Agreement is a first for MMV, which has until now concentrated only on research and development of treatments for P.falciparum.
MMV has executed an agreement with GlaxoSmithKline (GSK) to develop tafenoquine as a radical cure for Plasmodium vivax malaria. This marks a first for MMV, which has until now concentrated only on research and development of treatments for P.falciparum. Under the terms of the agreement, MMV will provide funding in order to advance the development of tafenoquine at GSK under the joint oversight of MMV and GSK.
P. vivax infection results in an acute infection of human erythrocytes (red blood cells) and liver cells with dormant parasites (hypnozoites). These dormant hypnozoites can become active resulting in a reappearance of blood stage parasites and a new outbreak of malaria. A radical cure implies the complete elimination of malaria parasites from the body; specifically of the hypnozoites
Research will initially focus on Phase I trials conducted on G6PD-deficient volunteers to determine the safety of tafenoquine on people who do not have enough of the enzyme glucose-6-phosphate dehydrogenase, (G6PD) which helps red blood cells (RBCs) function normally.
"Tafenoquine is a novel inclusion for MMV’s portfolio. Given its activity against the liver stages of malaria, or hypnozoites, it is an essential part of the fight against P vivax infections. As the malaria elimination agenda moves forwards we need an increasing array of tools against the parasite,” said Dr. Timothy Wells, Chief Scientific Officer at the Medicines for Malaria Venture. "MMV and GSK have worked successfully on a number of malaria projects in the past. Together, we hope to develop a radical cure for P.vivax malaria.”
Notes for editors
About Plasmodium vivax malaria
Malaria is among the world’s worst communicable diseases, causing over a million deaths each year and imposing major economic burdens on disease endemic countries. Over three billion people, half the world’s population, are at risk from this deadly disease. The recently released World Malaria Report 2008 (WMR) states that fewer people are dying of malaria than a decade ago, but attributes this reduction to a change in calculation methods. According to the WMR, 247 million cases of malaria and 881,000 deaths due to malaria occurred in 2006 in 109 countries. Ninety eight per cent of these deaths were in 35 countries, 91% of lives were lost in Africa and 85% were children under the age of five. That means one child dies of malaria every 30 seconds. Though the majority of the cases and approximately 90% of the malaria deaths are found in Sub-Saharan Africa, the disease is growing in Asia and Latin America.
P. vivax is one of four species of malarial parasite that commonly infect in humans and is the most frequent and widely distributed cause of recurring malaria. It is seldom fatal and is less virulent thanP. falciparum, the deadliest of the four. P. vivax is found mainly in Asia, Latin America, and in some parts of Africa. P. vivax can cause death due to splenomegaly, but more often it causes debilitating symptoms.
About G6PD Deficiency
Glucose-6-phosphate dehydrogenase G6PD is one of many enzymes that help the body process carbohydrates and turn them into energy. G6PD also protects red blood cells from potentially harmful by- products that can accumulate when a person takes certain medications or when the body is fighting an infection.
G6PD deficiency is known as ’favism’ after the Italian word for broad beans (fava), which cause a classic reaction when eaten by people with G6PD deficiency. In males, who have only one X chromosome, mutations in the gene for G6PD on the X chromosome cause G6PD deficiency. Females who have mutations on both X chromosomes will also be deficient. People of Mediterranean heritage, including Italians, Greeks, Arabs, and Sephardic Jews, are commonly affected. The severity of G6PD deficiency varies among these groups.
It is known that Africa and the Mediterranean basin are high-risk areas for the infectious disease malaria. Researchers have found evidence that the parasite that causes this disease does not survive well in G6PD-deficient cells. So they believe that the deficiency may have developed as a protection against malaria.