DPQ hydrochloride
Based on 4 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.
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- Pureté: 98.97%
- CAS No.: 84050-22-6
- Formule: C14H20ClN5O2
- Masse moléculaire:325.79
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Stockage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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Activité biologique
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Chemical Information
- Pureté et documentation
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Publications Citing Use of MedChemExpress (MCE) DPQ hydrochloride
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Activité biologique
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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.
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Cell Line:Mixed murine cortical neurons
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Concentration:10 μM
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Incubation Time:10 min pretreatment + 20 min NMDA exposure
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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.
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Cell Line:Murine peritoneal macrophages
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Concentration:10 μM
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Incubation Time:30 min pretreatment + 2-8 h LPS stimulation
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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%).
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Cell Line:Murine peritoneal macrophages
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Concentration:10 μM
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Incubation Time:30 min pretreatment + 15-60 min LPS stimulation
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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.
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Animal Model:LPS-Induced Acute Lung Injury Model in C57BL/6 mice (male, 8-10 weeks old)[2]
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Dosage:10 μg/kg (dissolved in 0.01% DMSO (PBS)
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Administration:Intraperitoneal injection, 30 min after LPS chanllenge (7.5 mg/kg; ip; single dose)
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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.
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Animal Model:Wistar rats (male, 4 months old) + MI via coronary artery ligation[3]
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Dosage:10 mg/kg (dissolved in DMSO)
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Administration:Intraperitoneal injection, single dose immediately after MI induction
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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
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CAS No. 84050-22-6
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Appearance Solid
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Masse moléculaire 325.79
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Formule C14H20ClN5O2
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Color White to off-white
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SMILES
NC1=C2C=C(OC)C(OC)=CC2=NC(N3CCNCC3)=N1.[H]Cl
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Synonyms
6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Publications (4)
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Journal Impact Factor
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Most Recent
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J Adv Res
Targeting myofibroblast copper vulnerability reverses pulmonary fibrosis via METTL3-directed STAT6 m6A driving cuproptosis. [Abstract]2026 May 21:S2090-1232(26)00436-4. PMID: 42173361 -
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
Pureté et documentation
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Fiche technique (281 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instruction de manipulation (2659 KB)
Références
[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)
DPQ hydrochloride Related Classifications
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