Acetaminophen

Research use only, not for human use.

A well-known analgesic and antipyretic agent that selectively inhibits COX activities in the brain.

A well-known analgesic and antipyretic agent that selectively inhibits COX activities in the brain; might modulate the endogenous cannabinoid system in the brain through paracetamol's metabolite, AM404; is typically used for mild to moderate pain.Pain Approved(In Vitro):n 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. 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.(In Vivo):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%).

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. 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.

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Paracetamol | 4-Acetamidophenol | APAP

Chromatin/Epigenetic

COX

COX-1|COX-2

Neurological Disease

Pain

103-90-2

151.1626

C8H9NO2

>98% (HPLC)

10 mM in DMSO

CC(NC1=CC=C(O)C=C1)=O

Acetamide, N-(4-hydroxyphenyl)-

(-20℃)

With Ice Pack

≥ 2 years