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MedChemExpressModel Aspirin lithium - 552-98-7

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Aspirin (Acetylsalicylic Acid) lithium 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 lithium induces apoptosis. Aspirin lithium inhibits the activation of NF-κB. Aspirin lithium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis[1][2][3][4][5][6].
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Aspirin lithium

MCE China:Aspirin lithium

Brand:MedChemExpress (MCE)

Cat. No.HY-14654A

CAS:552-98-7

Synonyms:Acetylsalicylic Acid lithium; ASA lithium

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

Shipping:Room temperature in continental US; may vary elsewhere.

Description:Aspirin (Acetylsalicylic Acid) lithium 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 lithium induces apoptosis. Aspirin lithium inhibits the activation of NF-κB. Aspirin lithium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis.

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

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

IC50 & Target:COX-1 COX-2

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References:

[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]

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