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    Aspirin (Acetylsalicylic Acid; ASA)
    Aspirin (Acetylsalicylic Acid; ASA)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1062
    CAS #: 50-78-2 Purity ≥98%

    Description: Aspirin (Acetylsalicylic acid; ASA; Acetylin; Claradin), a widely used analgesic and a salicylate analog, is a non-selective and covalent/irreversible inhibitor of COX1 and COX2 enzymes with a broad range of biological activities such as anti-inflammatory and pain relieving effects. It has been used to relieve minor aches and pains as an analgesic agent, to reduce fever as an antipyretic agent, and to treat inflammation conditions as an anti-inflammatory drug. Aspirin also shows potent anti-proliferative activity in vitro against many cancer cell lines such as ovarian cell harboring COX-1 by acting as histone deacetylase inhibitors to upregulate the cell cycle arrest protein p21.

    References: Science. 1994 Aug 12;265(5174):956-9; Nature. 1998 Nov 5;396(6706):77-80.

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    Molecular Weight (MW)180.16 
    FormulaC9H8O4 
    CAS No.50-78-2 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 36 mg/mL (199.8 mM) 
    Water: <1 mg/mL
    Ethanol: 36 mg/mL (199.8 mM) 
    Solubility (In vivo)4% DMSO+PBS: 10mg/mL
    SynonymsAcetylsalicylic acid; Acetylin; Claradin


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    In Vitro

    In vitro activity: 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.


    Cell Assay: Chondrocytes are isolated from articular cartilage of donors with no articular disease. Unstimulated and interleukin 1 (IL-1) stimulated chondrocytes are used as models to study the effects of drugs on COX-1 and COX-2. Cells are incubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in each sample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by different concentrations of the test substance by linear regression analysis.

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    References

    Science. 1994 Aug 12;265(5174):956-9; Nature. 1998 Nov 5;396(6706):77-80. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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