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The most severe form of human malaria is caused by the parasite  Plasmodium falciparum . The second messenger cAMP has been shown to be important for the parasite’s ability to infect the host’s liver, but its role during parasite growth inside erythrocytes, the stage responsible for symptomatic malaria, is less clear. The  P. falciparum  genome encodes two adenylyl cyclases, the enzymes that synthesize cAMP,  Pf ACα and  Pf ACβ. We now show that one of these,  Pf ACβ, plays an important role during the erythrocytic stage of the  P. falciparum  life cycle. Biochemical characterization of  Pf ACβ revealed a marked pH dependence, and sensitivity to a number of small molecule inhibitors. These inhibitors kill parasites growing inside red blood cells. One particular inhibitor is selective for  Pf ACβ relative to its human ortholog, soluble adenylyl cyclase (sAC); thus,  Pf ACβ represents a potential target for development of safe and effective antimalarial therapeutics.

Characterization of Plasmodium falciparum Adenylyl Cyclase-β and Its Role in Erythrocytic Stage Parasites