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- W2320437121 endingPage "5246" @default.
- W2320437121 startingPage "5231" @default.
- W2320437121 abstract "Historically, the most successful molecular target for antimalarial drugs has been heme biomineralization within the malarial parasite digestive vacuole. Heme released from catabolized host red blood cell hemoglobin is toxic, so malarial parasites crystallize heme to nontoxic hemozoin. For years it has been accepted that a number of effective quinoline antimalarial drugs (e.g., chloroquine, quinine, amodiaquine) function by preventing hemozoin crystallization. However, recent studies over the past decade have revealed a surprising molecular diversity in quinoline–heme molecular interactions. This diversity shows that even closely related quinoline drugs may have quite different molecular pharmacology. This paper reviews the molecular diversity and highlights important implications for understanding quinoline antimalarial drug resistance and for future drug design." @default.
- W2320437121 created "2016-06-24" @default.
- W2320437121 creator A5022780309 @default.
- W2320437121 creator A5060238138 @default.
- W2320437121 creator A5085883866 @default.
- W2320437121 date "2013-04-29" @default.
- W2320437121 modified "2023-10-02" @default.
- W2320437121 title "Quinoline Drug–Heme Interactions and Implications for Antimalarial Cytostatic versus Cytocidal Activities" @default.
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