lithium O-acetylsalicylate

Names

[ CAS No. ]:
552-98-7

[ Name ]:
lithium O-acetylsalicylate

[Synonym ]:
lithium 2-acetoxybenzoate
EINECS 209-029-5
lithium O-acetylsalicylate
Lithium acetylsalicylate
2-acetoxy-benzoic acid,lithium-salt
2-Acetoxy-benzoesaeure,Lithium-Verbindung
2-Acetoxy-benzoesaeure,Lithium-Salz

Biological Activity

[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[1][2][3][4][5][6].

[Related Catalog]:

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Research Areas >> Cardiovascular Disease

Research Areas >> Infection

Signaling Pathways >> Autophagy >> Autophagy

Signaling Pathways >> Apoptosis >> Caspase

Signaling Pathways >> MAPK/ERK Pathway >> p38 MAPK

Research Areas >> Inflammation/Immunology

Signaling Pathways >> Immunology/Inflammation >> COX

Signaling Pathways >> Autophagy >> Mitophagy

Research Areas >> Metabolic Disease

[Target]

COX-1

COX-2

[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]. Animal Model: Male albino Charles River rats (200-250 g, 8 animals/group, fever was induced by 20 ml/kg of a 20 % aqueous suspension of brewer’s yeast which was injected SC in the back below the nape of the neck)[7] Dosage: 5, 25, 50, 100 and 150 mg/kg Administration: PO, once Result: Produced a statistically significant decrease of 0.23 ℃ at 15 min post-drug at the dose of 150 mg/kg. Antipyretic effect gradually increased in magnitude until a peak effect of 1.96 ℃ was reached at 120 min post-drug. The ED50 of aspirin was found to be 10.3 mg/kg with confidence limits of 1.8-23.0 mg/kg. The antipyretic response to aspirin is dependent on the dose of the compound administered.

[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.

[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.

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

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

[5]. Burch JW, et al. Inhibition of platelet prostaglandin synthetase by oral aspirin. J Clin Invest. 1978 Feb;61(2):314-9.

[6]. Elwood PC, et al. Aspirin, salicylates, and cancer. Lancet. 2009 Apr 11;373(9671):1301-9.

[7]. Loux JJ, DePalma PD, Yankell SL. Antipyretic testing of aspirin in rats. Toxicol Appl Pharmacol. 1972 Aug;22(4):672-5.