| Literature DB >> 32568511 |
Fabian Hulpia1, Gustavo D Campagnaro2, Khalid J Alzahrani2,3, Ibrahim A Alfayez2, Marzuq A Ungogo2,4, Dorien Mabille5, Louis Maes5, Harry P de Koning2, Guy Caljon5, Serge Van Calenbergh1.
Abstract
Human African trypanosomiasis is a neglected tropical disease caused by Trypanosoma brucei parasites. These protists are unable to produce the purine ring, making them vulnerable to the effects of purine nucleoside analogues. Starting from 3'-deoxytubercidin (5), a lead compound with activity against central-nervous-stage human African trypanosomiasis, we investigate the structure-activity relationships of the purine and ribofuranose rings. The purine ring tolerated only modifications at C7, while from the many alterations of the 3'-deoxyribofuranosyl moiety only the arabino analogue 48 showed pronounced antitrypanosomal activity. Profiling of the most potent analogues against resistant T. brucei strains (resistant to pentamidine, diminazene, and isometamidium) showed reduced dependence on uptake mediated by the P2 aminopurine transporter relative to 5. The introduction of a 7-substituent confers up to 10-fold increased affinity for the P1 nucleoside transporter while generally retaining high affinity for P2. Four of the most promising analogues were found to be metabolically stable, earmarking them as suitable backup analogues for lead 5.Entities:
Keywords: Trypanosoma brucei; nucleoside transporter; purine nucleoside
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Year: 2020 PMID: 32568511 DOI: 10.1021/acsinfecdis.0c00105
Source DB: PubMed Journal: ACS Infect Dis ISSN: 2373-8227 Impact factor: 5.084