ArticleCancers2020
BMS-599626, a Highly Selective Pan-HER Kinase Inhibitor, Antagonizes ABCG2-Mediated Drug Resistance.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Differential response of HER2 - and HER2 + breast cancer cells to quinazoline and triazole derivatives: advancing receptor subtype-specific phytochemical targeting.Molecular diversity · 2026Article
- Article
- B-9-8, a Novel Harman Dimer, Reverses ABCG2-mediated Chemotherapeutic Drug Resistance.Recent patents on anti-cancer drug discovery · 2026Article
- Reversal of ABCG2-mediated drug resistance by tinodasertib (ETC-206).Frontiers in pharmacology · 2025Article
- Naturally occurring plant-based anticancerous candidates as prospective ABCG2 inhibitors: an in silico drug discovery study.Molecular diversity · 2022Article
- Strategies and Mechanism in Reversing Intestinal Drug Efflux in Oral Drug Delivery.Pharmaceutics · 2022Review
- KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal CancerFrontiers in genetics · 2022Article
- MG53 inhibits cellular proliferation and tumor progression in colorectal carcinoma.International journal of biological sciences · 2022Article
- A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors.Molecules (Basel, Switzerland) · 2021Review
- Structure-Based Discovery of ABCG2 Inhibitors: A Homology Protein-Based Pharmacophore Modeling and Molecular Docking Approach.Molecules (Basel, Switzerland) · 2021Article
- Article
- Scaffold fragmentation and substructure hopping reveal potential, robustness, and limits of computer-aided pattern analysis (C@PA).Computational and structural biotechnology journal · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multidrug resistance (MDR) associated with the overexpression of ABC transporters is one of the key causes of chemotherapy failure. Various compounds blocking the function and/or downregulating the expression of these transporters have been developed over the last few decades. However, their potency and toxicity have always been a concern. In this report, we found that BMS-599626 is a highly potent inhibitor of the ABCG2 transporter, inhibiting its efflux function at 300 nM. Our study repositioned BMS-599626, a highly selective pan-HER kinase inhibitor, as a chemosensitizer in ABCG2-overexpressing cell lines. As shown by the cytotoxicity assay results, BMS-599626, at noncytotoxic concentrations, sensitizes ABCG2-overexpressing cells to topotecan and mitoxantrone, two well-known substrates of ABCG2. The results of our radioactive drug accumulation experiment show that the ABCG2-overexpressing cells, treated with BMS-599626, had an increase in the accumulation of substrate chemotherapeutic drugs, as compared to their parental subline cells. Moreover, BMS-599626 did not change the protein expression or cell surface localization of ABCG2 and inhibited its ATPase activity. Our in-silico docking study also supports the interaction of BMS-599626 with the substrate-binding site of ABCG2. Taken together, these results suggest that administration of chemotherapeutic drugs, along with nanomolar concentrations (300 nM) of BMS-599626, may be effective against ABCG2-mediated MDR in clinical settings.
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