The apicoplast is essential to the malaria parasite and its main function during asexual blood stages is to provide the isoprenoid precursor isopentenyl diphosphate (MEP) pathway. Without IPP, the parasite cannot synthesize isoprenoids; this IPP deficit is cytocidal and may also reduce the ability of the parasite to invade host cells. Since humans synthesize IPP through the mevalonic acid pathway, compounds that block one or more of the enzymes of the MEP pathway could have an antimalarial action while having no impact on human isoprenoid biosynthesis. We have identified a series of compounds that are toxic to the malaria parasite due to blockage of the MEP pathway. Since other apicoplexan protozoan parasites and several pathogenic bacteria also use the MEP pathway, specifically tailored analogs of our lead compounds could be useful to treat a variety of other human infections, including: toxoplasmosis (Toxoplasma gondii), tuberculosis (Mycobacterium tuberculosis), Anthrax (Baccillus anthracis), cholera (V. cholera), Clostridum difficile, Clostridium botullinum, Helicobactor pylori, Campylobacter jejuni, and Chlamydia (trachomatis 434/Bu and pneumoniae). Furthermore, many pathogens with veterinary relevance also us the MEP pathway, such as Brucella abortus (brucellosis), and Eimeria tenella (hemorrhagic cecal coccidiosis in young poultry). In addition, since plants use the MEP pathway, herbicidal applications of MEP pathway inhibitors can also be envisioned.