Aspirin

别名: NSC 27223, Acetylsalicylic acid, ASA 中文名称:阿司匹林,乙酰水杨酸

Aspirin (NSC 27223, Acetylsalicylic acid, ASA)是水杨酸类不可逆的COX1 and COX2抑制剂,常用作止痛药来缓解轻微疼痛,作为解热药减少发热,并作为一种抗炎药物。Aspirin 可诱导自噬并激发线粒体自噬。

Aspirin Chemical Structure

Aspirin Chemical Structure

CAS: 50-78-2

规格 价格 库存 购买数量
10mM (1mL in DMSO) RMB 737.51 现货
50mg RMB 573.87 现货
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产品质控

批次: S301702 DMSO] 36 mg/mL] false] Ethanol] 36 mg/mL] false] Water] Insoluble] false 纯度: 99.99%
99.99

Aspirin相关产品

相关信号通路图

COX抑制剂选择性比较

细胞实验数据示例

细胞系 实验类型 给药浓度 孵育时间 活性描述 文献信息
PANC1 Growth inhibition assay 300 uM 48 hrs Growth inhibition of human PANC1 cells at 300 uM after 48 hrs by alamar blue assay 22494617
PC3 Growth inhibition assay 300 uM 48 hrs Growth inhibition of human PC3 cells at 300 uM after 48 hrs by alamar blue assay 22494617
SKBR3 Growth inhibition assay 300 uM 48 hrs Growth inhibition of human SKBR3 cells at 300 uM after 48 hrs by alamar blue assay 22494617
HCT116 Function assay 1 mM 6 hrs Inhibition of TNF-alpha-induced NF-kappaB activation in human HCT116 cells at 1 mM after 6 hrs by luciferase reporter gene assay 22154834
AGS Function assay 15 to 60 umol/L after 12 hrs Inhibition of Escherichia coli-stimulated IL-8 production in human AGS cells at 15 to 60 umol/L after 12 hrs by ELISA 20153183
MDA-MB-231 Function assay 100 uM 30 mins Irreversible inhibition of COX-1 in human MDA-MB-231 cells assessed as inhibition of arachidonic acid-induced PGE2 formation at 100 uM incubated for 30 mins followed by compound washout measured 30 mins post arachidonic acid challenge by radioimmunoassay 23651359
THP1 Function assay 100 uM 30 mins Irreversible inhibition of COX-1 in human THP1 cells assessed as inhibition of arachidonic acid-induced TXB2 formation at 100 uM incubated for 30 mins followed by compound washout measured 30 mins post arachidonic acid challenge by radioimmunoassay 23651359
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-6 in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of TNF-alpha in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by E 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring reduction in MDA levels at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in SOD activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in catalase activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of TNF-alpha in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-1beta in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as reduction in MDA levels at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by spectrophotometry 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in SOD activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by spec 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-6 in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by ELISA 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-1beta in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by EL 27575471
H9c2 Cardioprotective assay 1 uM 8 hrs Cardioprotective activity against hypoxia-induced cytotoxicity in rat H9c2 cells assessed as increase in cell viability at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by MTT assay 27575471
stem cells Function assay 100 uM 5 days Induction of adipogenesis in human bone marrow-derived mesenchymal stem cells assessed as increase in adiponectin production at 100 uM measured on day 5 in presence of IDX by ELISA 29398443
RPMI8226 Cell cycle assay 1.7 uM 48 hrs Cell cycle arrest in human RPMI8226 cells assessed as accumulation at G0/G1 phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib 30590258
RPMI8226 Cell cycle assay 1.7 uM 48 hrs Cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib 30590258
RPMI8226 Cell cycle assay 1.7 uM 48 hrs Cell cycle arrest in human RPMI8226 cells assessed as reduction in accumulation at G2/M phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib 30590258
HaCaT Antipyretic assay 100 uM 2 hrs Antipyretic activity in human HaCaT cells assessed as inhibition of TNFalpha-induced PGE2 production at 100 uM pre-incubated for 2 hrs before TNFalpha stimulation for 24 hrs by ELISA 31393125
OVCAR5 Function assay 300 uM to 1 mM 72 hrs Inhibition of NAPRT in human OVCAR5 cells assessed as potentiation of NAMPT inhibitor FK866-induced cytotoxicity by measuring reduction in cell viability at 300 uM to 1 mM incubated for 72 hrs by SRB assay ChEMBL
CCRF-CEM Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human CCRF-CEM cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further ChEMBL
Jurkat Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human Jurkat cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further i ChEMBL
ML2 Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human ML2 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further incu ChEMBL
NOMO Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human NOMO cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc ChEMBL
NB4 Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human NB4 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further incu ChEMBL
NAMALWA Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human NAMALWA cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further ChEMBL
Daudi Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human Daudi cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further in ChEMBL
Raji Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human Raji cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc ChEMBL
ARH77 Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human ARH77 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further in ChEMBL
RPMI8226 Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human RPMI8226 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further ChEMBL
U266 Function assay 3.5 mM 48 hrs Inhibition of NAPRT in human U266 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc ChEMBL
NAMALWA Function assay 35 mg/kg 45 days Potentiation of NAMPT inhibitor 10 mg/kg, ip bid FK866-induced antitumor activity in human NAMALWA cells xenografted in SCID mouse assessed as increase in mouse survival at 35 mg/kg, ip bid up to 45 days ChEMBL
microglia cells Antineuroinflammatory assay 15 mins Antineuroinflammatory activity in LPS-stimulated rat microglia cells assessed as inhibition of PMA-stimulated TXB2 release preincubated for 15 mins measured 70 mins after PMA challenge, IC50=3.12μM 22153874
HCT116 Cytotoxicity assay 48 hrs Cytotoxicity against human HCT116 cells assessed as reduction in cell viability after 48 hrs MTT assay 26750401
peritoneal cells Function assay 5 hrs Inhibition of LPS-induced PGE2 production in C57BL6 mouse peritoneal cells measured at 5 hrs time interval by ELISA, IC50=4.08μM 30006172
HCT8 Antiproliferative assay 72 hrs Antiproliferative activity against human HCT8 cells after 72 hrs in presence of cinnamaldehyde by MTT assay, IC50=15.6μM 30037494
RAW264.7 Antiinflammatory assay Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production by measuring nitrite accumulation by Griess method, IC50=43.2μM 28561586
DAOY qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells 29435139
Rh30 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells 29435139
Rh41 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells 29435139
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生物活性

产品描述 Aspirin (NSC 27223, Acetylsalicylic acid, ASA)是水杨酸类不可逆的COX1 and COX2抑制剂,常用作止痛药来缓解轻微疼痛,作为解热药减少发热,并作为一种抗炎药物。Aspirin 可诱导自噬并激发线粒体自噬。
靶点
COX2 [1] COX1 [1]
体外研究(In Vitro)
体外研究活性 Aspirin抑制NF-κB的活化,从而防止NF-κB抑制剂,IκB的降解,因此NF-κB保留在细胞质中。在转染的T细胞中,Aspirin也会抑制NF-κB依赖性Igκ增强子和人免疫缺陷病毒(HIV)长末端重复序列(LTR) 的转录。[1] Aspirin和salicylate在一定程度上被它们对IKK-β的特定抑制介导,从而防止涉及炎症反应发病机理的NF-κB基因激活。[2]在大鼠神经元原代培养物和海马脑片中,Aspirin对兴奋性氨基酸谷氨酸引发的神经毒性具有保护作用。[3]人脐静脉内皮细胞(HUVEC)和中性粒细胞[多形核白细胞(PMN)]共培养时,Aspirin引起一种先前未识别的类花生酸跨细胞生物合成。Aspirin引起乙酰化的PGHS-2和5-脂氧合酶相互作用形成一类独特的类花生酸。[4] Aspirin治疗抑制IRS-1在Ser307上的磷酸化和JNK,c-Jun磷酸化,以及IkappaBalpha在肿瘤坏死因子(TNF)-α处理的3T3-L1和Hep G2细胞中的降解。Aspirin治疗抑制Akt磷酸化和rapamycin (但不作用于细胞外调节激酶或PKCzeta)的哺乳动物靶点对TNF-α的响应。在TNF-α预处理的3T3-L1脂肪细胞,Aspirin减少胰岛素诱导的葡萄糖摄取。[5]
实验图片 检测方法 检测指标 实验图片 PMID
Western blot MCL-1 p-AKT / AKT / p-ERK / ERK p-AMPKα / AMPKα / p-ACC / ACC SHH / SMO / GLI1 / Bcl-2 / Foxm1 26918349
Growth inhibition assay Cell proliferation Cell viability 28446712
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06197009 Not yet recruiting
Axial Spondyloarthritis
Sinocelltech Ltd.
July 1 2024 Phase 2
NCT05861128 Not yet recruiting
Ankylosing Spondylitis
Suzhou Zelgen Biopharmaceuticals Co.Ltd
June 2024 Phase 3
NCT05868525 Recruiting
Blunt Cerebrovascular Injury
Loma Linda University
April 2024 Phase 4
NCT05960864 Not yet recruiting
Ankylosing Spondylitis (AS) / Radiographic Axial SpA (r-axSpA)|Non-radiographic Axial Spondyloarthritis (Nr-axSpA)|Axial Psoriatic Arthritis (axPsA)|Acute Anterior Uveitis (AAU)|Crohn Disease (CD)|Ulcerative Colitis (UC)|Reactive Arthritis (ReA)
Southwest Hospital China
February 2024 --
NCT06066983 Recruiting
Autism Spectrum Disorder|Anxiety Disorders
Hugo W. Moser Research Institute at Kennedy Krieger Inc.
January 2024 Not Applicable

化学信息&溶解度

分子量 180.16 分子式

C9H8O4

CAS号 50-78-2 SDF Download Aspirin SDF
Smiles CC(=O)OC1=CC=CC=C1C(=O)O
储存条件(自收到货起)

体外溶解度
批次:

DMSO : 36 mg/mL ( 199.82 mM; DMSO吸湿会降低化合物溶解度,请使用新开封DMSO)

Ethanol : 36 mg/mL

Water : Insoluble

摩尔浓度计算器

体内溶解度
批次:

现配现用,请按从左到右的顺序依次添加,澄清后再加入下一溶剂

动物体内配方计算器

实验计算

摩尔浓度计算器

质量 浓度 体积 分子量

动物体内配方计算器(澄清溶液)

第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)

mg/kg g μL

第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系Selleck为您提供正确的澄清溶液配方)

% DMSO % % Tween 80 % ddH2O
%DMSO %

计算结果:

工作液浓度: mg/ml;

DMSO母液配制方法: mg 药物溶于μL DMSO溶液(母液浓度mg/mL,:如该浓度超过该批次药物DMSO溶解度,请先联系Selleck);

体内配方配制方法:μL DMSO母液,加入μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入μL ddH2O,混匀澄清。

体内配方配制方法:μL DMSO母液,加入μL Corn oil,混匀澄清。

注意:1. 首先保证母液是澄清的;
2.一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。

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