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Small-molecule intervention and stabilization of G-quadruplexes (G4s) have been investigated for the potential as therapeutic approaches. MYC plays diverse roles in cellular functions, making it a highly desirable yet challenging target. One promising strategy includes DNA G4 structures, which mediate transcriptional control over MYC in the presence of small-molecule ligands. Unraveling the effects of these ligands on G4 stability and functionality is seldom achieved yet essential for designing potent ligands against these intractable targets. This study introduces BTO-28, a benzothiazole-based ligand that binds with high affinity to the MYC G4. In vitro experiments, NMR analysis, and intracellular assays collectively indicate that BTO-28 potentially downregulates MYC transcription through a G4-mediated mechanism. Structural determination of the 2:1 benzothiazole–MYC G4 complex provides insights into unexpected molecular interactions, highlighting for the first time a unique hydrogen-bonding pattern involving the nucleobase surrogate and flanking residues. The protonated pyrrolidine side chains of BTO-28 reorient to form hydrogen bonding with the external G-tetrad, establishing a previously uncharacterized ligand–G4 interface. This work advances the rational design of G4-binding ligands and clarifies the molecular basis underlying MYC recognition.
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Xiao et al. (2025) studied this question.
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