Evidence map›Paper›PMID 29302757›Full record

ArticlePharmaceutical research2018

Indinavir Alters the Pharmacokinetics of Lamivudine Partially via Inhibition of Multidrug and Toxin Extrusion Protein 1 (MATE1).

Qing Li, Zhi Ye, Peng Zhu, Dong Guo, Hong Yang, Jin Huang, Wei Zhang, James E Polli, Yan Shu

Abstract read
PubMed Publisher
In one paragraph

Article in Pharmaceutical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Article
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

9 authors at 2 institutions in 2 countries.

Qing LiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Zhi YeDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Maryland at Baltimore, 20 N Pine Street, PH N519, Baltimore, 21201, Maryland, USA.
Peng ZhuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Dong GuoDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Maryland at Baltimore, 20 N Pine Street, PH N519, Baltimore, 21201, Maryland, USA.
Hong YangDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Maryland at Baltimore, 20 N Pine Street, PH N519, Baltimore, 21201, Maryland, USA.
Jin HuangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Wei ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Road, Changsha, 410078, China.
James E PolliDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Maryland at Baltimore, 20 N Pine Street, PH N519, Baltimore, 21201, Maryland, USA.
Yan ShuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Road, Changsha, 410078, China. yshu@rx.umaryland.edu.ORCID http://orcid.org/0000-0002-4044-3610
University of Maryland, Baltimore · USCentral South University · CN

Funding

Xenobiotic Transporter Regulation and IRIP FunctionR01GM099742 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI SHU, YAN · 2012 to 2016
$1.6M
National Natural Science Foundation (NNSF) of China 81373477, 81570533 & 81273595NIGMS NIH HHS R01 GM099742the National Institute of General Medical Sciences of the National Institutes of Health (NIH) R01GM099742the US Food and Drug Administration 1U01FD005946the US Food and Drug Administration (FDA) U01FD004320
6 · The paper itself

Abstract

purposeLamivudine, a characterized substrate for human multidrug and toxin extrusion protein 1 (hMATE1) in vitro, was commonly used with indinavir as a therapy against human immunodeficiency virus (HIV). We aimed to investigate whether mouse MATE1 is involved in the disposition of lamivudine in vivo, and whether there is any transporter-mediated interaction between indinavir and lamivudine.

methodsThe role of MATE1 in the disposition of lamivudine was determined using Mate1 wild type (+/+) and knockout (-/-) mice. The inhibitory potencies of indinavir on lamivudine uptake mediated by OCT2 and MATE1 were determined in human embryonic kidney 293 (HEK 293) cells stably expressing these transporters. The role of MATE1 in the interaction between indinavir and lamivudine in vivo was determined using Mate1 (+/+) and Mate1 (-/-) mice.

resultsThe plasma concentrations and tissue accumulation of lamivudine were markedly elevated in Mate1 (-/-) mice as compared to those in Mate1 (+/+) mice. Indinavir significantly increased the pharmacokinetic exposure of lamivudine in mice; however, the effect by indinavir was significantly less pronounced in Mate1 (-/-) mice as compared to Mate1(+/+) mice.

conclusionMATE1 played an important role in lamivudine pharmacokinetics. Indinavir could cause drug-drug interaction with lamivudine in vivo via inhibition of MATE1 and additional mechanism.

Indexed as

AnimalsAnti-HIV AgentsBiological TransportCell Culture TechniquesDrug InteractionsHEK293 CellsHIV-1HumansIndinavirKidneyLamivudineMaleMiceMice, Inbred C57BLMice, KnockoutOrganic Cation Transport ProteinsAnti-HIV AgentsIndinavirLamivudineOrganic Cation Transport ProteinsSLC47A1 protein, humandrug-drug interactionindinavirlamivudinemultidrug and toxin extrusion proteinorganic cation transporter

Identifiers

PMID29302757
OpenAlexW2782255115

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.