ArticlePloS one2020
Identification of tyrosine kinase inhibitors that halt Plasmodium falciparum parasitemia.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- High-throughput screening and meta-analysis for lead compounds in antimalarial drug discovery.Malaria journal · 2025Pooled it
- Imatinib augments standard malaria combination therapy without added toxicity.The Journal of experimental medicine · 2021Trial
- Computationally guided optimization of the antimalarial activity and physicochemical properties of 2,4-diaminopyrimidines.RSC medicinal chemistry · 2025Article
- Host metabolomic responses in recurrent P. vivax malaria.Scientific reports · 2024Article
- Mesenchymal Stem Cell Behavior under Microgravity: From Stress Response to a Premature Senescence.International journal of molecular sciences · 2023Article
- Tyrosine Kinase Inhibitors Display Potent Activity against Cryptosporidium parvum.Microbiology spectrum · 2023Article
- Preparation, biological evaluation and QSAR analysis of urea substituted 2,4-diamino-pyrimidine anti-malarials.RSC medicinal chemistry · 2022Article
- MAPPINGS, a tool for network analysis of large phospho-signalling datasets: application to host erythrocyte response toCurrent research in microbial sciences · 2022Article
- Cell physiology and molecular mechanism of anion transport by erythrocyte band 3/AE1.American journal of physiology. Cell physiology · 2021Review
- Host-directed therapy, an untapped opportunity for antimalarial intervention.Cell reports. Medicine · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Although current malaria therapies inhibit pathways encoded in the parasite's genome, we have looked for anti-malaria drugs that can target an erythrocyte component because development of drug resistance might be suppressed if the parasite cannot mutate the drug's target. In search for such erythrocyte targets, we noted that human erythrocytes express tyrosine kinases, whereas the Plasmodium falciparum genome encodes no obvious tyrosine kinases. We therefore screened a library of tyrosine kinase inhibitors from Eli Lilly and Co. in a search for inhibitors with possible antimalarial activity. We report that although most tyrosine kinase inhibitors exerted no effect on parasite survival, a subset of tyrosine kinase inhibitors displayed potent anti-malarial activity. Moreover, all inhibitors found to block tyrosine phosphorylation of band 3 specifically suppressed P. falciparum survival at the parasite egress stage of its intra-erythrocyte life cycle. Conversely, tyrosine kinase inhibitors that failed to block band 3 tyrosine phosphorylation but still terminated the parasitemia were observed to halt parasite proliferation at other stages of the parasite's life cycle. Taken together these results suggest that certain erythrocyte tyrosine kinases may be important to P. falciparum maturation and that inhibitors that block these kinases may contribute to novel therapies for P. falciparum malaria.
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