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.
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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- Erratum issued
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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.
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