DPQ hydrochloride
Based on 3 publication(s) in Google Scholar
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.
- CAS No.: 84050-22-6
- Formula: C14H20ClN5O2
- Molecular Weight:325.79
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
-
Biological Activity
-
Chemical Information
- Purity & Documentation
- References
-
Help & FAQs
Publications Citing Use of MedChemExpress (MCE) DPQ hydrochloride
More
Biological Activity
|
PARP-1 |
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.
-
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.
-
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%).
-
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).
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.
Chemical Information
-
CAS No. 84050-22-6
-
Molecular Weight 325.79
-
Formula C14H20ClN5O2
-
SMILES
NC1=C2C=C(OC)C(OC)=CC2=NC(N3CCNCC3)=N1.[H]Cl
-
Synonyms
6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (3)
-
Journal Impact Factor
-
Most Recent
-
Sci Immunol
Schlafen 11 triggers innate immune responses through its ribonuclease activity upon detection of single-stranded DNA. [Abstract]2024 Jun 14;9(96):eadj5465. PMID: 38875319 -
Adv Sci (Weinh)
Cuproptosis and Disulfidptosis Converge to Empower PD-L1 Checkpoint Therapy via Cadict-Induced PD-L1 Translation. [Abstract]2026 May;13(25):e15367. PMID: 41722054 -
Stem Cell Res Ther
MSC-derived exosomes attenuate cell death through suppressing AIF nucleus translocation and enhance cutaneous wound healing. [Abstract]2020 May 11;11(1):174. PMID: 32393338
Purity & Documentation
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. [Content Brief]
[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. [Content Brief]
[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. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Powered by Bioz