The current drugs against sleeping sickness are derived from cancer chemotherapeutic approaches. Herein, we aimed at evaluating the in vitro effect of alcoholic extracts of Artemisia annua (AMR), Rumex abyssinicus (RMA), and Catha edulis Forsk (CEF) on proliferation/viability of 1321N1 astrocytoma, MCF-7 breast cancer, THP-1 leukemia, and LNCaP, Du-145, and PC-3 prostate cancer cells and on Trypanosoma brucei cells. Proliferation of tumor cells was evaluated by WST-1 assay and viability/behaviour of T. brucei by cell counting and light microscopy. CEF was the most efficient growth inhibitor in comparison to AMR and RMA. Nevertheless, in LNCaP and THP-1 cells, all extracts significantly inhibited tumor growth at 3？μg/mL. All extracts inhibited proliferation of T. brucei cells in a concentration-dependent manner. Microscopic analysis revealed that 95% of the T. brucei cells died when exposed to 33？μg/mL CEF for 3 hrs. Similar results were obtained using 33？μg/mL AMR for 6？hrs. In case of RMA, however, higher concentrations were necessary to obtain similar effects on T. brucei. This demonstrates the antitumor efficacy of these extracts as well as their ability to dampen viability and proliferation of T. brucei, suggesting a common mechanism of action on highly proliferative cells, most probably by targeting cell metabolism. 1. Introduction Many anticancer reagents, including nucleotide analogues and other DNA synthesis inhibitors (e.g., methotrexate), aim at exerting a specific activity against rapidly proliferating cell types. Because of the capacity of trypanosomes for rapid growth within mammals, they have been linked to some types of cancer cells. D,L-α-Difluoromethylornithine (DFMO), a polyamine synthesis inhibitor, was originally developed as a potential anticancer reagent before it has been proved useful in trypanosomiasis therapy. Furthermore, suramin, melarsoprol, and pentamidine which are drugs licensed for the treatment of human African trypanosomiasis (HAT) are known to arise from cancer research studies [1–3]. If left untreated, sleeping sickness patients die within months when infected with T. brucei rhodesiense (acute form of the disease in East and Southern Africa) or within years when infected with T. brucei gambiense (chronic form of the disease in West and Central Africa) [4]. It is estimated that at least people are presently infected [5]. Above this burden of the disease, all the available drugs have a number of shortcomings during treatment because of resistance development against them, allergic reactions, undesirable effects in the
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