Dual Plasmepsin-Targeting Antimalarial Agents Disrupt Multiple Stages of the Malaria Parasite Life Cycle

Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identi...

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Bibliographic Details
Published inCell host & microbe Vol. 27; no. 4; pp. 642 - 658.e12
Main Authors Favuzza, Paola, de Lera Ruiz, Manuel, Thompson, Jennifer K., Triglia, Tony, Ngo, Anna, Steel, Ryan W.J., Vavrek, Marissa, Christensen, Janni, Healer, Julie, Boyce, Christopher, Guo, Zhuyan, Hu, Mengwei, Khan, Tanweer, Murgolo, Nicholas, Zhao, Lianyun, Penington, Jocelyn Sietsma, Reaksudsan, Kitsanapong, Jarman, Kate, Dietrich, Melanie H., Richardson, Lachlan, Guo, Kai-Yuan, Lopaticki, Sash, Tham, Wai-Hong, Rottmann, Matthias, Papenfuss, Tony, Robbins, Jonathan A., Boddey, Justin A., Sleebs, Brad E., Sabroux, Hélène Jousset, McCauley, John A., Olsen, David B., Cowman, Alan F.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 08.04.2020
Cell Press
Subjects
Animals
antimalarial
Antimalarials - pharmacology
Aspartic Acid Endopeptidases - drug effects
Disease Transmission, Infectious - prevention & control
humanized mouse
Life Cycle Stages - drug effects
malaria
Malaria - drug therapy
merozoite
Merozoites - drug effects
Mice
Mice, Transgenic
plasmepsin
plasmepsin IX
plasmepsin X
Plasmodium
Plasmodium berghei - drug effects
Plasmodium falciparum - drug effects
Plasmodium
humanized mouse
plasmepsin IX
merozoite
plasmepsin X
malaria
antimalarial
plasmepsin
Online AccessGet full text
ISSN1931-3128
1934-6069
1934-6069
DOI10.1016/j.chom.2020.02.005

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Abstract Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention. [Display omitted] •Specific compounds against P. falciparum Plasmepsin IX and X were identified•PMIX and PMX are modulators of parasite proteins for egress, invasion, and development•Anti-PMIX and anti-PMX compounds inhibit liver, blood, and mosquito stages of Plasmodium•One compound, WM382, can clear mouse models of P. berghei and P. falciparum parasites We describe inhibitors of essential aspartic proteases from malaria parasites that block multiple life cycle stages. PMIX and PMX are master modulators processing proteins required for invasion, development, and egress. Administration of WM382 cured mice of malaria infection, showing that these inhibitors are promising candidates for malaria treatment and prevention.
AbstractList Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention. [Display omitted] •Specific compounds against P. falciparum Plasmepsin IX and X were identified•PMIX and PMX are modulators of parasite proteins for egress, invasion, and development•Anti-PMIX and anti-PMX compounds inhibit liver, blood, and mosquito stages of Plasmodium•One compound, WM382, can clear mouse models of P. berghei and P. falciparum parasites We describe inhibitors of essential aspartic proteases from malaria parasites that block multiple life cycle stages. PMIX and PMX are master modulators processing proteins required for invasion, development, and egress. Administration of WM382 cured mice of malaria infection, showing that these inhibitors are promising candidates for malaria treatment and prevention.
Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention.
Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention. • Specific compounds against P. falciparum Plasmepsin IX and X were identified • PMIX and PMX are modulators of parasite proteins for egress, invasion, and development • Anti-PMIX and anti-PMX compounds inhibit liver, blood, and mosquito stages of Plasmodium • One compound, WM382, can clear mouse models of P. berghei and P. falciparum parasites We describe inhibitors of essential aspartic proteases from malaria parasites that block multiple life cycle stages. PMIX and PMX are master modulators processing proteins required for invasion, development, and egress. Administration of WM382 cured mice of malaria infection, showing that these inhibitors are promising candidates for malaria treatment and prevention.
Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention.Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased resistance to ACT highlights the importance of finding new drugs. Recently, the aspartic proteases Plasmepsin IX and X (PMIX and PMX) were identified as promising drug targets. In this study, we describe dual inhibitors of PMIX and PMX, including WM382, that block multiple stages of the Plasmodium life cycle. We demonstrate that PMX is a master modulator of merozoite invasion and direct maturation of proteins required for invasion, parasite development, and egress. Oral administration of WM382 cured mice of P. berghei and prevented blood infection from the liver. In addition, WM382 was efficacious against P. falciparum asexual infection in humanized mice and prevented transmission to mosquitoes. Selection of resistant P. falciparum in vitro was not achievable. Together, these show that dual PMIX and PMX inhibitors are promising candidates for malaria treatment and prevention.
Author Robbins, Jonathan A.
Christensen, Janni
Reaksudsan, Kitsanapong
Triglia, Tony
Sabroux, Hélène Jousset
McCauley, John A.
Tham, Wai-Hong
Jarman, Kate
Sleebs, Brad E.
Richardson, Lachlan
Ngo, Anna
Papenfuss, Tony
Khan, Tanweer
Guo, Zhuyan
Penington, Jocelyn Sietsma
Olsen, David B.
Healer, Julie
Steel, Ryan W.J.
Vavrek, Marissa
Cowman, Alan F.
Hu, Mengwei
Boyce, Christopher
Murgolo, Nicholas
Zhao, Lianyun
Rottmann, Matthias
Boddey, Justin A.
de Lera Ruiz, Manuel
Dietrich, Melanie H.
Favuzza, Paola
Thompson, Jennifer K.
Guo, Kai-Yuan
Lopaticki, Sash
AuthorAffiliation 3 Merck & Co., Inc., 770 Sumneytown Pike, West Point, PA 19486, USA
4 Swiss Tropical and Public Health Institute, Basel 4002, Switzerland
1 The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
2 University of Melbourne, Melbourne, VIC 3010, Australia
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32109369$$D View this record in MEDLINE/PubMed
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Keywords Plasmodium
humanized mouse
plasmepsin IX
merozoite
plasmepsin X
malaria
antimalarial
plasmepsin
Language English
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Snippet Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased...
Artemisin combination therapy (ACT) is the main treatment option for malaria, which is caused by the intracellular parasite Plasmodium. However, increased...
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StartPage 642
SubjectTerms Animals
antimalarial
Antimalarials - pharmacology
Aspartic Acid Endopeptidases - drug effects
Disease Transmission, Infectious - prevention & control
humanized mouse
Life Cycle Stages - drug effects
malaria
Malaria - drug therapy
merozoite
Merozoites - drug effects
Mice
Mice, Transgenic
plasmepsin
plasmepsin IX
plasmepsin X
Plasmodium
Plasmodium berghei - drug effects
Plasmodium falciparum - drug effects
Title Dual Plasmepsin-Targeting Antimalarial Agents Disrupt Multiple Stages of the Malaria Parasite Life Cycle
URI https://dx.doi.org/10.1016/j.chom.2020.02.005
https://www.ncbi.nlm.nih.gov/pubmed/32109369
https://www.proquest.com/docview/2369421874
https://pubmed.ncbi.nlm.nih.gov/PMC7146544
Volume 27
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