2. Cell Cycle/DNA Damage Epigenetics
  3. PARP
  4. DPQ hydrochloride

DPQ hydrochloride  (Synonyms: 6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride)

Cat. No.: HY-W424851
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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.

For research use only. We do not sell to patients.

DPQ hydrochloride Chemical Structure

DPQ hydrochloride Chemical Structure

CAS No. : 84050-22-6

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DPQ hydrochloride Related Antibodies

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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

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Description

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].

IC50 & Target

PARP-1

 

In Vitro

DPQ hydrochloride (10 μM; pretreatment 30 min, treatment 2-8 h) significantly inhibited the mRNA expression of TNF-α, IL-1β, IL-6, CXCL-1, MIP-2 and iNOS in mouse peritoneal macrophages stimulated by LPS (100 ng/mL) [2].

DPQ hydrochloride (10 μM; pretreatment 30 min, treatment 2-8 h) inhibited the degradation of IkB-α and phosphorylation of NF-κB p65 in macrophages induced by LPS (100 ng/mL), blocking the inflammatory signaling pathway[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

DPQ hydrochloride Related Antibodies

Apoptosis Analysis[1]

Cell Line: Mixed murine cortical neurons
Concentration: 10 μM
Incubation Time: 10 min pretreatment + 20 min NMDA exposure
Result: Reduced NMDA-induced neuronal apoptosis by 84% at 6 h and 50% at 24 h, restored ATP levels from 4% to 72% of control, and suppressed PARP activation.

Real Time qPCR[2]

Cell Line: Murine peritoneal macrophages
Concentration: 10 μM
Incubation Time: 30 min pretreatment + 2-8 h LPS stimulation
Result: Significantly decreased LPS-induced mRNA expression of TNF-α (50% reduction), IL-1β (40%), IL-6 (45%), CXCL-1 (35%), MIP-2 (40%), and iNOS (50%).

Western Blot Analysis[2]

Cell Line: Murine peritoneal macrophages
Concentration: 10 μM
Incubation Time: 30 min pretreatment + 15-60 min LPS stimulation
Result: Blocked LPS-induced IkB-α degradation (50% inhibition at 15 min) and NF-κB p65 phosphorylation (40% reduction at 30 min).

Immunofluorescence[2][3]

Cell Line: Murine peritoneal macrophages
Concentration: 10 μM
Incubation Time: 30 min pretreatment + 1 h LPS stimulation
Result: Reduced LPS-induced PARP activation (40% decrease in PAR fluorescence intensity) and nitrotyrosine formation (35% reduction).
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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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 (O2-, nitrotyrosine) were reduced by 30-40% in infarcted myocardium.
Molecular Weight

325.79

Formula

C14H20ClN5O2
CAS No.
SMILES

NC1=C2C=C(OC)C(OC)=CC2=NC(N3CCNCC3)=N1.[H]Cl
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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DPQ hydrochloride Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

DPQ84050-22-66,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinaminePARPpoly ADP ribose polymeraseInhibitorAnti-inflammationAntiviralAcute lung injuryinhibitorinhibit

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