In-silico identification of antimalarial compounds targeting PfMDR1 of Plasmodium falciparum

利用计算机模拟方法鉴定靶向恶性疟原虫 PfMDR1 的抗疟化合物

阅读:1

Abstract

PfMDR1, a key transporter protein in Plasmodium falciparum, contributes to antimalarial drug resistance by actively expelling drugs like chloroquine from the parasite's digestive vacuole, lowering their intracellular efficacy. In this study, our aim was to identify the antimalarial compounds with unknown targets on the basis of cellular assays from the Chembl and IUPHAR databases against the target protein PfMDR1, having PDB ID: 8JWI, using molecular docking with GLIDE and GOLD. The top-ranking compound demonstrated a GLIDE docking score of - 12.169 kcal/mol, surpassing the benchmark compound (- 5.435 kcal/mol) and other experimentally tested drugs. Post-docking analyses using LigPlot and PyMOL revealed strong hydrogen bonding and hydrophobic interactions with key active site residues. Binding affinity predictions using X-SCORE further supported the superior binding of the top compound. To evaluate stability and inhibitory potential, we performed molecular dynamics (MD) simulations using GROMACS, analyzing protein-ligand interactions throughout the trajectory. The top compound maintained stable binding throughout the simulation, with minimal fluctuations. The binding free energy calculations using MM/PBSA method further confirmed its inhibitory effect, with a binding free energy of - 130.971 ± 14.283 kJ/mol, significantly higher as compared to the benchmark and other experimentally tested compounds, indicating stronger and more stable interactions. These findings suggest that the identified inhibitor exhibits greater potency against PfMDR1 than the benchmark and other screened antimalarial drugs, making it a promising candidate for overcoming P. falciparum drug resistance. This study provides valuable insights for future structure-based drug design targeting PfMDR1 and developing next-generation antimalarial therapies. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40203-025-00486-3.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。