{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Edgar RCS"],"funding":["DHAC | National Health and Medical Research Council","Therapeutic Innovation Australia (TIA)","Therapeutic Innovation Australia","DHAC | National Health and Medical Research Council (NHMRC)"],"pagination":["e0096624"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11237774"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(6)"],"pubmed_abstract":["To combat the global burden of malaria, development of new drugs to replace or complement current therapies is urgently required. Here, we show that the compound <b>MMV1557817</b> is a selective, nanomolar inhibitor of both <i>Plasmodium falciparum</i> and <i>Plasmodium vivax</i> aminopeptidases M1 and M17, leading to inhibition of end-stage hemoglobin digestion in asexual parasites. <b>MMV1557817</b> can kill sexual-stage <i>P. falciparum</i>, is active against murine malaria, and does not show any shift in activity against a panel of parasites resistant to other antimalarials. <b>MMV1557817</b>-resistant <i>P. falciparum</i> exhibited a slow growth rate that was quickly outcompeted by wild-type parasites and were sensitized to the current clinical drug, artemisinin. Overall, these result"],"journal":["mBio"],"pubmed_title":["On-target, dual aminopeptidase inhibition provides cross-species antimalarial activity."],"pmcid":["PMC11237774"],"funding_grant_id":["1136300","1185354","1150359"],"pubmed_authors":["Price RN","Suraweera CD","Malcolm TR","Avery VM","Creek DJ","de Koning-Ward TF","Giannangelo C","Duffy S","Drinkwater N","Counihan NA","Daware K","Charman SA","Chowdhury M","Noviyanti R","McGowan S","Wirjanata G","Scammells PJ","Wittlin S","Siddiqui G","Marfurt J","Dans M","Challis M","Edgar RCS"],"additional_accession":[]},"is_claimable":false,"name":"On-target, dual aminopeptidase inhibition provides cross-species antimalarial activity.","description":"To combat the global burden of malaria, development of new drugs to replace or complement current therapies is urgently required. Here, we show that the compound <b>MMV1557817</b> is a selective, nanomolar inhibitor of both <i>Plasmodium falciparum</i> and <i>Plasmodium vivax</i> aminopeptidases M1 and M17, leading to inhibition of end-stage hemoglobin digestion in asexual parasites. <b>MMV1557817</b> can kill sexual-stage <i>P. falciparum</i>, is active against murine malaria, and does not show any shift in activity against a panel of parasites resistant to other antimalarials. <b>MMV1557817</b>-resistant <i>P. falciparum</i> exhibited a slow growth rate that was quickly outcompeted by wild-type parasites and were sensitized to the current clinical drug, artemisinin. Overall, these result","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-04-29T12:04:37.208Z","creation":"2025-04-05T15:47:20.051Z"},"accession":"S-EPMC11237774","cross_references":{"pubmed":["38717141"],"doi":["10.1128/mbio.00966-24"]}}