| CAS NO: | 103-90-2 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 10g | 电议 |
| 25g | 电议 |
| 50g | 电议 |
| 100g | 电议 |
| 200g | 电议 |
| 500g | 电议 |
| Molecular Weight (MW) | 151.16 |
|---|---|
| Formula | C8H9NO2 |
| CAS No. | 103-90-2 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 30 mg/mL (198.5 mM) |
| Water: 13 mg/mL (86.0 mM) | |
| Ethanol: 30 mg/mL (198.5 mM) | |
| Other info | Chemical Name: Acetamide, N-(4-hydroxyphenyl)- InChi Key: RZVAJINKPMORJF-UHFFFAOYSA-N InChi Code: InChI=1S/C8H9NO2/c1-6(10)9-7-2-4-8(11)5-3-7/h2-5,11H,1H3,(H,9,10) SMILES Code: CC(NC1=CC=C(O)C=C1)=O |
| Synonyms | 4'-Hydroxyacetanilide; 4-Acetamidophenol; Paracetamol, Tylenol; Acetaminophen; Tylenol; 4-Acetamidophenol; APAP; 4'-Hydroxyacetanilide; NSC 3991; NSC 109028; Paracetamol. |
| In Vitro | In vitro activity: Acetaminophen is functionally active as a selective COX-2 inhibitor, exhibiting a 4.4-fold specificity towards COX-2 (IC50 is 113.7 μM for COX-1 and IC50 of 25.8 μM for COX-2). Acetaminophen demonstrates selective toxicity towards melanoma cells, such as SK-MEL-28, MeWo, SK-MEL-5, B16-F0 and B16-F10, with IC50 of 100 μM, and shows no significant toxicity towards BJ, Saos-2, SW-620, and PC-3 non-melanoma cells. Acetaminophen induces the apoptosis of SK-MEL-28 cells through intracellular GSH depletion, ROS formation and induced mitochondrial toxicity, which can be enhanced by Dicoumarol and 1-bromoheptane and allayed by Ascorbic acid, GSH, Trifluoperazine and cyclosporin A. Acetaminophen significantly inhibits the activity of COX-2 which has been induced by diclofenac than that induced by bacterial lipopolysaccharide in murine J774.2 macrophages. However in the presence of diclofenac, LPS-induced COX-2 activity is inhibited by acetaminophen to the same extent as the COX-2 activity induced by diclofenac alone. Kinase Assay: For COX-1 assay, aliquots of human whole blood drawn from healthy volunteers without anticoagulant are transferred to glass tubes containing Acetaminophen or DMSO, serum is separated by centrifugation after clotting, and serum TxB2 levels are determined. For COX-2 assay, aliquots of heparinized whole blood are incubated with LPS (10 μg/mL) and aspirin (10 μg/mL), plus Acetaminophen or DMSO for 24 hours at 37 °C, plasma is separated by centrifugation, and PGE2 levels are determined subsequently. The degree of COX-1 or COX-2 inhibition is calculated as the percentage change of plasma eicosanoid (TxB2 for COX-1 and PGE2 for COX-2).Concentration response curves are fitted by a sigmoidal regression with variable slope for both enzymatic assays, and the 50% inhibitory concentration (IC50) values are derived by using of PRISM Version 3.0. Cell Assay: Cells are exposed to Acetaminophen for 48 hours. Cell viability is determined by the trypan blue exclusion method. Intracellular GSH is measured by recording the disulfide, GS-TNB and 5-thio-nitrobenzoic acid (TNB), the yellow colored compound formed by the reaction between GSH with DTNB. |
|---|---|
| In Vivo | Overdose of Acetaminophen leads to liver toxicity, which is well correlated with liver protein arylation by Acetaminophen metabolites. Administration of Acetaminophen (1 g/kg) in male Long Evans Hooded rats causes damage to centrilobular regions of the liver, increases serum transaminase levels significantly within 6 hours of treatment, reaching a maximum at 24 hours. This can be correlated to expression of the inducible nitric oxide synthase (iNOS) protein. |
| Animal model | B6C3F1 mice |
| Formulation & Dosage | Dissolved in DMSO and diluted to a final concentration 20 mg/mL in aqueous solutions; 350 mg/kg; p.o. administration |
| References | FASEB J. 2008 Feb;22(2):383-90; J Pharm Sci. 2009 Apr;98(4):1409-25; J Biol Chem. 1998 Jul 10;273(28):17940-53; Hepatology. 1998 Mar;27(3):748-54. |
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