Dapagliflozin in Chronic Kidney Disease: Insights from Network Pharmacology and Molecular Docking Simulation
Issued Date
2025-03-01
Resource Type
eISSN
20751729
Scopus ID
2-s2.0-105001035052
Journal Title
Life
Volume
15
Issue
3
Rights Holder(s)
SCOPUS
Bibliographic Citation
Life Vol.15 No.3 (2025)
Suggested Citation
Phongphithakchai A., Tedasen A., Netphakdee R., Leelawattana R., Srithongkul T., Raksasuk S., Huang J.C., Chatatikun M. Dapagliflozin in Chronic Kidney Disease: Insights from Network Pharmacology and Molecular Docking Simulation. Life Vol.15 No.3 (2025). doi:10.3390/life15030437 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/108618
Title
Dapagliflozin in Chronic Kidney Disease: Insights from Network Pharmacology and Molecular Docking Simulation
Corresponding Author(s)
Other Contributor(s)
Abstract
Chronic kidney disease (CKD) involves inflammation, oxidative stress, and fibrosis, leading to renal dysfunction. Dapagliflozin, an SGLT2 inhibitor, shows renoprotective effects beyond glucose control, but its precise molecular mechanisms remain unclear. This study utilizes network pharmacology and molecular docking to elucidate its multi-target effects in CKD. Dapagliflozin’s SMILES structure was analyzed for ADMET properties. Potential targets were identified via SwissTargetPrediction, GeneCards, and SEA, and common CKD-related targets were determined. A protein–protein interaction (PPI) network was constructed, and key pathways were identified using GO and KEGG enrichment analyses. Molecular docking was conducted to validate dapagliflozin’s binding affinities with hub proteins. A total of 208 common targets were identified, including EGFR, GSK3β, and IL-6. GO and KEGG analyses highlighted key pathways, such as PI3K-Akt, MAPK, and AGE-RAGE, involved in inflammation, oxidative stress, and metabolic regulation. Molecular docking confirmed strong binding affinities with EGFR (−8.42 kcal/mol), GSK3β (−7.70 kcal/mol), and IL-6 (−6.83 kcal/mol). Dapagliflozin exhibits multi-target therapeutic potential in CKD by modulating inflammation, oxidative stress, and metabolic pathways. This integrative approach enhances the understanding of its mechanisms, supporting future experimental validation and clinical application in CKD management.