In the malarial research program conducted on a national scale during World War II, several drugs were developed which had marked superiority over quinacrine (atabrine) and quinine in their ability to terminate individual attacks of vivax malaria (1). For example, chloroquine (SN-7618) in terms of oral dosage and the resulting plasma concentration can be administered in amounts many times that required to suppress the disease (2). The margin between the therapeutic and toxic dose of chloroquine is several times that which exists for quinine and quinacrine. When these new compounds, however, failed, even at high dosages, to affect the relapse rate it seemed doubtful that further extension of research aimed chiefly towards finding a more effective and less toxic, and primarily suppressive, drug would lead