Local view for "https://dbmi-icode-01.dbmi.pitt.edu/dikb/resource/Evidence/359"

Predicate	Value (sorted: default)
rdfs:label	"evidence_1193"
rdf:type	?:Evidence ?:Item
?:Evidence_assump_list_id	"65"
?:Evidence_enzyme_system	""
?:Evidence_type	?:EV_EX_Met_Enz_ID_Cyp450_Hum_Microsome_Chem
?:claim_assumed_valid_for_evidence_application_evidence_1193	?:furafylline_in_vitro_selective_inhibitor_of_enzyme_cyp1a2
?:content	"Enzyme system: human liver microsomes: NADPH added: yes inhibitor used: furafylline 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."
dc:creator	"boycer"
dc:date	"06/15/2009 14:26:44"
rdfs:seeAlso	?:11136295

The resource appears as object in one triple:

{ perphenazine_substrate_of_cyp1a2, <http://purl.org/swan/1.2/swan-commons#citesAsSupportingEvidence>, evidence_1193 }

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