction | | Result: | Improved cardiac function (FS increased by 25%, EDD/ESD reduced by 15%), decreased apoptotic cardiomyocytes (TUNEL-positive cells reduced by 40%), and suppressed cleaved caspase-3 and PARP1 expression. Oxidative stress markers (O2-, nitrotyrosine) were reduced by 30-40% in infarcted myocardium. |
| [IC 50]
PARP-1 | [storage]
+4°C | [References]
[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 |
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Energy Chemical
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