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Drug-Target Interaction

Drug

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PubChem ID:2165
Structure:
Synonyms:
2-[(diethylamino)methyl]-4-[(7-chloro(4-quinolyl))amino]phenol
2aou
4-((7-Chloro-4-quinolinyl)amino)-2-((diethylamino)methyl)phenol
4-((7-Chloro-4-quinolyl)amino)-alpha-(diethylamino)-o-cresol
4-(7-Chloro-quinolin-4-ylamino)-2-diethylaminomethyl-phenol
4-[(7-Chloro-4-quinolinyl)amino]-2-[(diethylamino)methyl]phenol
4-[(7-chloroquinolin-4-yl)amino]-2-(diethylaminomethyl)phenol
4-[(7-CHLOROQUINOLIN-4-YL)AMINO]-2-[(DIETHYLAMINO)METHYL]PHENOL
5-22-10-00283 (Beilstein Handbook Reference)
6398-98-7(DIHYDROCHLORIDE, DIHYDRATE)
7-Chloro-4-(3-diethylaminomethyl-4-hydroxyanilino)
7-Chloro-4-(3-diethylaminomethyl-4-hydroxyanilino)quinoline
7-Chloro-4-(3-diethylaminomethyl-4-hydroxyphenylamino)quinoline
86-42-0
AC-13295
AC1L1D2F
AIDS-002325
AIDS002325
AKOS000538864
Amodiachin
Amodiachinum
Amodiaquin
Amodiaquina
Amodiaquina [INN-Spanish]
Amodiaquine
Amodiaquine (USAN/INN)
Amodiaquine (USAN/INN)
Amodiaquine hydrochloride
Amodiaquine USP24
Amodiaquine [USAN:BAN:INN]
Amodiaquine [USAN:INN:BAN]
AMODIAQUINE, FLAVOQUINE
Amodiaquine, ring-closed
Amodiaquinum
Amodiaquinum [INN-Latin]
BAS 00327385
Basoquin
Bio-0471
BPBio1_000306
BRN 0300962
BSPBio_000278
C07626
C20H22ClN3O
CAM-AQ 1
CAM-AQ1
CAM-AQI
Camochin
Camoquin
Camoquin Hcl
Camoquinal
Camoquine
CCG-103317
CCRIS 8486
CHEBI:2674
CHEMBL682
CPD-10889
CQA
D02922
DB00613
EINECS 201-669-3
Flavoquin
Flavoquine
HMS2236K03
HSDB 7457
LS-55353
Miaquin
MLS001304065
NCGC00244901-01
NSC 13453
NSC13453
o-Cresol, 4-((7-chloro-4-quinolyl)amino)-alpha-(diethylamino)-
o-Cresol, 4-[(7-chloro-4-quinolyl)amino]-.alpha.-(diethylamino)-
Oprea1_019229
Phenol, 4-((7-chloro-4-quinolinyl)amino)-2-((diethylamino)methyl)-
Phenol, 4-[(7-chloro-4-quinolinyl)amino]-2-[(diethylamino)methyl]-
Prestwick0_000309
Prestwick1_000309
Prestwick2_000309
Prestwick3_000309
Quinoline, 7-chloro-4-[[3-[(diethylamino)methyl]-4-hydroxyphenyl]amino]-
Quinoline, 7-chloro-4-[[3-[(diethylamino)methyl]-4-hydroxyphenyl]amino]-|
S. N. 10751
SMR000718769
SN 10,751
SN 10751
SPBio_002497
ST095174
STOCK2S-53274
Sunoquine
UNII-220236ED28
WR-002977
||SN 10,751
ATC-Codes:

Target

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Uniprot ID:CP1A1_HUMAN
Synonyms:
CYPIA1
Cytochrome P450 1A1
P450 form 6
P450-C
P450-P1
EC-Numbers:1.14.14.1
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

11805197
Amodiaquine clearance and its metabolism to N-desethylamodiaquine is mediated by CYP2C8: a new high affinity and turnover enzyme-specific probe substrate.. Xue-Qing Li; Anders Björkman; Tommy B Andersson; Marianne Ridderström; Collen M Masimirembwa (2002) The Journal of pharmacology and experimental therapeutics display abstract
Amodiaquine (AQ) metabolism to N-desethylamodiaquine (DEAQ) is the principal route of disposition in humans. Using human liver microsomes and two sets of recombinant human cytochrome P450 isoforms (from lymphoblastoids and yeast) we performed studies to identify the CYP isoform(s) involved in the metabolism of AQ. CYP2C8 was the main hepatic isoform that cleared AQ and catalyzed the formation of DEAQ. The extrahepatic P450s, 1A1 and 1B1, also cleared AQ and catalyzed the formation of an unknown metabolite M2. The K(m) and V(max) values for AQ N-desethylation were 1.2 microM and 2.6 pmol/min/pmol of CYP2C8 for recombinant CYP2C8, and 2.4 microM and 1462 pmol/min/mg of protein for human liver microsomes (HLMs), respectively. Relative contribution of CYP2C8 in the formation of DEAQ was estimated at 100% using the relative activity factor method. Correlation analyses between AQ metabolism and the activities of eight hepatic P450s were made on 10 different HLM samples. Both the formation of DEAQ and the clearance of AQ showed excellent correlations (r(2) = 0.98 and 0.95) with 6alpha-hydroxylation of paclitaxel, a marker substrate for CYP2C8. The inhibition of DEAQ formation by quercetin was competitive with K(i) values of 1.96 for CYP2C8 and 1.56 microM for HLMs. Docking of AQ into the active site homology models of the CYP2C isoforms showed favorable interactions with CYP2C8, which supported the likelihood of an N-desethylation reaction. These data show that CYP2C8 is the main hepatic isoform responsible for the metabolism of AQ. The specificity, high affinity, and high turnover make AQ desethylation an excellent marker reaction for CYP2C8 activity.