The purpose of this topic is to explore how the stereochemical configuration of the drug molecule (especially the C3 isomer) regulates the balance between primary target inhibition and secondary bactericidal mechanisms in the development of novel antibiotics against bacterial ATP synthase. The analysis focuses on whether such drugs can still retain effective bactericidal activity through non-target-dependent pathways (e. g., affecting cell membrane potential or fluidity) when bacteria are resistant to the main target (e. g., atpE gene).