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

DPQ hydrochloride Chemical Structure

CAS No. : 84050-22-6

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DPQ

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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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