Acetaminophen (Paracetamol) is a selective cyclooxygenase-2 (COX-2) inhibitor with anIC₅₀of 25.8 μM; is a widely used antipyretic and analgesic agent^[1][2][3]. Acetaminophen is a potenthepatic N-acetyltransferase 2 (NAT2)inhibitor^[4].

In vitro, acetaminophen elicites a 4.4-fold selectivity toward COX-2 inhibition (IC₅₀113.7 μM for COX-1; IC₅₀25.8 μM for COX-2). Following oral administration of the drug, maximalex vivoinhibitions are 56% (COX-1) and 83% (COX-2). Acetaminophen plasma concentrations remaine above thein vitroIC₅₀for COX-2 for at least 5 h postadministration.Ex vivoIC₅₀values (COX-1: 105.2 μM; COX-2: 26.3 μM) of acetaminophen compared favorably with itsin vitroIC₅₀values. 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].

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].

151.16

Solid

C₈H₉NO₂

103-90-2

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

Room temperature in continental US; may vary elsewhere.

*该产品在溶液状态不稳定，建议您现用现配，即刻使用。

DMSO : 250 mg/mL(1653.88 mM;Need ultrasonic)

H₂O : 10 mg/mL(66.16 mM;Need ultrasonic)

请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液；该产品在溶液状态不稳定，建议您现用现配，即刻使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 0.5%CMC-Na/saline water

  Solubility: 10 mg/mL (66.16 mM); Suspended solution; Need ultrasonic
• 2.

  请依序添加每种溶剂： saline  0.5%Tween-80

  Solubility: 10 mg/mL (66.16 mM); Clear solution; Need ultrasonic
• 3.

  请依序添加每种溶剂： PBS

  Solubility: 6.67 mg/mL (44.13 mM); Clear solution; Need ultrasonic
• 4.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.08 mg/mL (13.76 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (13.76 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 5.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: ≥ 2.08 mg/mL (13.76 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (13.76 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 6.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.08 mg/mL (13.76 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (13.76 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。