Catalog No.S3017 Synonyms: Acetylsalicylic acid
Molecular Weight(MW): 180.16
Aspirin is a salicylate, and irreversible COX1 and COX2 inhibitor, used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication.
Purity & Quality Control
Choose Selective COX Inhibitors
|Description||Aspirin is a salicylate, and irreversible COX1 and COX2 inhibitor, used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication.|
Aspirin inhibits the activation of NF-kappa B, thus prevents the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B is retained in the cytosol. Aspirin also inhibits NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.  Aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response.  Aspirin is protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices.  Aspirin triggers transcellular biosynthesis of a previously unrecognized class of eicosanoidsduring coincubations of human umbilical vein endothelial cells (HUVEC) and neutrophils [polymorphonuclear leukocytes (PMN)]. Aspirin evokes a unique class of eicosanoids formed by acetylated PGHS-2 and 5-lipoxygenase interactions.  Aspirin treatment inhibits the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha in 3T3-L1 and Hep G2 cells treated with tumor necrosis factor (TNF)-alpha. Aspirin treatment inhibits phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha. Aspirin rescues insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. 
-  Kopp E, et al. Science, 1994, 265(5174), 956-959.
-  Yin MJ, et al. Nature, 1998, 396(6706), 77-80.
-  Grilli M, et al. Science, 1996, 274(5291), 1383-1385.
|In vitro||DMSO||36 mg/mL (199.82 mM)|
|Ethanol||36 mg/mL (199.82 mM)|
|In vivo||Add solvents to the product individually and in order:
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02007837||Not yet recruiting||Pregnancy Induced Hypertension||UMC Utrecht|Ghana Health Services|University of Ghana||January 2018||Phase 3|
|NCT02735902||Not yet recruiting||Transcatheter Aortic Valve Replacement||Centre Hospitalier Universitaire de Nīmes|Medtronic||April 2017||Phase 4|
|NCT02797548||Not yet recruiting||Antiplatelet Drugs||Seung-Jung Park|CardioVascular Research Foundation, Korea|Asan Medical Center||March 2017||Phase 4|
|NCT02666742||Not yet recruiting||Ventricular Tachycardia||Dhanunjaya Lakkireddy, MD, FACC|Bristol-Myers Squibb|University of Kansas Medical Center||February 2017||Phase 4|
|NCT03023020||Not yet recruiting||High Bleeding Risk|Coronary Artery Disease|PCI||ECRI bv|Cardialysis B.V.|European Cardiovascular Research Center|University of Bern|Terumo Medical Corporation||February 2017||--|
|NCT02984384||Not yet recruiting||Blood Clot|Trauma||Major Extremity Trauma Research Consortium|Patient-Centered Outcomes Research Institute||February 2017||Phase 3|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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