Aspirin  (Synonyms: Acetylsalicylic Acid; ASA)

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^{[1][2][3][4][5][6]}.

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].

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

Aspirin can be used to induce gastrointestinal ulcer models^[8].

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

180.16

C₉H₈O₄

50-78-2

Solid

White to off-white

OC(C1=C(OC(C)=O)C=CC=C1)=O

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [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.