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Aspirin

MCE China：Aspirin

Brand：MedChemExpress (MCE)

Cat. No.HY-14654

CAS：50-78-2

Synonyms：Acetylsalicylic Acid; ASA

Purity：99.82%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year

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

Description：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.

In Vitro：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].

In Vivo：Aspirin can be used to induce gastrointestinal ulcer models[8]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } 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): /

IC50 & Target：COX-1 27.75 μM (IC50) COX-2 1.17 mM (IC50)

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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]

[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.