Inhibition Mechanism and Target Reassessment of Potent Piperaquine Analogs: Evidence for PfLDH over PfDHODH

强效哌喹类似物的抑制机制及靶点重新评估:PfLDH优于PfDHODH的证据

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Abstract

Malaria remains a major global health concern, with Plasmodium falciparum (Pf) responsible for the most severe and drug-resistant infections. In earlier work, Boechat et al. synthesized two novel series of piperaquine analogs via molecular hybridization, identifying compounds M9 and M11 as promising antiplasmodial leads. These compounds showed significant activity against both asexual and gametocyte stages. Despite incorporating structural features typically associated with Pf dihydroorotate dehydrogenase (PfDHODH) inhibition, enzymatic assays revealed negligible activity against this enzyme, suggesting an alternative molecular target. This prompted the current study, which explores Pf lactate dehydrogenase (PfLDH) as a potential target. An in-silico investigation including molecular docking, molecular dynamics (MD) simulations, DFT calculations, and Quantum Theory of Atoms in Molecules (QTAIM) analysis was conducted to validate this hypothesis. The findings supported PfLDH as a likely target and emphasized the role of linker length in enhancing hydrophobic interactions and conformational flexibility. Among the candidates, compound M9 exhibited strong and stable binding within the PfLDH active site, characterized by a low RMSD (0.5 Å), favorable binding energy (-5.06 kcal/mol), and sustained hydrogen bonding with key catalytic residues (Thr101 and Asn140). Frontier molecular orbital analysis indicated a reduced HOMO-LUMO energy gap upon binding, while Mulliken charge and QTAIM analyses confirmed significant electronic redistribution and stabilizing noncovalent interactions. These results provide mechanistic insights into the compound's bioactivity and support the further development of antimalarials.

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