. . . . . . . . . . . . . . "1 to 4 hours"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . " "@en . . . . "For temporary relief of fever, minor aches, and pains."@en . . . . . "103-90-2"@en . . . . . . . . . . . . . . . . "Tylenol"@en . "N-acetyl-p-aminophenol"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "# Kis B, Snipes JA, Busija DW: Acetaminophen and the cyclooxygenase-3 puzzle: sorting out facts, fictions, and uncertainties. J Pharmacol Exp Ther. 2005 Oct;315(1):1-7. Epub 2005 May 6. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15879007 # Aronoff DM, Oates JA, Boutaud O: New insights into the mechanism of action of acetaminophen: Its clinical pharmacologic characteristics reflect its inhibition of the two prostaglandin H2 synthases. Clin Pharmacol Ther. 2006 Jan;79(1):9-19. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/16413237 # Bertolini A, Ferrari A, Ottani A, Guerzoni S, Tacchi R, Leone S: Paracetamol: new vistas of an old drug. CNS Drug Rev. 2006 Fall-Winter;12(3-4):250-75. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/17227290 # Graham GG, Scott KF: Mechanism of action of paracetamol. Am J Ther. 2005 Jan-Feb;12(1):46-55. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/15662292 # Ohki S, Ogino N, Yamamoto S, Hayaishi O: Prostaglandin hydroperoxidase, an integral part of prostaglandin endoperoxide synthetase from bovine vesicular gland microsomes. J Biol Chem. 1979 Feb 10;254(3):829-36. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/104998 # Bertolini A, Ferrari A, Ottani A, Guerzoni S, Tacchi R, Leone S: Paracetamol: new vistas of an old drug. CNS Drug Rev. 2006 Fall-Winter;12(3-4):250-75. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/17227290 # Chandrasekharan NV, Dai H, Roos KL, Evanson NK, Tomsik J, Elton TS, Simmons DL: COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: cloning, structure, and expression. Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13926-31. Epub 2002 Sep 19. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/12242329 # Adjei AA, Gaedigk A, Simon SD, Weinshilboum RM, Leeder JS: Interindividual variability in acetaminophen sulfation by human fetal liver: implications for pharmacogenetic investigations of drug-induced birth defects. Birth Defects Res A Clin Mol Teratol. 2008 Mar;82(3):155-65. doi: 10.1002/bdra.20535. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/18232020 # Hazai E, Vereczkey L, Monostory K: Reduction of toxic metabolite formation of acetaminophen. Biochem Biophys Res Commun. 2002 Mar 8;291(4):1089-94. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/11866476"@en . . . . . . . "Approximately 80% of acetaminophen is excreted in the urine after conjugation and about 3% is excreted unchanged."@en . . . "Avoid alcohol (may increase risk of hepatotoxicity)."@en . . . . . . . . . . . . . . . . . . "25%"@en . "p-acetamidophenol"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "p-acetaminophenol"@en . . . "Acetaminophen"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "4-(Acetylamino)phenol"@en . . . . . "Take without regard to meals."@en . . . . "Paracetamol"@en . . "Acetaminofen"@en . . . "Jeffrey L. Finnan, Rudolph E. Lisa, Douglass N. Schmidt, \"Process for preparing spray dried acetaminophen powder and the powder prepared thereby.\" U.S. Patent US4710519, issued October, 1975."@en . "Acetaminophen, also known as paracetamol, is commonly used for its analgesic and antipyretic effects. Its therapeutic effects are similar to salicylates, but it lacks anti-inflammatory, antiplatelet, and gastric ulcerative effects. "@en . "Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation. "@en . . . . "p-Acetylaminophenol"@en . . . . . . . . . . . . . . "Oral, mouse: LD50 = 338 mg/kg; Oral, rat: LD50 = 1944 mg/kg. Acetaminophen is metabolized primarily in the liver, where most of it is converted to inactive compounds by conjugation with glucuronic acid and, to a lesser extent, sulfuric acid. Conjugates are then excreted by the kidneys. Only a small portion is excreted in unchanged in urine or oxidized via the hepatic cytochrome P450 enzyme system (CYP2E1). Metabolism via CYP2E1 produces a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). The toxic effects of acetaminophen are due to NAPQI, not acetaminophen itself nor any of the major metabolites. At therapeutic doses, NAPQI reacts with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is excreted by the kidneys. High doses of acetaminophen may cause glutathione depletion, accumulation of NAPQI and hepatic necrosis. The maximum daily dose of acetaminophen is 4 g. Liver failure has been observed at doses as low as 6 g per day. As such, the maximum daily and single dose of acetaminophen is currently being reviewed in some countries. N-acetyl-cysteine, a precursor of glutathione, may be administered in the event of acetaminophen toxicity. "@en . . . . . . . . . "4'-hydroxyacetanilide"@en . "APAP"@en . "Rapid and almost complete"@en . "p-hydroxyacetanilide"@en . . . . . . . . . . . . "p-hydroxyphenolacetamide"@en . "Acetaminophene"@en . "Humans and other mammals"@en . . . . . . . "Panadol"@en . . "Acenol"@en . . . . . "4-acetamidophenol"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "Paracetamolum"@en . "approved"@en . . . . . . . . . . . . . . . "Acetaminophen"@en . . . . . . . . . . .