Evidence map›Paper›PMID 27519550›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2016

Identification and Characterization of CINPA1 Metabolites Facilitates Structure-Activity Studies of the Constitutive Androstane Receptor.

Milu T Cherian, Lei Yang, Sergio C Chai, Wenwei Lin, Taosheng Chen

Open access · bronzeAbstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Milu T CherianDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee.
Lei YangDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee.
Sergio C ChaiDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee.
Wenwei LinDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee.
Taosheng ChenDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee taosheng.chen@stjude.org.
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Regulation of xenobiotic receptors PXR and CAR: implications in drug dispositionR35GM118041 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Taosheng Chen · 2016 to 2026
$4.3M
Regulation of PXR by cell cycle and phosphorylationR01GM086415 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHEN, TAOSHENG · 2010 to 2013
$1.3M
Regulation of drug disposition by a novel microRNA-mediated pathwayR01GM110034 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHEN, TAOSHENG · 2014 to 2016
$998k
NCI NIH HHS P30 CA021765NIGMS NIH HHS R01 GM086415NIGMS NIH HHS R01 GM110034NIGMS NIH HHS R35 GM118041
6 · The paper itself

Abstract

The constitutive androstane receptor (CAR) regulates the expression of genes involved in drug metabolism and other processes. A specific inhibitor of CAR is critical for modulating constitutive CAR activity. We recently described a specific small-molecule inhibitor of CAR, CINPA1 (ethyl (5-(diethylglycyl)-10,11-dihydro-5H-dibenzo[b,f]azepin-3-yl)carbamate), which is capable of reducing CAR-mediated transcription by changing the coregulator recruitment pattern and reducing CAR occupancy at the promoter regions of its target genes. In this study, we showed that CINPA1 is converted to two main metabolites in human liver microsomes. By using cell-based reporter gene and biochemical coregulator recruitment assays, we showed that although metabolite 1 was very weak in inhibiting CAR function and disrupting CAR-coactivator interaction, metabolite 2 was inactive in this regard. Docking studies using the CAR ligand-binding domain structure showed that although CINPA1 and metabolite 1 can bind in the CAR ligand-binding pocket, metabolite 2 may be incapable of the molecular interactions required for binding. These results indicate that the metabolites of CINPA1 may not interfere with the action of CINPA1. We also used in vitro enzyme assays to identify the cytochrome P450 enzymes responsible for metabolizing CINPA1 in human liver microsomes and showed that CINPA1 was first converted to metabolite 1 by CYP3A4 and then further metabolized by CYP2D6 to metabolite 2. Identification and characterization of the metabolites of CINPA1 enabled structure-activity relationship studies of this family of small molecules and provided information to guide in vivo pharmacological studies.

Indexed as

AnimalsBenzazepinesCaco-2 CellsCell Line, TumorConstitutive Androstane ReceptorCytochrome P-450 CYP2B6Cytochrome P-450 CYP3AGenes, ReporterHepatocytesHep G2 CellsHumansLigandsMiceMicrosomes, LiverReceptors, Cytoplasmic and NuclearStructure-Activity RelationshipBenzazepinesConstitutive Androstane ReceptorCytochrome P-450 CYP2B6Cytochrome P-450 CYP3Aethyl (5-(diethylglycyl)-10,11-dihydro-5H-dibenzo(b,f)azepin-3-yl)carbamateLigandsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID27519550
PMCPMC5074473
OpenAlexW2507551009

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.