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
CAS: 50-78-2
产品质控
Aspirin相关产品
相关信号通路图
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 | ||
| 点击查看更多细胞系数据 | |||||
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。 | ||
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| 靶点 |
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| 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] | |||
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| 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 |
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26918349 | |
| Growth inhibition assay | Cell proliferation Cell viability |
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28446712 | |
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| 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 |
September 2024 | -- |
| NCT05868525 | Recruiting | Blunt Cerebrovascular Injury |
Loma Linda University |
July 2024 | Phase 4 |
| NCT06197009 | Not yet recruiting | Axial Spondyloarthritis |
Sinocelltech Ltd. |
July 1 2024 | Phase 2 |
| NCT06378398 | Not yet recruiting | Colorectal Neoplasia |
University of Michigan Rogel Cancer Center|National Cancer Institute (NCI) |
May 2024 | Early Phase 1 |
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) | |||
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体外溶解度 |
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 (199.82 mM) Water : Insoluble |
摩尔浓度计算器 |
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体内溶解度 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
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
只
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，注：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：取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：取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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