As an obligate intracellular pathogen that can invade and replicate in any nucleated mammalian cell, T. gondii is in stringent dependence on specific host cell resources . This parasite lacks many genes encoding the entire metabolic pathways, but has evolved efficient strategies to acquire crucial metabolites from the host cells . For survival, T. gondii is auxotrophic for numerous nutrients and has acquired salvage mechanisms to import the vital compounds that it cannot synthesize, as for example various metabolites including polyamines, cholesterol, purine derivatives and essential amino acids . Chemotherapeutic targeting of the parasitic cell cycle and of the specific metabolic defects of T. gondii based on its auxotrophic nature was already explored (e.g., starving the parasite by nutrient depletion or disrupting the salvage pathways) . Various approaches can be considered: (i) using specific inhibitors of transporters/enzymes involved in the salvage pathway (nutrients uptake and metabolism) while exploiting the large phylogenic separation between the mammalian host and T. gondii ; (ii) developing 'subversive' substrate analogues that are metabolized to toxic molecules ; (iii) using a 'Trojan horse' like strategy by conjugating essential nutrients to an active compound to increase internalization based on the ability of T. gondii to sequester and scavenge this type of the hybrid molecules. Some of the most striking biochemical and physiological differences between pathogens and mammalian hosts are found in purine metabolism , with the respective parasite and mammalian enzymes showing discrepancies in substrate specificity . Targeting the T. gondii purine salvage pathways represents a potential pharmacological strategy and former studies explored this approach . However, this stratagem was not widely applied due to the apprehension that compounds targeting parasite metabolism can also be toxic to the host .