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Drug-Target Interaction

Drug

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PubChem ID:4754
Structure:
Synonyms:
1-Acetamido-4-ethoxybenzene
1-Acetyl-p-phenetidin
314005_SIGMA
4'-Ethoxyacetanilide
4'-Ethoxyacetanilide-ring-UL-14C
4-(Acetylamino)phenetole
4-13-00-01092 (Beilstein Handbook Reference)
4-Ethoxyacetanilide
62-44-2
77440_ALDRICH
77440_FLUKA
A2500_SIGMA
AB00052135
AC1L1IVN
AC1Q37RD
AC1Q37RE
acet-p-phenal ide
Acet-p-phenalide
Acet-p-phenetidin
Acetamide, N-(4-ethoxyphenol)-
Acetamide, N-(4-ethoxyphenyl)-
Acetamide, N-(4-ethoxyphenyl)- (9CI)
Acetanilide, 4'-ethoxy-
Acetic acid amide, N-(4-ethoxyphenyl)-
Aceto-4-phenetidine
Aceto-para-phenalide
Aceto-para-phenetidide
Acetophenetidin
Acetophenetidine
Acetophenetin
Acetphenetidin
Acetylphenetidin
Achrocidin
AE-848/04969036
AI3-00783
AKOS000370201
Anapac
BBL004038
BIM-0051571.0001
BPBio1_000601
BRD-K38323065-001-05-8
BRN 1869238
Bromo seltzer
BSPBio_000545
BSPBio_003048
Buff-A-Comp
C07591
C10H13NO2
CAS-62-44-2
CCG-39439
CCRIS 496
CHEBI:8050
CHEMBL16073
Citra-fort
Clistanol
Codempiral
Commotional
component of A.S.A. and Codeine compound
component of A.S.A. compound
component of Ansemco 2
component of Butigetic
component of P-A-C compound
component of Percodan
component of Phensal
Contradol
Contradouleur
Coricidin
Coriforte
Coryban-D
D00569
D010615
Daprisal
Darvon compound
Dasikon
Dasin
Dasin CH
DB03783
DB08243
DivK1c_000580
Dolostop
Edrisal
EINECS 200-533-0
Empiral
empirin compound
Emprazil
Emprazil-C
Epragen
Fenacetin
Fenacetin [Czech]
Fenacetina
Fenacetina [INN-Spanish]
Fenia
Fenidina
Fenina
Fiorinal
Fortacyl
Gelonida
Gewodin
Helvagit
Hjorton's powder
HMS1569L07
HMS1921M21
HMS2092E14
HMS2096L07
HMS2234P11
HMS501M22
Hocophen
HSDB 3152
IDI1_000580
KAFA
Kalmin
KBio1_000580
KBio2_001262
KBio2_003830
KBio2_006398
KBio3_002268
KBioGR_001089
KBioSS_001262
LS-269
Malex
Melabon
Melaforte
Mixture Name
MLS001304971
MLS002153862
MLS002303055
MolPort-000-626-710
N-(4-Ethoxyphenyl) Acetamide
N-(4-ethoxyphenyl)-acetamide
N-(4-Ethoxyphenyl)acetamide
N-Acetyl-4-ethoxyani line
N-Acetyl-4-ethoxyaniline
N-Acetyl-p-phenetidine
N-Acetyl-para-phenetidine
N-p-phenetylacetamide
N-para-Ethoxyphenylacetamide
N-[4-(ethyloxy)phenyl]acetamide
N4E
NCGC00016281-01
NCGC00016281-02
NCGC00016281-03
NCGC00016281-04
NCGC00016281-05
NCGC00016281-06
NCGC00016281-07
NCGC00016281-08
NCGC00091376-01
NCGC00091376-02
NCGC00091376-03
NCGC00091376-04
NCGC00091376-05
NINDS_000580
Norgesic
NSC 7651
NSC7651
P-A-C Compound
p-Acetophenetide
p-Acetophenetidide
p-Acetophenetidide (8CI)
p-Acetophenetidine
p-Acetphenetidin
p-Ethoxyacetanilide
p-Ethoxyanilid kyseliny octove
p-Ethoxyanilid kyseliny octove [Czech]
p-Phenetidine, N-acetyl-
P1669
Pamprin
para-Acetophenetidide
para-Acetophenetidine
para-Acetphenetidin
para-Ethoxyacetanilide
para-Phenacetin
Paracetophenetidin
paracetophentidin
Paramette
Paratodol
Pertonal
Phenacet
Phenacetin
Phenacetin (JAN/INN)
Phenacetin [Analgesic mixtures containing phenacetin]
Phenacetin [INN:JAN]
Phenacetin-ring-UL-14C
Phenacetine
Phenacetine [INN-French]
Phenacetinum
Phenacetinum [INN-Latin]
Phenacitin
Phenacon
Phenaphen
Phenaphen plus
Phenazetin
Phenazetina
Phenedina
Phenidin
Phenin
Phenodyne
Phensal
Phorazetim
Prestwick0_000533
Prestwick1_000533
Prestwick2_000533
Prestwick3_000533
Prestwick_862
Pyraphen
Pyrroxate
Quadronal
RCRA waste no. U187
RCRA waste number U187
Robaxisal-PH
Salgydal
Sanalgine
Saridon
Seranex
Sinedal
Sinubid
Sinutab
Sinutabs
SMR000752916
SPBio_001979
SPBio_002466
SPECTRUM1500642
Spectrum2_001940
Spectrum3_001404
Spectrum4_000515
Spectrum5_001902
Spectrum_000782
ST5405359
Stellacyl
STK011463
Super anahist
Synalgos-DC
Synalogos
Tacol
Tetracydin
Thephorin A-C
Treupel
UNII-ER0CTH01H9
Veganine
Viden
Wigraine
WLN: 2OR DMV1
Xaril
ZINC00000602
ATC-Codes:

Target

show target details
Uniprot ID:CP1A2_HUMAN
Synonyms:
CYPIA2
Cytochrome P450 1A2
P(3)450
P450 4
P450-P3
EC-Numbers:1.14.14.1
Organism:Homo sapiens
Human
PDB IDs:2HI4
Structure:
2HI4

Binding Affinities:

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

References:

10383922
10805063
10901704
11159803
11284709
11353760
Evaluation of methoxsalen, tranylcypromine, and tryptamine as specific and selective CYP2A6 inhibitors in vitro.. W Zhang; T Kilicarslan; R F Tyndale; E M Sellers (2001) Drug metabolism and disposition: the biological fate of chemicals display abstract
CYP2A6 is the principle enzyme metabolizing nicotine to its inactive metabolite cotinine. In this study, the selective probe reactions for each major cytochrome P450 (P450) were used to evaluate the specificity and selectivity of the CYP2A6 inhibitors methoxsalen, tranylcypromine, and tryptamine in cDNA-expressing and human liver microsomes. Phenacetin O-deethylation (CYP1A2), coumarin 7-hydroxylation (CYP2A6), diclofenac 4'-hydroxylation (CYP2C9), omeprazole 5-hydroxylation (CYP2C19), dextromethorphan O-demethylation (CYP2D6), 7-ethoxy-4-trifluoromethylcoumarin deethylation (CYP2B6), p-nitrophenol hydroxylation (CYP2E1), and omeprazole sulfonation (CYP3A4) were used as index reactions. Apparent K(i) values for inhibition of P450s' (1A2, 2A6, 2B6, 2C9, 2C19, 2D6, 2E1, and 3A4) activities showed that tranylcypromine, methoxsalen, and tryptamine have high specificity and relative selectivity for CYP2A6. In cDNA-expressing microsomes, tranylcypromine inhibited CYP2A6 (K(i) = 0.08 microM) with about 60- to 5000-fold greater potency relative to other P450s. Methoxsalen inhibited CYP2A6 (K(i) = 0.8 microM) with about 3.5- 94-fold greater potency than other P450s, except for CYP1A2 (K(i) = 0.2 microM). Tryptamine inhibited CYP2A6 (K(i) = 1.7 microM) with about 6.5- 213-fold greater potency relative to other P450s, except for CYP1A2 (K(i) = 1.7 microM). Similar results were also obtained with methoxsalen and tranylcypromine in human liver microsomes. R-(+)-Tranylcypromine, (+/-)-tranylcypromine, and S-(-)-tranylcypromine competitively inhibited CYP2A6-mediated metabolism of nicotine with apparent K(i) values of 0.05, 0.08, and 2.0 microM, respectively. Tranylcypromine [particularly R-(+) isomer], tryptamine, and methoxsalen are specific and relatively selective for CYP2A6 and may be useful in vivo to decrease smoking by inhibiting nicotine metabolism with a low risk of metabolic drug interactions.
145
15231049
17178771
7617560
Kinetics and inhibition by fluvoxamine of phenacetin O-deethylation in V79 cells expressing human CYP1A2.. K G Jensen; H E Poulsen; J Doehmer; S Loft (1995) Pharmacology & toxicology display abstract
The kinetics of phenacetin O-deethylation and its inhibition by fluvoxamine was investigated in a V79 cell line (V79MZh1A2) transfected with human CYP1A2. In four sets of experiments the apparent Km values for phenacetin O-deethylation ranged from 35 to 95 microM and the Ki for fluvoxamine-mediated inhibition of the reaction ranged from 2.7 to 14.5 nM, i.e. comparable to values obtained in human liver microsomes. The kinetic performance of the V79MZh1A2 cell line demonstrates its usefulness as an analytical tool in a variety of toxicological and drug metabolism studies involving CYP1A2.
9152599
Inhibition of human drug metabolizing cytochromes P450 by anastrozole, a potent and selective inhibitor of aromatase.. S W Grimm; M C Dyroff (1997) Drug metabolism and disposition: the biological fate of chemicals display abstract
Anastrozole (2,2'[5(1H-1,2,4-triazol-1-ylmethyl)-1,3-phenylene]- bis(2-methylproprionitrile)) is a potent third-generation inhibitor of aromatase, currently marketed as a treatment for postmenopausal women with advanced breast cancer. While its potency and selectivity for inhibition of estrogen synthesis has been established in both preclinical and clinical studies, this study used in vitro methods to examine the effects of anastrozole on several drug metabolizing CYP enzymes found in human liver. Human liver microsomes were co-incubated with anastrozole and probe substrates for CYP1A2 (phenacetin), CYP2A6 (coumarin), CYP2C9 (tolbutamide), CYP2D6 (dextromethorphan), and CYP3A (nifedipine). The formation of the CYP-specific metabolites following co-incubation with various anastrozole concentrations was determined to establish IC50 and Ki values for these enzymes. While anastrozole did not inhibit CYP2A6 and CYP2D6 activities at concentrations below 500 microM, this compound inhibited CYP1A2, CYP2C9, and CYP3A activities with Ki values of 8, 10, and 10 microM, respectively. Dixon plots used to determine the Ki values for the inhibition of CYP1A2 and CYP3A activities by anastrozole were biphasic, indicating additional lower affinity Ki values. Major metabolites of anastrozole did not retain the ability to inhibit the metabolism of nifedipine (CYP3A). The results of this study indicate that, although anastrozole can inhibit CYP1A2, 2C9, and 3A-mediated catalytic activities, this compound would not be expected to cause clinically significant interactions with other CYP-metabolized drugs at physiologically relevant concentrations achieved during therapy with Arimidex (Zeneca, Ltd., Macclesfield, UK) 1-mg.
9825829
Inhibitory monoclonal antibodies to human cytochrome P450 1A2: analysis of phenacetin O-deethylation in human liver.. T J Yang; Y Sai; K W Krausz; F J Gonzalez; H V Gelboin (1998) Pharmacogenetics display abstract
Human cytochrome P450 1A2 metabolizes a large number of common drugs and engages in carcinogen metabolism and activation. Baculovirus-expressed 1A2 was used to immunize mice producing hybridomas yielding monoclonal antibodies (MAbs). Three of 2050 clones assayed yielded the MAbs, MAb 26-7-5, MAb 951-5-1, MAb 1812-2-4, which were specific for 1A2 as assessed by enzyme-linked immunosorbent assay and immunoblots. The three MAbs inhibited 1A2-catalysed metabolism of phenacetin, 7-ethoxycoumarin, chlorzoxazone and phenanthrene by more than 85%. The MAbs were highly specific to 1A2 and did not inhibit 11 other human P450s. The phenancetin O-deethylation activity varied from 0.44-2.49 nmol/min/nmol P450 in eight human liver microsomes samples. MAb 26-7-5 inhibited 1A2-dependent phenacetin O-deethylation in these samples by 64-84% indicating the amount of 1A2 contribution to this reaction and in addition a role for other P450s in the O-deethylation. Independent analysis of recombinant human P450s showed that 1A1, 1A2, 2A6 and 2C19 exhibited phenacetin O-deethylation activity, with 1A1 and 1A2 being the most active followed by 2C19 and 2A6. Eight other P450s were inactive towards phenacetin O-deethylation. The role of different P450 in eight liver samples was analysed with specific individual inhibitory MAbs. Inhibitory antibodies to 1A2, 2C8/9/18/19, 2A6, 2D6, 2E1, and 1A1 were combinatorially added to the microsomes. The O-deethylation activity was inhibited by antibodies to 1A2 (64-84%), to 2C19 (4.6-20%) and to 2A6 (0-8.8%). The total activity inhibited by antibodies to P450 2E1, 2D6 and 1A1 was less than 4.5%, indicating a minor role for these P450s in phenancetin metabolism in human liver microsomes. Thus, 1A2, 2C 9 and 2A6 are the dominant P450s for phenacetin O-deethylation. These studies demonstrate the use of inhibitory MAbs to P450s for a simple and precise assessment of the quantitative role of each P450 in the metabolism of substrates, including drugs, carcinogens, mutagens, environmental chemicals and endobiotics.