Malaria is a global challenge, and its infection is propagated through Plasmodium falciparum, an obligate human parasite. The genome of P. falciparum encodes many proteases that play significant roles in their survival and pathogenesis thus being considered as attractive drug targets. P. falciparum metacaspase-3 (PfMCA3) is one such protease and a validated drug target to control malarial infection.
The continuous emergence of resistance to the available drugs poses major constraints in the development of effective therapeutics against Malaria. The Malaria drug resistance has been attributed to be the manifestation of numerous factors. For example, mutations in the parasite transporter protein acetyl-CoA transporter (Pfact) can remarkably affect its uptake affinity for a drug molecule against malaria, and hence enhance its susceptibility to resistance.