Department of Cellular Biology, Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia 30602, USA.
Cleveland BioLabs, Inc., Buffalo, New York 14203, USA.
Sci Rep. 2016 Aug 26;6:32083. doi: 10.1038/srep32083.
The protozoan parasite Trypanosoma brucei causes the fatal illness human African trypanosomiasis (HAT). Standard of care medications currently used to treat HAT have severe limitations, and there is a need to find new chemical entities that are active against infections of T. brucei. Following a "drug repurposing" approach, we tested anti-trypanosomal effects of carbazole-derived compounds called "Curaxins". In vitro screening of 26 compounds revealed 22 with nanomolar potency against axenically cultured bloodstream trypanosomes. In a murine model of HAT, oral administration of compound 1 cured the disease. These studies established 1 as a lead for development of drugs against HAT. Pharmacological time-course studies revealed the primary effect of 1 to be concurrent inhibition of mitosis coupled with aberrant licensing of S-phase entry. Consequently, polyploid trypanosomes containing 8C equivalent of DNA per nucleus and three or four kinetoplasts were produced. These effects of 1 on the trypanosome are reminiscent of "mitotic slippage" or endoreplication observed in some other eukaryotes.
原生动物寄生虫布氏锥虫会引起致命的人类非洲锥虫病(HAT)。目前用于治疗 HAT 的标准护理药物存在严重的局限性,因此需要寻找新的对 T. brucei 感染具有活性的化学实体。我们采用“药物再利用”方法,测试了称为“Curaxin”的咔唑衍生化合物的抗锥虫作用。对 26 种化合物进行体外筛选,发现有 22 种对体外培养的血淋巴锥虫具有纳摩尔效力。在 HAT 的小鼠模型中,化合物 1 的口服给药治愈了该疾病。这些研究确立了 1 作为开发抗 HAT 药物的先导化合物。药理学时程研究表明,1 的主要作用是同时抑制有丝分裂,并伴有 S 期进入的异常许可。因此,每个核包含 8C 当量 DNA 的多倍体锥虫和三个或四个动基体被产生。1 对锥虫的这些作用类似于在一些其他真核生物中观察到的“有丝分裂滑溜”或内复制。