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Drug-Target Interaction

Drug

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PubChem ID:3675
Structure:
Synonyms:
1-Hydrazino-2-phenylethane
2-Phenethylhydrazine
2-Phenylethylhydrazine
4-15-00-01269 (Beilstein Handbook Reference)
51-71-8
AB00053520
AC1L1GGN
AKOS000131105
BBV-011834
beta-Phenylethylhydrazine
BPBio1_000043
BRD-K87024524-065-05-2
BRN 0742354
BSPBio_000039
BSPBio_002373
C07430
C8H12N2
CAS-156-51-4
CBChromo1_000176
CCG-205051
CHEBI:248018
CHEMBL1089
cMAP_000003
CPD001496977
D08349
DB00780
DivK1c_000062
EINECS 200-117-9
Fenelzin
Fenelzina
Fenelzina [INN-Spanish]
Fenelzyna
Fenelzyna [Polish]
Fenelzyne
Fenelzyne [Polish]
HMS3259L04
Hydrazine, (2-phenylethyl)-
HYDRAZINE, PHENETHYL-
IDI1_000062
KBio1_000062
KBio2_001331
KBio2_002265
KBio2_003899
KBio2_004833
KBio2_006467
KBio2_007401
KBio3_001593
KBio3_002745
KBioGR_000950
KBioGR_002265
KBioSS_001331
KBioSS_002266
Lopac-P-6777
Lopac0_000971
LS-76934
MLS000758253
Nardil
NCGC00015830-01
NCGC00015830-02
NCGC00015830-03
NCGC00015830-04
NCGC00015830-05
NCGC00162301-01
NINDS_000062
Phenelezine
Phenelzine
Phenelzine (BAN)
Phenelzine sulfate
Phenelzine [INN:BAN]
Phenelzinum
Phenelzinum [INN-Latin]
Phenethylhydrazine
Phenylethyl hydrazine-HCl
Phenylethylhydrazine
Prestwick0_000170
Prestwick1_000170
Prestwick2_000170
Prestwick3_000170
SAM002589985
SMR000058500
SPBio_001137
SPBio_001960
Spectrum2_001009
Spectrum3_000677
Spectrum4_000475
Spectrum5_000990
Spectrum_000851
Stinerval
UNII-O408N561GF
W 1544-A
W1544
ATC-Codes:
Side-Effects:
Side-EffectFrequency
euphoria0
psychosis0
shock0
vomiting0
nystagmus0
convulsions0
sweating0
insomnia0
tachycardia0
glaucoma0
urinary retention0
nausea0
manic0
hypernatremia0
leukopenia0
headache0
metabolic acidosis0
somnolence0
malaise0
tremor0
delirium0
jaundice0
postural hypotension0
blurred vision0
fever0
coma0
schizophrenia0
paresthesia0
weakness0
constipation0
agitation0
rash0
nightmares0
lupus0
fatigue0
dry mouth0
hypoxia0
pruritus0
impotence0
hypersomnia0
edema0
ataxia0
dizziness0
weight gain0

Target

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Uniprot ID:Q38LG2_HUMAN
Synonyms:
Cytochrome P450 2D6
EC-Numbers:1.14.14.1
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

16669850
An evaluation of potential mechanism-based inactivation of human drug metabolizing cytochromes P450 by monoamine oxidase inhibitors, including isoniazid.. Thomas M Polasek; David J Elliot; Andrew A Somogyi; Elizabeth M J Gillam; Benjamin C Lewis; John O Miners (2006) British journal of clinical pharmacology display abstract
AIMS: To characterize potential mechanism-based inactivation (MBI) of major human drug-metabolizing cytochromes P450 (CYP) by monoamine oxidase (MAO) inhibitors, including the antitubercular drug isoniazid. METHODS: Human liver microsomal CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A activities were investigated following co- and preincubation with MAO inhibitors. Inactivation kinetic constants (KI and kinact) were determined where a significant preincubation effect was observed. Spectral studies were conducted to elucidate the mechanisms of inactivation. RESULTS: Hydrazine MAO inhibitors generally exhibited greater inhibition of CYP following preincubation, whereas this was less frequent for the propargylamines, and tranylcypromine and moclobemide. Phenelzine and isoniazid inactivated all CYP but were most potent toward CYP3A and CYP2C19. Respective inactivation kinetic constants (KI and kinact) for isoniazid were 48.6 microm and 0.042 min-1 and 79.3 microm and 0.039 min-1. Clorgyline was a selective inactivator of CYP1A2 (6.8 microm and 0.15 min-1). Inactivation of CYP was irreversible, consistent with metabolite-intermediate complexation for isoniazid and clorgyline, and haeme destruction for phenelzine. With the exception of phenelzine-mediated CYP3A inactivation, glutathione and superoxide dismutase failed to protect CYP from inactivation by isoniazid and phenelzine. Glutathione partially slowed (17%) the inactivation of CYP1A2 by clorgyline. Alternate substrates or inhibitors generally protected against CYP inactivation. CONCLUSIONS: These data are consistent with mechanism-based inactivation of human drug-metabolizing CYP enzymes and suggest that impaired metabolic clearance may contribute to clinical drug-drug interactions with some MAO inhibitors.