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Mucormycosis (a.k.a. zygomycosis) is an often-life-threatening disease caused by fungi from the ancient fungal division Mucoromycota. Globally, there are nearly a million people with the disease. <i>Rhizopus</i> spp., and <i>R. delemar</i> (<i>R. oryzae, R. arrhizus</i>) in particular, are responsible for most of the diagnosed cases. Pulmonary, rhino-orbito-cerebral, and invasive mucormycosis are most effectively treated with amphotericin B (AmB) and particularly with liposomal formulations (e.g., AmBisome^®). However, even after antifungal therapy, there is still a 50% mortality rate. Hence, there is a critical need to improve therapeutics for mucormycosis. Targeting AmB-loaded liposomes (AmB-LLs) with the pathogen receptor Dectin-1 (DEC1-AmB-LLs) to the beta-glucans expressed on the surface of <i>Aspergillus fumigatus</i> and <i>Candida albicans</i> lowers the effective dose required to kill cells relative to untargeted AmB-LLs. Because Dectin-1 is an immune receptor for <i>R. delemar</i> infections and may bind it directly, we explored the Dectin-1-mediated delivery of liposomal AmB to <i>R. delemar</i>. DEC1-AmB-LLs bound 100- to 1000-fold more efficiently to the exopolysaccharide matrix of <i>R. delemar</i> germlings and mature hyphae relative to AmB-LLs. DEC1-AmB-LLs delivering sub-micromolar concentrations of AmB were an order of magnitude more efficient at inhibiting and/or killing <i>R. delemar</i> than AmB-LLs. Targeted antifungal drug-loaded liposomes have the potential to improve the treatment of mucormycosis.