| Literature DB >> 16516467 |
Radim Vicik1, Verena Hoerr, Melanie Glaser, Martina Schultheis, Elizabeth Hansell, James H McKerrow, Ulrike Holzgrabe, Conor R Caffrey, Alicia Ponte-Sucre, Heidrun Moll, August Stich, Tanja Schirmeister.
Abstract
The protozoan parasite Trypanosoma brucei causes Human African trypanosomiasis, which is fatal if left untreated. Due to the toxicity of currently used drugs and emerging drug resistance, there is an urgent need for novel therapies. The major trypanosome papain-like cysteine protease expressed by the parasite (e.g., rhodesain in T. b. rhodesiense) is considered an important target for the development of new trypanocidal drugs. Series of aziridine-2,3-dicarboxylate-based cysteine protease inhibitors have been tested, most of them inhibiting rhodesain in the low micromolar range. Among these, only dibenzyl aziridine-2,3-dicarboxylates display trypanocidal activity being equipotent to the drug eflornithine. The Leu-Pro-containing aziridinyl tripeptides 13a-f are the most promising as they are not cytotoxic to macrophages up to concentrations of 125microM.Entities:
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Year: 2006 PMID: 16516467 DOI: 10.1016/j.bmcl.2006.02.026
Source DB: PubMed Journal: Bioorg Med Chem Lett ISSN: 0960-894X Impact factor: 2.823