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infecting a red blood cell
Image courtesy of St. Jude
Children’s Research Hospital
Researchers have found that a screening model can classify antimalarial drugs and reveal drug targets for Plasmodium falciparum, according to a paper published in Scientific Reports.
The team performed chemogenomic profiling of P falciparum for the first time.
They used a collection of malaria parasite mutants that each had altered metabolism linked to a defect in a single P falciparum gene.
They then screened 53 drugs and compounds against 71 of these P falciparum piggyBac single-insertion mutant parasites.
Computational analysis of the response patterns linked the different antimalarial drug candidates and metabolic inhibitors to the specific gene defect.
This revealed new insights into the drugs’ mechanism of action and uncovered 6 new genes that were involved in P falciparum’s response to artemisinin but were associated with increased susceptibility to the drugs tested.
“That represents 6 new targets potentially as effective as artemisinin for killing the malaria parasite,” said study author Dennis Kyle, PhD, of the University of South Florida in Tampa.
“There is definitely a sense of urgency for discovering new antimalarial drugs that may replace artemisinin, or work better with artemisinin, to prevent or delay drug resistance.”
P falciparum, which is becoming increasingly resistant to artemisinin, causes three-quarters of all malaria cases in Africa and 95% of malaria deaths worldwide. 
infecting a red blood cell
Image courtesy of St. Jude
Children’s Research Hospital
Researchers have found that a screening model can classify antimalarial drugs and reveal drug targets for Plasmodium falciparum, according to a paper published in Scientific Reports.
The team performed chemogenomic profiling of P falciparum for the first time.
They used a collection of malaria parasite mutants that each had altered metabolism linked to a defect in a single P falciparum gene.
They then screened 53 drugs and compounds against 71 of these P falciparum piggyBac single-insertion mutant parasites.
Computational analysis of the response patterns linked the different antimalarial drug candidates and metabolic inhibitors to the specific gene defect.
This revealed new insights into the drugs’ mechanism of action and uncovered 6 new genes that were involved in P falciparum’s response to artemisinin but were associated with increased susceptibility to the drugs tested.
“That represents 6 new targets potentially as effective as artemisinin for killing the malaria parasite,” said study author Dennis Kyle, PhD, of the University of South Florida in Tampa.
“There is definitely a sense of urgency for discovering new antimalarial drugs that may replace artemisinin, or work better with artemisinin, to prevent or delay drug resistance.”
P falciparum, which is becoming increasingly resistant to artemisinin, causes three-quarters of all malaria cases in Africa and 95% of malaria deaths worldwide.
infecting a red blood cell
Image courtesy of St. Jude
Children’s Research Hospital
Researchers have found that a screening model can classify antimalarial drugs and reveal drug targets for Plasmodium falciparum, according to a paper published in Scientific Reports.
The team performed chemogenomic profiling of P falciparum for the first time.
They used a collection of malaria parasite mutants that each had altered metabolism linked to a defect in a single P falciparum gene.
They then screened 53 drugs and compounds against 71 of these P falciparum piggyBac single-insertion mutant parasites.
Computational analysis of the response patterns linked the different antimalarial drug candidates and metabolic inhibitors to the specific gene defect.
This revealed new insights into the drugs’ mechanism of action and uncovered 6 new genes that were involved in P falciparum’s response to artemisinin but were associated with increased susceptibility to the drugs tested.
“That represents 6 new targets potentially as effective as artemisinin for killing the malaria parasite,” said study author Dennis Kyle, PhD, of the University of South Florida in Tampa.
“There is definitely a sense of urgency for discovering new antimalarial drugs that may replace artemisinin, or work better with artemisinin, to prevent or delay drug resistance.”
P falciparum, which is becoming increasingly resistant to artemisinin, causes three-quarters of all malaria cases in Africa and 95% of malaria deaths worldwide.