For research use only.
Catalog No.S3017 Synonyms: Acetylsalicylic acid
CAS No. 50-78-2
Aspirin (Acetylsalicylic acid) 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 induces autophagy and stimulates mitophagy.
Selleck's Aspirin has been cited by 9 publications
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|Description||Aspirin (Acetylsalicylic acid) 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 induces autophagy and stimulates mitophagy.|
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)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
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* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
In vivo Formulation Calculator (Clear solution)
|Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)|
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|% DMSO % % Tween 80 % ddH2O|
Working concentration： mg/ml；
Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL，)
Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH2O，mix and clarify.
1.Please make sure the liquid is clear before adding the next solvent.
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04356326||Not yet recruiting||Drug: Aspirin 150 mg|Drug: Placebo||Chronic Hypertension Complicating Pregnancy|Pre-Eclampsia|Intrauterine Growth Restriction|Aspirin|Perinatal Death|Placental Abruption||Centre Hospitalier Intercommunal Creteil||January 2021||Phase 3|
|NCT04308551||Not yet recruiting||Drug: Indobufen|Drug: Aspirin||Stable Coronary Heart Disease||Henan Institute of Cardiovascular Epidemiology||October 30 2020||Not Applicable|
|NCT03615846||Not yet recruiting||--||Platelet Aggregation|Coronary Artery Disease||Accriva Diagnostics||October 20 2020||--|
|NCT04442256||Recruiting||Drug: Dupilumab||AERD - Aspirin Exacerbated Respiratory Disease||Medical University of Vienna||June 1 2020||Phase 4|
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