Malaria, a disease caused by several species of obligate protozoan parasites, remains one of the most prevalent and persistent diseases to affect the global population; with hundreds of millions of people infected and over a million deaths each year. This situation is compounded by the increasing resistance of the malaria parasites, particularly Plasmodium falciparum, to conventional drugs. There is a great need to identify new therapeutically amenable targets and/or mechanisms with a view to developing small molecule inhibitors and/or vaccines to treat malaria.
Falcipain-2 (FP-2) and falcipain-3 (FP-3) are cysteine peptidases of the same CAC1 family as the human cathepsins and are produced by the human malaria parasite Plasmodium falciparum. FP-2 and FP-3 catalyse the proteolysis of host proteins as a means of completing various stages of the parasites life-cycle as well as acquiring nutrients. FP-2 and FP-3 have been found to be essential for parasite growth and completion of the blood stage of their life-cycle. Selective inhibition of FP-2 and/or FP-3 may provide a novel treatment for malaria.
General information on Malaria: link here
Search MEROPS peptidase database: link to MEROPS here
Amura has developed low nanomolar inhibitors of falcipain-2 (FP-2) and falcipain-3 (FP-3) with excellent selectivity (greater than a hundred fold) versus closely related homologs. Our current lead inhibitors exhibit a significant reduction in parasitaemia in an in vivo model of a Plasmodium chabaudi disease. These lead compounds are the product of Amura’s AMcore™ platform which has reproducibly provided ‘fast-on, slow-off rate’ enzyme inhibitors with good pharmacokinetic half-lives and a very strong IP position.
PubMed link to Amura falcipain paper: here
Amura is seeking funding opportunities or partners with a common vision towards progression and commercialisation of these first in class therapeutics.
Amura has licensing opportunities for its AMcore™-based programmes.