Acetaminophen  (Synonyms: 对乙酰氨基酚; Paracetamol; 4-Acetamidophenol; 4'-Hydroxyacetanilide)

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].

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Administering Acetaminophen (250 mg/kg, orally) to the mice causes significant (p<0.001) 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. Conversely, effects of pretreatment with different doses of citral (125, 250, and 500 mg/kg) exhibited a significant (p<0.05) decrease in serum activities of ALT (91.79%, 93.07%, and 95.61%, resp.), AST (93.40%, 91.89%, and 96.52%, resp.), ALP (39.29%, 37.07%, and 59.80%, resp.), and γGT (92.83%, 91.59%, and 93.0%, resp.), when compared to the Acetaminophen group. Similar results were found in pretreatment with SLM on the activity of ALT (95.90%), AST (95.03%), ALP (70.52%), and γGT (92.69%)^[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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

151.16

C₈H₉NO₂

103-90-2

固体

White to off-white

对乙酰氨基酚；乙酰氨基酚；扑热息痛；退热净；醋氨酚；对醋氨酚；索密痛；乙酰氨基苯酚；二醋洛尔

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Store at room temperature 3 years

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• [1]. Hinz, B, et al. Acetaminophen (paracetamol) is a selective cyclooxygenase-2 inhibitor in man. FASEB J, 2008. 22(2): p. 383-90.  [Content Brief]

  [2]. Miroslav Dinić, et al. Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment ofAcetaminophen Hepatotoxicity. Front Microbiol. 2017 Apr 6;8:594.  [Content Brief]

  [3]. Uchida NS, et al. Hepatoprotective Effect of Citral on Acetaminophen-Induced Liver Toxicity in Mice. Evid Based Complement Alternat Med. 2017;2017:1796209.  [Content Brief]

  [4]. Rothen JP, et al. Acetaminophen is an inhibitor of hepatic N-acetyltransferase 2 in vitro and in vivo. Pharmacogenetics. 1998 Dec;8(6):553-9.  [Content Brief]

  [5]. An Y, et al., Abietic acid inhibits acetaminophen-induced liver injury by alleviating inflammation and ferroptosis through regulating Nrf2/HO-1 axis. Int Immunopharmacol. 2023 May;118:110029.  [Content Brief]