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

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

目录号: HY-W424851
产品使用指南 技术支持

DPQ hydrochloride 是一种具有血脑屏障透过性和选择性的 PARP-1 抑制剂，可阻断 PARP-1 介导的 DNA 损伤修复及 NAD+/ATP 消耗，从而抑制过度炎症反应。DPQ hydrochloride 抑制 NF-κB 通路激活、减少促炎因子 (如 TNF-α、IL-6) 表达及氧化应激。DPQ hydrochloride 可用于急性肺损伤、心肌梗死及神经退行性疾病的炎症相关研究。

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DPQ hydrochloride Chemical Structure

DPQ hydrochloride Chemical Structure

CAS No. : 84050-22-6

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DPQ hydrochloride 的其他形式现货产品:

DPQ

Customer Review

Other Forms of DPQ hydrochloride:

DPQ hydrochloride 相关抗体

Top Publications Citing Use of Products

MCE 顾客使用本产品发表的 1 篇科研文献

查看 PARP 亚型特异性产品:

查看所有亚型
PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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

 

体外研究
(In Vitro)

DPQ hydrochloride (10 μM；预处理 30 min，处理 2-8 h) 显著抑制 LPS (100 ng/mL) 刺激的小鼠腹腔巨噬细胞中 TNF-α、IL-1β、IL-6、CXCL-1、MIP-2 和 iNOS 的 mRNA 表达[2]。
DPQ hydrochloride (10 μM；预处理 30 min，处理 2-8 h) 抑制 LPS (100 ng/mL) 诱导的巨噬细胞中 IkB-α 降解及 NF-κB p65 磷酸化，阻断炎症信号通路[2]。

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

DPQ hydrochloride 相关抗体:

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).
体内研究
(In Vivo)

DPQ hydrochloride (10 mg/kg；腹腔注射；单次；6 小时) 在 LPS 诱导的 C57BL/6 小鼠急性肺损伤模型中显著减轻肺炎症、中性粒细胞浸润及血管渗漏，抑制 NF-κB 通路激活[2]。
DPQ hydrochloride (10 mg/kg；腹腔注射；单次；4 周) 在 Wistar 大鼠心肌梗死模型中改善心脏功能，减少细胞凋亡及氧化应激损伤[3]。

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.
分子量

325.79

同用名

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

Formula

C14H20ClN5O2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

DPQ hydrochloride 相关分类

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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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