Monoclonal antibodies targeting Candida disrupt biofilms and inhibit growth across global clinical isolates.

Candida species are a major cause of severe fungal infections, particularly in immunocompromised individuals and hospitalized patients. Among these, Candida auris stands out as an emerging "superbug", responsible for life-threatening bloodstream infections with mortality rates up to 60%. This multidrug-resistant, hospital-acquired pathogen has been declared a serious global health threat, complicating effective treatment and increasing mortality risks. Our research has identified universal monoclonal antibodies (mAbs) targeting Candida albicans cell wall epitopes, which are highly homologous to those in other pathogenic Candida species, including C. auris. Passive transfer of mAbs-C3.1 (anti-β-1,2-mannotriose) and 9F2 (anti-phosphoglycerate kinase 1)-significantly extended survival and improved fungal clearance in a complement C5-deficient A/J murine model. Additionally, C3.1 and 9F2 mAbs show direct fungicidal effects against C. auris isolates, presenting a promising therapeutic option against this critical threat.