DNA-binding drugs have shown potential against the parasitic disease African trypanosomiasis (sleeping sickness), but they have several disadvantages, such as toxic effects or inability to cross the blood-brain barrier, which may prevent them from treating individuals in which the parasites have entered the central nervous system.

Human African trypanosomiasis (HAT) is a neglected tropical disease caused by the vector-borne parasites Trypanosoma brucei gambiens or Trypanosoma brucei rhodesiense. Despite the recent approval of fexinidazole, novel antitrypanosomal agents are needed to attain its targeted eradication by 2030.

Researchers at the Salk Institute for Biological Studies have shown a possible beneficial role for muscle wasting in mice infected with Trypanosoma brucei, a parasite that causes sleeping sickness in humans. The team assessed the impact of both fat and muscle wasting on survival of mice with T. brucei infection. They found that while fat wasting appeared to have no impact on survival, mice that were unable to undergo muscle wasting died more quickly from the infection than those that experienced muscle loss.

Parasitic diseases caused by trypanosomatid protozoa have long been treated with traditional methods. However, the effectiveness of current treatments for leishmaniasis is limited. Some are toxic, or have been abandoned, such as in the cases of Chagas disease and human African trypanosomiasis (HAT), commonly known as sleeping sickness.