There are an estimated 200 million people infected with malaria annually, with an estimated 400,000-500,000 deaths, and 40% of the world’s population at risk of contracting the disease.  While artemisinin and mosquito reduction are the current treatments, there are artemisinin-resistant parasites emerging, underscoring the need for the next generation of antimalarial drugs.

Researchers in Drexel’s Department of Microbiology & Immunology and Rutgers University have used a hybrid structure-based method to design pyrazole-urea compounds that may be effective antimalarial agents.  These agents inhibit a protein-protein interaction that allows for host cell invasion by the parasite.  Because these structures are new molecular scaffolds that are unrelated to the pathways targeted by current malaria drugs, the likelihood of parasite resistance is minimized.  The myosin motor components in the P. falciparum parasite were targeted, as the interaction between the carboxy terminal tail of myosin A and the myosin tail interacting protein contributes to parasite motility and entry into the host cell.