EU-funded study shows that drugs originally designed to inhibit the growth of cancer cells can also kill the parasite that causes malaria. The idea is to make the host cell environment useless to it, by blocking the kinases in the cell. This strategy deprives the parasite of a major 'modus operandi' for development of drug resistance.

Malaria is caused by a parasite called Plasmodium, which is transmitted via the bites of infected mosquitoes. In the human body, the parasites reproduce in the liver, and then infect and multiply in red blood cells. Until now the malaria parasite has managed to avoid control by rapidly developing drug resistance through mutations and hiding from the immune system inside liver and red blood cells in the body of the host, where it proliferates. The discovery that the parasite needs to hijack some enzymes from the cell it lives in opens up a whole new strategy for fighting the disease.

According to World Health Organisation statistics, in 2009 there were infected around 225 million and killed nearly 800,000 people worldwide. Since 2002, the EU has invested nearly €180 million in malaria research through the EU's Framework Programmes for Research (FP6, 2002-2006, and FP7, 2007-2013). So far, efforts to find a treatment have been hampered by the parasite’s ability to quickly develop drug resistance.

The research involved four projects funded by the EU (ANTIMAL, BIOMALPAR, MALSIG and EVIMALAR) and was led by laboratories in the UK, France and Switzerland with partners from Belgium, Germany, Denmark, Greece, Spain, Italy, Netherlands, Portugal, and Sweden, along with many developing nations severely affected by malaria. Now, the UE has to mobilise public and industrial partners to verify the efficacy of kinase inhibitors in malaria patients and to adjust the dose through clinical trials