Evidence map›Paper›PMID 21212239›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2011

Comparison of the inhibitory profiles of itraconazole and cimetidine in cytochrome P450 3A4 genetic variants.

Takeshi Akiyoshi, Takashi Saito, Saori Murase, Mitsue Miyazaki, Norie Murayama, Hiroshi Yamazaki, F Peter Guengerich, Katsunori Nakamura, Koujirou Yamamoto, Hisakazu Ohtani

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Genomewide Association Study of Simvastatin Pharmacokinetics.Clinical pharmacology and therapeutics · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Takeshi AkiyoshiKeio University Faculty of Pharmacy, Tokyo, Japan.
Takashi Saito
Saori Murase
Mitsue Miyazaki
Norie Murayama
Hiroshi Yamazaki
F Peter Guengerich
Katsunori Nakamura
Koujirou Yamamoto
Hisakazu Ohtani
Gunma University · JPShowa Pharmaceutical University · JPVanderbilt University · USKeio University · JP

Funding

Structural Biology Facility CoreP30ES000267 · NIEHS · VANDERBILT UNIVERSITY · PI GUENGERICH, F PETER · 1985 to 2014
$20.3M
Metabolism of Carcinogens and Drugs by Human P450sR37CA090426 · NCI · VANDERBILT UNIVERSITY · PI GUENGERICH, F PETER · 2006 to 2015
$3.6M
NCI NIH HHS R37 CA090426NCI NIH HHS R37-CA090426NIEHS NIH HHS P30 ES000267NIEHS NIH HHS P30-ES000267
6 · The paper itself

Abstract

CYP3A4, an important drug-metabolizing enzyme, is known to have genetic variants. We have previously reported that CYP3A4 variants such as CYP3A4.2, 7, 16, and 18 show different enzymatic kinetics from CYP3A4.1 (wild type). In this study, we quantitatively investigated the inhibition kinetics of two typical inhibitors, itraconazole (ITCZ) and cimetidine (CMD), on CYP3A4 variants and evaluated whether the genetic variation leads to interindividual differences in the extent of CYP3A4-mediated drug interactions. The inhibitory profiles of ITCZ and CMD on the metabolism of testosterone (TST) were analyzed by using recombinant CYP3A4 variants. The genetic variation of CYP3A4 significantly affected the inhibition profiles of the two inhibitors. In CYP3A4.7, the K(i) value for ITCZ was 2.4-fold higher than that for the wild-type enzyme, whereas the K(i) value for CMD was 0.64-fold lower. In CYP3A4.16, the K(i) value for ITCZ was 0.54-fold lower than that for wild-type CYP3A4, whereas the K(i) value for CMD was 3.2-fold higher. The influence of other genetic variations also differed between the two inhibitors. Docking simulations could explain the changes in the K(i) values, based on the accessibility of TST and inhibitors to the heme moiety of the CYP3A4 molecule. In conclusion, the inhibitory effects of an inhibitor differ among CYP3A4 variants, suggesting that the genetic variation of CYP3A4 may contribute, at least in part, to interindividual differences in drug interactions mediated by CYP3A4 inhibition, and the pattern of the influences of genetic variation differs among inhibitors as well as substrates.

Indexed as

Cytochrome P-450 CYP3A Inhibitors14-alpha Demethylase InhibitorsAndrogensCimetidineCytochrome P-450 CYP3ADrug InteractionsEnzyme InhibitorsGenetic VariationHemeHumansHydroxytestosteronesItraconazoleRecombinant ProteinsTestosterone14-alpha Demethylase Inhibitors6 beta-hydroxytestosteroneAndrogensCimetidineCYP3A4 protein, humanCytochrome P-450 CYP3ACytochrome P-450 CYP3A InhibitorsEnzyme InhibitorsHemeHydroxytestosteronesItraconazoleRecombinant ProteinsTestosterone

Identifiers

PMID21212239
PMCPMC3063718
OpenAlexW2139936026

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.