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2-Piperazine-4-amino-6,7-dimethoxy quinoline hydrochloride

Product Name2-Piperazine-4-amino-6,7-dimethoxy quinoline hydrochloride
CAS84050-22-6
MFC14H20ClN5O2
MW325.79
EINECS
MOL File84050-22-6.mol

Chemical Properties

CAS DataBase Reference

84050-22-6(CAS DataBase Reference)

Usage And Synthesis

Uses

DPQ hydrochloride is a blood-brain barrier permeable and selective PARP-1 inhibitor that blocks PARP-1-mediated DNA damage repair and NAD+/ATP consumption, thereby inhibiting excessive inflammatory responses. DPQ hydrochloride inhibits NF-κB pathway activation, reduces the expression of pro-inflammatory factors (such as TNF-α, IL-6) and oxidative stress. DPQ hydrochloride can be used in inflammation-related studies of acute lung injury, myocardial infarction, and neurodegenerative diseases[1][2][3].

in vivo

DPQ hydrochloride (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 hydrochloride (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)^[2]
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:	Wistar rats (male, 4 months old) + MI 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 (O^2-, nitrotyrosine) were reduced by 30-40% in infarcted myocardium.

IC 50

PARP-1

References

[1] Meli E, et al. Differential role of poly (ADP-ribose) polymerase-1in apoptotic and necrotic neuronal death induced by mild or intense NMDA exposure in vitro. Mol Cell Neurosci. 2004;25 (1) :172-180. DOI:10.1016/j.mcn.2003.09.016
[2] Wang G, et al. PARP-1 inhibitor, DPQ, attenuates LPS-induced acute lung injury through inhibiting NF-κB-mediated inflammatory response. PLoS One. 2013 Nov 21;8 (11) :e79757. DOI:10.1371/journal.pone.0079757
[3] Wang J, et al. Inhibition of poly (ADP-ribose) polymerase and inducible nitric oxide synthase protects against ischemic myocardial damage by reduction of apoptosis. Mol Med Rep. 2015 Mar;11 (3) :1768-76. DOI:10.3892/mmr.2014.2977

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