Evidence map›Paper›PMID 41120063›Full record

ArticleEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences2025

The fourth-generation EGFR tyrosine kinase inhibitor BLU-945 resensitizes ABCG2-overexpressing multidrug-resistant non-small cell lung cancer cells to cytotoxic anticancer drugs.

Yen-Ching Li, Bing-Huan Lin, Megumi Murakami, Yu-Shan Wu, Tai-Ho Hung, Suresh V Ambudkar, Chung-Pu Wu

Erratum issuedAbstract read
In one paragraph

Article in European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Yen-Ching LiGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Bing-Huan LinGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Megumi MurakamiLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Yu-Shan WuDepartment of Chemistry, Tunghai University, Taichung 40704, Taiwan.
Tai-Ho HungDepartment of Obstetrics and Gynecology, Taipei Chang Gung Memorial Hospital, Taipei 10507, Taiwan; Department of Medicine, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan; Department of Obstetrics and Gynecology, Keelung Chang Gung Memorial Hospital, Keelung 20401, Taiwan. Electronic address: thh20@adm.cgmh.org.tw.
Suresh V AmbudkarLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA. Electronic address: ambudkar@mail.nih.gov.
Chung-Pu WuGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan; Department of Obstetrics and Gynecology, Taipei Chang Gung Memorial Hospital, Taipei 10507, Taiwan; Department of Physiology and Pharmacology, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan; Molecular Medicine Research Center, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan. Electronic address: wuchung@mail.cgu.edu.tw.

Funding

Multidrug Resistance-linked Transport ProteinsZ01BC010030 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBUDKAR, SURESH · 1996 to 2008
$2.3M
Intramural NIH HHS Z01 BC010030
6 · The paper itself

Abstract

ABCG2, a key ATP-binding cassette (ABC) transporter, contributes significantly to multidrug resistance (MDR) by actively effluxing a wide range of chemotherapeutic agents from cancer cells, thereby lowering intracellular drug concentrations and reducing therapeutic efficacy. This mechanism poses a major challenge in treating cancers such as non-small-cell lung cancer (NSCLC). Despite extensive research, no clinically approved agents specifically target ABCG2-mediated MDR. Given the success of combining tyrosine kinase inhibitors (TKIs) with chemotherapy, we explored whether BLU-945, a fourth-generation epidermal growth factor receptor (EGFR) TKI with potent activity against resistant EGFR mutations, could modulate ABCG2 function to reverse MDR. Our findings reveal that BLU-945 stimulates the ATPase activity of ABCG2, indicating direct interaction as a potential substrate or modulator. However, ABCG2-overexpressing NSCLC cells did not display resistance to BLU-945, suggesting that its antitumor activity remains intact despite high ABCG2 expression. Importantly, BLU-945 significantly resensitized these resistant cells to multiple cytotoxic agents in a concentration-dependent manner, with effects evident even at nanomolar levels. Mechanistic studies indicate that this chemosensitizing effect results from functional inhibition of ABCG2-mediated drug efflux, without affecting ABCG2 protein expression, thereby enhancing intracellular drug retention and cytotoxicity. These findings reveal a previously unrecognized pharmacological property of BLU-945 as an inhibitor of ABCG2-mediated drug efflux, supporting its potential role in combination therapies aimed at overcoming MDR in patients with ABCG2-overexpressing tumors. Further preclinical and clinical studies are warranted to validate the translational relevance of this approach and to identify patient populations that may benefit most from this combinatorial strategy.

Indexed as

Antineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Carcinoma, Non-Small-Cell LungDrug Resistance, MultipleDrug Resistance, NeoplasmLung NeoplasmsNeoplasm ProteinsProtein Kinase InhibitorsAcrylamidesCell Line, TumorErbB ReceptorsHumansTyrosine Kinase InhibitorsABCG2 protein, humanAcrylamidesAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2EGFR protein, humanErbB ReceptorsNeoplasm ProteinsProtein Kinase InhibitorsTyrosine Kinase InhibitorsABCG2ABC transporterBLU-945Drug repositioningmultidrug resistance

Identifiers

PMID41120063
PMCPMC13356819

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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.