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Drug-Target Interaction

Drug

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PubChem ID:15625
Structure:
Synonyms:
1746-01-6
2,3,7,8-:tetrachlorodibenzo-p-dioxin
2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny
2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny [Polish]
2,3,7,8-T4CDD
2,3,7,8-TCDD
2,3,7,8-Tetra polychlorinated dibenzo-p-dioxin
2,3,7,8-Tetrachloro(b,e)dibenzodioxin
2,3,7,8-Tetrachloro(b,f)dibenzodioxin
2,3,7,8-Tetrachloro-dibenzo[b,e][1,4]dioxin
2,3,7,8-Tetrachlorodibenzo(b,e)(1,4)dioxin
2,3,7,8-Tetrachlorodibenzo-1,4-dioxin
2,3,7,8-Tetrachlorodibenzo-p-dioxin
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (SEE ALSO TRANSGENIC MODEL EVALUATION
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (SEE ALSO TRANSGENIC MODEL EVALUATION (2,3,7,8-TETRACHLORODIBENZODIOXIN))
2,3,7,8-Tetrachlorodibenzo-p-dioxin [Dioxin and dioxin-like compounds]
2,3,7,8-Tetrachlorodibenzodioxin
2,3,7,8-tetrachlorodibenzodioxine
2,3,7,8-Tetrachlorodibenzo[b,e][1,4]dioxin
2,3,7,8-tetrachlorooxanthrene
5-19-02-00041 (Beilstein Handbook Reference)
56795-67-6
AC1L26AF
AIDS-105033
AIDS105033
BRN 0271116
C07557
CCRIS 576
CHEBI:28119
CHEMBL30327
D013749
Dibenzo(b,e)(1,4)dioxin, 2,3,7,8-tetrachloro-
dibenzo-dioxin, 2,3,7,8-tetrachlorinated
Dibenzo-p-dioxin, 2,3,7,8-tetrachloro-
Dioksyny
Dioksyny [Polish]
Dioxin
Dioxin (herbicide contaminant)
Dioxin mixture
Dioxine
EINECS 217-122-7
HSDB 4151
LS-938
NCI-C03714
PCDD 48
TCDB D
TCDBD
TCDD
TEF TRANSGENICS (TCDD)
Tetrachlorodibenzo-1,4-dioxin
Tetrachlorodibenzo-p-dioxin
Tetrachlorodibenzodioxin
Tetradioxin
TOXIC EQUIVALENCY FACTOR EVALUATION (TCDD) (SEE ALSO TCDD & TRANSGENIC MODEL EVALUATION)
TRANSGENIC MODEL EVALUATION (2,3,7,8-TETRACHLORODIBENZODIOXIN)
[3H]-TCDD

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:

19070657
CYP1A1 induction and CYP3A4 inhibition by the fungicide imazalil in the human intestinal Caco-2 cells-comparison with other conazole pesticides.. Thérèse Sergent; Isabelle Dupont; Coralie Jassogne; Laurence Ribonnet; Edwige van der Heiden; Marie-Louise Scippo; Marc Muller; Dan McAlister; Luc Pussemier; Yvan Larondelle; Yves-Jacques Schneider (2009) Toxicology letters display abstract
Imazalil (IMA) is a widely used imidazole-antifungal pesticide and, therefore, a food contaminant. This compound is also used as a drug (enilconazole). As intestine is the first site of exposure to ingested drugs and pollutants, we have investigated the effects of IMA, at realistic intestinal concentrations, on xenobiotic-metabolizing enzymes and efflux pumps by using Caco-2 cells, as a validated in vitro model of the human intestinal absorptive epithelium. For comparison, other conazole fungicides, i.e. ketoconazole, propiconazole and tebuconazole, were also studied. IMA induced cytochrome P450 (CYP) 1A1 activity to the same extent as benzo(a)pyrene (B(a)P) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in a dose- and time-dependent manner. Cell-free aryl hydrocarbon receptor (AhR) binding assay and reporter gene assay suggested that IMA is not an AhR-ligand, implying that IMA-mediated induction should involve an AhR-independent pathway. Moreover, IMA strongly inhibited the CYP3A4 activity in 1,25-vitamin D(3)-induced Caco-2 cells. The other fungicides had weak or nil effects on CYP activities. Study of the apical efflux pump activities revealed that ketoconazole inhibited both P-glycoprotein (Pgp) and multidrug resistance-associated protein 2 (MRP-2) or breast cancer resistance protein (BCRP), whereas IMA and other fungicides did not. Our results imply that coingestion of IMA-contaminated food and CYP3A4- or CYP1A1-metabolizable drugs or chemicals could lead to drug bioavailability modulation or toxicological interactions, with possible adverse effects for human health.
9784250
Induction of cytochrome P-450 1A1 by omeprazole in human HepG2 cells is protein tyrosine kinase-dependent and is not inhibited by alpha-naphthoflavone.. H Kikuchi; A Hossain; H Yoshida; S Kobayashi (1998) Archives of biochemistry and biophysics display abstract
Benzimidazole compounds, such as omeprazole and thiabendazole, are a different type of CYP1A1 inducer from Ah receptor-ligands, such as TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and 3-methylcholanthrene. In HepG2 cells, the commonly used tyrosine kinase inhibitors, herbimycin-A and a series of tyrphostins, inhibited the induction of CYP1A1 produced by treatment with TCDD. Genistein, another type of tyrosine kinase inhibitor, inhibited the induction of CYP1A1 whether it was produced by omeprazole or TCDD; however, this inhibition was caused by a dual effect of genistein, that is an anti-tyrosine kinase and an anti-topoisomerase I effect. An antagonist of Ah receptor, alpha-naphthoflavone (0.1-10 microM), and 3'-methoxy-4'-aminoflavone (1 microM), did not inhibit the induction of CYP1A1 produced in HepG2 cells by omeprazole, but both of them did inhibit that produced by TCDD. In one of a number of human lung tumor cell lines, S6T, the inducibility of CYP1A1 was high by TCDD, whereas the inducibility by omeprazole was low. Thus, omeprazole appears to induce CYP1A1 by initiating a protein tyrosine kinase-mediated signal transduction pathway, a different pathway from that inhibited by TCDD.