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Aspirin

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Chemical Structure| 50-78-2 同义名 : 阿司匹林;邻乙酰水杨酸;2-乙酰氧基苯甲酸 ;Acetylsalicylic Acid;ASA;Claradin;Acetylin;NSC 406186;NSC 27223
CAS号 : 50-78-2
货号 : A1457229
分子式 : C9H8O4
纯度 : 99%
分子量 : 180.157
MDL号 : MFCD00002430
存储条件：

粉末 Sealed in dry,Room Temperature

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(582.82 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
靶点

  • COX-1
描述 Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL[1]. Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever[2]. Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation. Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer. Aspirin at suprapharmacological concentrations inhibits NF-kappaB-mediated gene transcription and protects tissue from injury[3]. Low-dose aspirin therapy (75-162 mg) is reasonable for patients with diabetes mellitus and a 10-year risk of cardiovascular events >10%[4]. Among those with suspected evolving MI (myocardial infarction), aspirin significantly reduces the risk of reinfarction, stroke, and vascular mortality[5].
细胞研究
细胞系 浓度 检测类型 检测时间 活动说明 数据源
human AGS cells 15-60 μmol/L Function assay 12 h Inhibition of Escherichia coli-stimulated IL-8 production in human AGS cells at 15 to 60 umol/L after 12 hrs by ELISA 20153183
human HCT116 cells 1 mM Function assay 6 h Inhibition of TNF-alpha-induced NF-kappaB activation in human HCT116 cells at 1 mM after 6 hrs by luciferase reporter gene assay 22154834
human MDA-MB-231 cells 100 μM Function assay 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
临床研究
NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT02326350 Acute Respiratory Distress Syn... 展开 >>drome 收起 << Phase 2 Enrolling by invitation July 2017 -
NCT01784159 Sepsis Phase 2 Active, not recruiting January 2019 Brazil ... 展开 >> Hospital São Paulo São Paulo, Brazil, 04024002 收起 <<
NCT00178464 - Completed - -
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

5.55mL

1.11mL

0.56mL

27.75mL

5.55mL

2.78mL

55.51mL

11.10mL

5.55mL
参考文献

[1]Yin MJ, Yamamoto Y, et al. The anti-inflammatory agents aspirin and salicylate inhibit the activity of I(kappa)B kinase-beta. Nature. 1998 Nov 5;396(6706):77-80.

[2]Kopp E, Ghosh S. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12;265(5174):956-9.

[3]Mitchell JA, Akarasereenont P, Thiemermann C, Flower RJ, Vane JR. Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase. Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):11693-7

[4]Vane JR, Botting RM. The mechanism of action of aspirin. Thromb Res. 2003 Jun 15;110(5-6):255-8

[5]Wu KK. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3(2):107-12

[6]Pignone M, Williams CD. Aspirin for primary prevention of cardiovascular disease in diabetes mellitus. Nat Rev Endocrinol. 2010 Nov;6(11):619-28

[7]Hennekens CH. Aspirin in chronic cardiovascular disease and acute myocardial infarction. Clin Cardiol. 1990 Mar;Suppl 5:V62-6; discussion V67-72