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- NCIT_C38970 NCIT_NHC0 "C38970" @default.
- NCIT_C38970 NCIT_P106 "Functional Concept" @default.
- NCIT_C38970 NCIT_P108 "Acetaminophen Pathway" @default.
- NCIT_C38970 NCIT_P207 "C1510757" @default.
- NCIT_C38970 NCIT_P216 "h_AcetaminophenPathway" @default.
- NCIT_C38970 NCIT_P325 "Acetaminophen is one of the world's most commonly used drugs, used for the treatment of pain and fever. Like other NSAIDs (non-steroidal anti-inflammatory drugs), acetaminophen has a unique activity profile based in part on its action at its molecular targets, the cyclooxygenase enzymes that produce prostaglandins responsible for pain, fever and inflammation. Until very recently, only two Cox enzymes, Cox-1 and Cox-2, were known to be targets of NSAIDS. Cox-1 is expressed in a constitutive manner throughout most tissues, and plays an essential role in maintaining the integrity of the stomach mucosal lining. Cox-2 is an inducible enzyme whose expression is induced by inflammation. NSAIDS selective for Cox-2 have been developed to avoid the development of ulcers by some non-selective NSAIDs, including aspirin. While these two isoforms were sufficient to account for most NSAIDs pharmacology, the actions of acetaminophen remained hard to explain on the basis of inhibiting Cox-1 and Cox-2 alone, such as its efficacy at reducing pain and fever but lack of anti-inflammatory effects. A novel Cox enzyme isoform encoded by the Cox-1 gene, Cox-3, contains an additional 30-34 amino acids and is expressed selectively in the brain. This insertion alters the pharmacology of the Cox enzyme, making Cox-3 sensitive to selective inhibition by acetaminophen and other drugs that reduce pain and fever but have weak anti-inflammatory activity, explaining the pharmacology of these drugs. Another characteristic of acetaminophen is its liver toxicity when taken at high doses. The target of this toxicity has also been recently been revealed. The nuclear receptor CAR is activated by many different exogenous compounds, including acetaminophen, inducing expression of three cytochrome P450 enzymes that transform acetaminophen into NAPQI, a reactive and toxic metabolite. Blocking CAR activation with an antagonist protects against acetaminophen liver toxicity, suggesting a strategy to treat acetaminophen toxicity. (This definition may be outdated - see the DesignNote.)" @default.
- NCIT_C38970 NCIT_P366 "Acetaminophen_Pathway" @default.
- NCIT_C38970 NCIT_P98 "The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA Definition might be outdated or inaccurate. Please see the Terms and Conditions for Use at http://www.biocarta.com/." @default.
- NCIT_C38970 normalizedInformationContent "84.76342111748103" @default.
- NCIT_C38970 referenceCount "10" @default.
- NCIT_C38970 hasExactSynonym "Acetaminophen Pathway" @default.
- NCIT_C38970 hasExactSynonym "Mechanism of Acetaminophen Activity and Toxicity" @default.
- NCIT_C38970 type Class @default.
- NCIT_C38970 isDefinedBy ncit.owl @default.
- NCIT_C38970 label "Acetaminophen Pathway" @default.
- NCIT_C38970 subClassOf NCIT_C20633 @default.
- NCIT_C38970 subClassOf NCIT_C38970 @default.
- NCIT_C38970 subClassOf NCIT_C91821 @default.