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Drug-Target Interaction

Drug

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PubChem ID:441233
Structure:
Synonyms:
(1R)-2-phenylcyclopropan-1-amine
155-09-9
AC1L9ASR
C07155
D08625
DB00752
Parnate
Tranylcypromine
Tranylcypromine (INN)
ATC-Codes:
Side-Effects:
Side-EffectFrequency
insomnia0
thrombocytopenia0
tachycardia0
spasm0
scleroderma0
paresthesia0
weakness0
palpitations0
numbness0
tinnitus0
tremor0
urinary incontinence0
memory loss0
urinary frequency0
manic0
blurred vision0
chills0
urinary retention0
dry mouth0
urticaria0
nausea0
leukopenia0
constipation0
confusion0
ataxia0
anxiety0
anorexia0
anemia0
alopecia0
agranulocytosis0
cystic acne0
diarrhea0
dizziness0
siadh0
impotence0
hepatitis0
blood dyscrasia0
headache0
rash0
edema0
somnolence0
abdominal pain0

Target

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Uniprot ID:CP2D6_HUMAN
Synonyms:
CYPIID6
Cytochrome P450 2D6
Debrisoquine 4-hydroxylase
P450-DB1
EC-Numbers:1.14.14.1
Organism:Homo sapiens
Human
PDB IDs:2F9Q
Structure:
2F9Q

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----
----

References:

11128045
Oxidation of ranitidine by isozymes of flavin-containing monooxygenase and cytochrome P450.. W G Chung; C S Park; H K Roh; W K Lee; Y N Cha (2000) Japanese journal of pharmacology display abstract
Rat and human liver microsomes oxidized ranitidine to its N-oxide (66-76%) and S-oxide (13-18%) and desmethylranitidine (12-16%). N- and S-oxidations of ranitidine were inhibited by metimazole [flavin-containing monooxygenase (FMO) inhibitor] to 96-97% and 71-85%, respectively, and desmethylation of ranitidine was inhibited by SKF525A [cytochrome P450 (CYP) inhibitor] by 71-95%. Recombinant FMO isozymes like FMO1, FMO2, FMO3 and FMO5 produced 39, 79, 2180 and 4 ranitinine N-oxide and 45, 0, 580 and 280 ranitinine S-oxide pmol x min(-1) x nmol(-1) FMO, respectively. Desmethyranitinine was not produced by recombinant FMOs. Production of desmethylranitidine by rat and human liver microsomes was inhibited by tranylcypromine, a-naphthoflavon and quinidine, which are known to inhibit CYP2C19, 1A2 and 2D6, repectively. FMO3, the major form in adult liver, produced both ranitidine N- and S-oxides at a 4 to 1 ratio. FMO1, expressed primarily in human kidney, was 55- and 13-fold less efficient than the hepatic FMO3 in producing ranitidine N- and S-oxides, respectively. FMO2 and FMO5, although expressed slightly in human liver, kidney and lung, were not efficient producers of ranitidine N- and S-oxides. Thus, urinary contents of ranitidine N-oxide can be used as the in vivo probe to determine the hepatic FMO3 activity.
15049511