The Candida genus is responsible for causing over 150 million fungal infections annually, with Candida albicans being the most clinically significant member of the genus. It is responsible for approximately 40% of fungal bloodstream infections and is particularly problematic in immunocompromised patients. Rising antimicrobial drug resistance has intensified the need for new antifungal agents with alternative mechanisms of action capable of bypassing existing resistance pathways. Silver-based complexes have emerged as promising antimicrobial candidates due to their ability to coordinate with biologically active ligands, including 1,10-phenanthroline and its derivatives. Two such derivatives, phenanthroline-oxazine and pyrido-phenanthroline, have shown notable antifungal potential. Previous studies demonstrated the in vitro activity of the phenanthroline-oxazine derivative PPO and its silver complex, Ag(PPO)₂, against C. albicans. However, their in vivo efficacy and mechanism of action remained unclear. In this study, label-free quantitative proteomics was used to investigate the antifungal mechanism of Ag(PPO)₂. Proteomic analysis revealed that the silver complex disrupted fungal respiration, with treated C. albicans cells showing reduced abundance of key respiratory enzymes, including succinate dehydrogenase and NADH-ubiquinone reductase, it wasfound that Ag(PPO)2 causes iron starvation, through sequestration, leading to a metabolic failure. Treatment also caused major changes in fungal cell wall structure and altered the abundance of adhesins, including adhesin 2 and adhesin 5, these changes to the cell wall were confirmed using SEM and fluorescence microscopy. The in vivo efficacy of Ag(PPO)₂ was assessed using the Galleria mellonella infection model, where treatment provided 80% protection against C. albicans infection.