AspirinAspirin
MedChemExpress (MCE)
HY-14654
50-78-2
Acetylsalicylic Acid
ASA
99.82%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Aspirin (Acetylsalicylic Acid) is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin induces apoptosis. Aspirin inhibits the activation of NF-κB. Aspirin also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis.
Aspirin inhibits COX-1 and COX-2 in human articular chondrocytes, with IC50 values of 3.57 μM and 29.3 μM, respectively[2]. Aspirin acetylates serine-530 of COX-1, thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation[3]. Aspirin inhibits 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[3]. Aspirin inhibits NF-κB-dependent transcription from the lgκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells[4]. Aspirin induces apoptosis by the activation of caspases, the activation of p38 MAP kinase, release of mitochondrial cytochrome c, and activation of the ceramide pathway[6].
Aspirin can be used to induce gastrointestinal ulcer models[8]. .f12{ font-size: 12px
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} Induction of gastric Ulcer Model[8] Background Aspirin inhibits the synthesis of endogenous prostaglandins (PGs) in animals. Aspirin can also lyse mucosal epithelial cells phospholipids, resulting in increased mucosal permeability. Specific Mmodeling Methods Mice: Albino • male • 6-week-old Administration: 500 mg/kg • oral • single dose Note Modeling Indicators Behavior Observation: Caused erosionof the surface epithelial cell. Resulted in a decrease in themucosal thickness. Induced ulcer without COX-1reaction. Correlated Product(s): / Opposite Product(s): /
COX-1 27.75 μM (IC50) COX-2 1.17 mM (IC50)
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[1]. Mitchell JA, et al. Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and induciblecyclooxygenase. Proc Natl Acad Sci U S A. 1993 Dec 15
90(24):11693-7. [Content Brief]
[2]. Blanco FJ, et al. Effect of antiinflammatory drugs on COX-1 and COX-2 activity in human articular chondrocytes. J Rheumatol. 1999 Jun
26(6):1366-73. [Content Brief]
[3]. Wu KK, et al. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May
3(2):107-12. [Content Brief]
[4]. Kopp E, et al. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12
265(5174):956-9. [Content Brief]
[5]. Burch JW, et al. Inhibition of platelet prostaglandin synthetase by oral aspirin. J Clin Invest. 1978 Feb
61(2):314-9. [Content Brief]
[6]. Elwood PC, et al. Aspirin, salicylates, and cancer. Lancet. 2009 Apr 11
373(9671):1301-9. [Content Brief]
[7]. Loux JJ, DePalma PD, Yankell SL. Antipyretic testing of aspirin in rats. Toxicol Appl Pharmacol. 1972 Aug
22(4):672-5. [Content Brief]
[8]. Yomna I Mahmoud, et al. Spirulina ameliorates aspirin-induced gastric ulcer in albino mice by alleviating oxidative stress and inflammation. Biomed Pharmacother. 2019. [Content Brief]
[9]. Zhongzhi Wang, et al. Protective Effects of Ginger against Aspirin-Induced Gastric Ulcers in Rats. Yonago Acta Med. 2011, 54, 1.
