Aspirin calcium  (Synonyms: Acetylsalicylic acid calcium; ASA calcium)

Aspirin calcium 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 calcium induces apoptosis. Aspirin calcium inhibits the activation of NF-κB. Aspirin calcium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis^{[1][2][3][4][5][6]}.

Aspirin calcium inhibits COX-1 and COX-2 in human articular chondrocytes, with IC₅₀ values of 3.57 μM and 29.3 μM, respectively^[2].
Aspirin calcium acetylates serine-530 of COX-1, thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation^[3].
Aspirin calcium 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 calcium 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 calcium 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.

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Aspirin (5-150 mg/kg, PO, once) calcium shows significant antipyretic activity in adult yeast-fevered male rats^[7].
Aspirin calcium 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.

200.20

C₉H₇O₄.1/2Ca

69-46-5

O=C(C1=C(OC(C)=O)C=CC=C1)[O-].[0.5].[Ca+2]

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.