| Summary: | The emerging spread of drug-resistant malaria parasites highlights the need for new antimalarial agents. This study evaluated the growth-inhibitory effects of sparsomycin (Sm), a peptidyl transferase inhibitor, against <i>Plasmodium falciparum</i> 3D7 (chloroquine-sensitive strain), <i>P. falciparum</i> K1 (resistant to multiple drugs, including chloroquine), <i>P. yoelii</i> 17XNL (cause of uncomplicated rodent malaria) and <i>P. berghei</i> ANKA (cause of complicated rodent malaria). Using a fluorescence-based assay, we found that Sm exhibited half-maximal inhibitory concentrations (IC<sub>50</sub>) of 12.07 and 25.43 nM against <i>P. falciparum</i> 3D7 and K1, respectively. In vitro treatment of <i>P. falciparum</i> 3D7 with Sm at 10 or 50 nM induced morphological alteration, blocked parasites in the ring state and prevented erythrocyte reinvasion, even after removal of the compound. In mice infected with <i>P. yoelii</i> 17XNL, the administration of 100 μg/kg Sm for 7 days did not affect parasitemia. Meanwhile, treatment with 300 μg/kg Sm resulted in a significantly lower parasitemia peak (18.85%) than that observed in the control group (40.13%). In mice infected with <i>P. berghei</i> ANKA, both four and seven doses of Sm (300 μg/kg) prolonged survival by 33.33%. Our results indicate that Sm has potential antiplasmodial activities in vitro and in vivo, warranting its further development as an alternative treatment for malaria.
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