Local view for "https://dbmi-icode-01.dbmi.pitt.edu/dikb/resource/Evidence/1100"
| Predicate | Value (sorted: none) |
|---|---|
| rdf:type | |
| rdf:type | |
| rdfs:label | |
| ?:Evidence_type | |
| ?:Evidence_assump_list_id |
"194"
|
| ?:Evidence_enzyme_system | |
| ?:claim_assumed_valid_for_evidence_application_evidence_1827 | |
| dc:creator | |
| dc:date |
"06/15/2009 16:47:08"
|
| ?:content |
"Enzyme system: human liver microsomes:
NADPH added: yes
inhibitor used: quinidine
reaction: perphenazine N-dealkylation
Quote:
To identify the human cytochrome P450 (CYP) isoforms mediating the N-dealkylation of the antipsychotic drug perphenazine in vitro and estimate the relative contributions of the CYP isoforms involved. METHODS: cDNA-expressed CYP isoforms were used to identify the isoforms that are able to mediate the N-dealkylation of perphenazine, which is considered a major metabolic pathway for the drug. Using human liver microsomal preparations (HLM), inhibition studies were carried out to establish the relative contributions of the CYP isoforms involved in the N-dealkylation reaction... Ketoconazole inhibition of N-dealkylation mediated by a mixed HLM indicated that CYP3A4 accounted for about 40% of perphenazine N-dealkylation at therapeutically relevant concentrations.The contribution of the CYP isoforms 1A2, 2C19 and 2D6 amounted to 20-25% each as measured by the percentage inhibition obtained by addition of furafylline, fluvoxamine or quinidine, respectively."
|
| rdfs:seeAlso |
All properties reside in the graph file:///home/swish/src/ClioPatria/guidelines/dikb.ttl
The resource appears as object in one triple:
{ cyp2d6_controls_formation_of_N-dealkylperphenazine, <http://purl.org/swan/1.2/swan-commons#citesAsSupportingEvidence>, evidence_1827 }