ArticleFrontiers in pharmacology2026
Reversal of ABCG2-mediated MDR by VEGFR3 inhibitor (S)-SAR131675.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Multidrug resistance (MDR) remains a major challenge in cancer treatment, as it is a significant factor contributing to chemotherapy failure and cancer recurrence. Among various resistance mechanisms, the overexpression of the breast cancer resistance protein (BCRP/ABCG2) has been identified as a cause of MDR in multiple cancers, including breast cancer, lung cancer, and colon cancer (S)-SAR131675 is the S-enantiomer of SAR131675 (HY-15458), which significantly and selectively suppresses the Vascular Endothelial Growth Factor Receptor 3 (VEGFR3). In this research (S)-SAR131675 shows the ability to overcome the ABCG2-mediated MDR in both the non-small cell lung cancer cell line NCI-H460 and its ABCG2-overexpressing cell line NCI-H460/TPT10, as well as the colorectal cancer cell line S1 and its ABCG2-overexpressing cell line S1-M1-80. Through several experiments, we demonstrate that (S)-SAR131675 targets the efflux function of ABCG2, resulting in an increased intracellular concentration of substrates of ABCG2, including mitoxantrone and topotecan. Additionally, this resensitizing effect did not affect the overall protein expression or subcellular localization of ABCG2 in the ABCG2-overexpressing cell lines. In summary (S)-SAR131675 can overcome ABCG2-mediated MDR by directly suppressing the drug efflux function, providing a promising basis for the further development of cancer treatments associated with MDR in the future.
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