Majed S. AlFayi , Mohd Saeed , Irfan Ahmad , Mohd Adnan Kausar , Samra Siddiqui , Saba Irem , Faisal Fawaz Alshammari , Riadh Badraoui , Dharmendra Kumar Yadav
{"title":"揭示戊氟利多和BMS-754,807: NUDT5抑制在乳腺癌中的治疗作用","authors":"Majed S. AlFayi , Mohd Saeed , Irfan Ahmad , Mohd Adnan Kausar , Samra Siddiqui , Saba Irem , Faisal Fawaz Alshammari , Riadh Badraoui , Dharmendra Kumar Yadav","doi":"10.1016/j.chphi.2025.100871","DOIUrl":null,"url":null,"abstract":"<div><div>Breast cancer (BC) remains a leading cause of cancer-related mortality among women, with hormone-receptor-positive subtypes frequently developing resistance to standard therapies. Nudix hydrolase 5 (NUDT5), an enzyme integral to ADP-ribose metabolism, DNA repair, and hormone-driven transcription, has emerged as a promising therapeutic target. This study employed computational drug discovery approaches to identify potential NUDT5 inhibitors from FDA-approved compounds in the Drug-Lib database. Virtual screening and molecular docking revealed four promising candidates: Afacifenacin, Penfluridol, Belaperidone, and BMS-754,807. Detailed molecular dynamics simulations validated their stability, with trajectory analyses, including RMSD, RMSF, and PCA-based free energy landscapes, highlighting consistent and favourable interactions. Among these, BMS-754,807 demonstrated the strongest inhibitory potential, with stable binding, superior hydrogen bonding interactions, and the lowest free energy values. These findings emphasize the therapeutic promise of these compounds, particularly BMS-754,807, in targeting hormone-resistant breast cancer. Future in vitro and in vivo studies will be crucial to confirm these results and advance these inhibitors toward clinical applications.</div></div>","PeriodicalId":9758,"journal":{"name":"Chemical Physics Impact","volume":"10 ","pages":"Article 100871"},"PeriodicalIF":3.8000,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Unveiling the therapeutic role of penfluridol and BMS-754,807: NUDT5 inhibition in breast cancer\",\"authors\":\"Majed S. AlFayi , Mohd Saeed , Irfan Ahmad , Mohd Adnan Kausar , Samra Siddiqui , Saba Irem , Faisal Fawaz Alshammari , Riadh Badraoui , Dharmendra Kumar Yadav\",\"doi\":\"10.1016/j.chphi.2025.100871\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Breast cancer (BC) remains a leading cause of cancer-related mortality among women, with hormone-receptor-positive subtypes frequently developing resistance to standard therapies. Nudix hydrolase 5 (NUDT5), an enzyme integral to ADP-ribose metabolism, DNA repair, and hormone-driven transcription, has emerged as a promising therapeutic target. This study employed computational drug discovery approaches to identify potential NUDT5 inhibitors from FDA-approved compounds in the Drug-Lib database. Virtual screening and molecular docking revealed four promising candidates: Afacifenacin, Penfluridol, Belaperidone, and BMS-754,807. Detailed molecular dynamics simulations validated their stability, with trajectory analyses, including RMSD, RMSF, and PCA-based free energy landscapes, highlighting consistent and favourable interactions. Among these, BMS-754,807 demonstrated the strongest inhibitory potential, with stable binding, superior hydrogen bonding interactions, and the lowest free energy values. These findings emphasize the therapeutic promise of these compounds, particularly BMS-754,807, in targeting hormone-resistant breast cancer. Future in vitro and in vivo studies will be crucial to confirm these results and advance these inhibitors toward clinical applications.</div></div>\",\"PeriodicalId\":9758,\"journal\":{\"name\":\"Chemical Physics Impact\",\"volume\":\"10 \",\"pages\":\"Article 100871\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-04-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Chemical Physics Impact\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2667022425000593\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CHEMISTRY, PHYSICAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chemical Physics Impact","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667022425000593","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CHEMISTRY, PHYSICAL","Score":null,"Total":0}
Unveiling the therapeutic role of penfluridol and BMS-754,807: NUDT5 inhibition in breast cancer
Breast cancer (BC) remains a leading cause of cancer-related mortality among women, with hormone-receptor-positive subtypes frequently developing resistance to standard therapies. Nudix hydrolase 5 (NUDT5), an enzyme integral to ADP-ribose metabolism, DNA repair, and hormone-driven transcription, has emerged as a promising therapeutic target. This study employed computational drug discovery approaches to identify potential NUDT5 inhibitors from FDA-approved compounds in the Drug-Lib database. Virtual screening and molecular docking revealed four promising candidates: Afacifenacin, Penfluridol, Belaperidone, and BMS-754,807. Detailed molecular dynamics simulations validated their stability, with trajectory analyses, including RMSD, RMSF, and PCA-based free energy landscapes, highlighting consistent and favourable interactions. Among these, BMS-754,807 demonstrated the strongest inhibitory potential, with stable binding, superior hydrogen bonding interactions, and the lowest free energy values. These findings emphasize the therapeutic promise of these compounds, particularly BMS-754,807, in targeting hormone-resistant breast cancer. Future in vitro and in vivo studies will be crucial to confirm these results and advance these inhibitors toward clinical applications.