Acetaminophen
CAS No. : 103-90-2
(Synonyms: Paracetamol; 4-Acetamidophenol; 4'-Hydroxyacetanilide)
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| Cat. No. : | HY-66005 |
| M.Wt: | 151.16 |
| Formula: | C8H9NO2 |
| Purity: | >98 % |
| Solubility: | DMSO : 250 mg/mL (ultrasonic);H2O : 10 mg/mL (ultrasonic) |
Acetaminophen (Paracetamol) is a selective cyclooxygenase-2 (COX-2) inhibitor with an IC50 of 25.8 μM; is a widely used antipyretic and analgesic agent.[1][2][3]. Acetaminophen is a potent hepatic N-acetyltransferase 2 (NAT2) inhibitor[4]. Acetaminophen induces ferroptosis and leads to acute liver injury in mice model[5].
IC50 & Target:IC50: 113.7 μM (COX-1), 25.8 μM (COX-2)[1]
In Vitro:In vitro, acetaminophen elicites a 4.4-fold selectivity toward COX-2 inhibition (IC50 113.7 μM for COX-1; IC50 25.8 μM for COX-2). Following oral administration of the drug, maximal ex vivo inhibitions are 56% (COX-1) and 83% (COX-2). Acetaminophen plasma concentrations remaine above the in vitro IC50 for COX-2 for at least 5 h postadministration. Ex vivo IC50 values (COX-1: 105.2 μM; COX-2: 26.3 μM) of acetaminophen compared favorably with its in vitro IC50 values. In contrast to previous concepts, acetaminophen inhibited COX-2 by more than 80%, i.e., to a degree comparable to nonsteroidal antiinflammatory drugs (NSAIDs) and selective COX-2 inhibitors. However, a >95% COX-1 blockade relevant for suppression of platelet function is not achieved[1]. MTT assay shows that Acetaminophen (APAP) in a dose of 50 mM significantly (p<0.001) reduces cell viability to 61.5±6.65%. Interestingly, the significant (p<0.01) increase in cell viability to 79.7±2.47% is observed in the Acetaminophen/HV110 co-treated cells, compared to Acetaminophen treated cells[2].
In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
Administering Acetaminophen (250 mg/kg, orally; once) to the mice causes significant liver damage and necrosis of cells as evidenced by the elevated serum hepatic enzymes alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transferase (γGT) compared with normal group[3].
Acetaminophen (300 mg/kg, i.p., single dose) induces ferroptosis, by enhancing levels of Fe2+ and malondialdehyde (MDA), and decreasing levels of glutathione (GSH) and glutathione peroxidase 4 (GPX4), and induces acut eliver injury in C57BL/6J mice model[5].
Administration: 250 mg/kg • p.o. • single dose
(2) Acetaminophen was dissolved in saline that contained 0.1% Tween 80 (HY-Y1891) solution.
Histopathological changes: Severe necrotic areas were visible in the APAP-treated group, characterized by large areas of necrosis with centrilobular vein congestion, presence of a dense and/or moderate polymorphonuclear infiltrate, and vacuolization of hepatocytes.
Biochemical changes: Caused significant liver damage and necrosis of cells as evidenced by the elevated serum hepatic enzymes ALT, AST, ALP, and γGT.
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