Marcel Kaiser

This paper uses human iPSC-derived macrophages to model T. cruzi infection and test trypanocidal compounds for Chagas disease drug discovery.

The paper shows that atovaquone and venturicidin A work together to kill Plasmodium falciparum by blocking two pathways that generate mitochondrial membrane potential.

This study shows venturicidin A targets ATP synthase in Trypanosoma brucei, causing mitochondrial membrane potential loss and kDNA loss, suggesting it as a potential antitrypanosomatid drug.

MEMO enables clustering of chemodiverse samples using LC-MS/MS profiles without feature alignment, achieving performance comparable to state-of-the-art methods faster.