The Institute of Biological, Environmental and Rural Sciences (IBERS), Aberystwyth University, SY23 3DA, Wales, UK.
School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff, CF10 3NB, United Kingdom.
Int J Parasitol Drugs Drug Resist. 2018 Dec;8(3):559-570. doi: 10.1016/j.ijpddr.2018.10.005. Epub 2018 Nov 13.
Schistosomiasis endangers the lives of greater than 200 million people every year and is predominantly controlled by a single class chemotherapy, praziquantel (PZQ). Development of PZQ replacement (to combat the threat of PZQ insensitivity/resistance arising) or combinatorial (to facilitate the killing of PZQ-insensitive juvenile schistosomes) chemotherapies would help sustain this control strategy into the future. Here, we re-categorise two families of druggable epigenetic targets in Schistosoma mansoni, the histone methyltransferases (HMTs) and the histone demethylases (HDMs). Amongst these, a S. mansoni Lysine Specific Demethylase 1 (SmLSD1, Smp_150560) homolog was selected for further analyses. Homology modelling of SmLSD1 and in silico docking of greater than four thousand putative inhibitors identified seven (L1 - L7) showing more favourable binding to the target pocket of SmLSD1 vs Homo sapiens HsLSD1; six of these seven (L1 - L6) plus three structural analogues of L7 (L8 - L10) were subsequently screened against schistosomula using the Roboworm anthelmintic discovery platform. The most active compounds (L10 - pirarubicin > L8 - danunorubicin hydrochloride) were subsequently tested against juvenile (3 wk old) and mature (7 wk old) schistosome stages and found to impede motility, suppress egg production and affect tegumental surfaces. When compared to a surrogate human cell line (HepG2), a moderate window of selectivity was observed for the most active compound L10 (selectivity indices - 11 for schistosomula, 9 for juveniles, 1.5 for adults). Finally, RNA interference of SmLSD1 recapitulated the egg-laying defect of schistosomes co-cultivated in the presence of L10 and L8. These preliminary results suggest that SmLSD1 represents an attractive new target for schistosomiasis; identification of more potent and selective SmLSD1 compounds, however, is essential. Nevertheless, the approaches described herein highlight an interdisciplinary strategy for selecting and screening novel/repositioned anti-schistosomals, which can be applied to any druggable (epigenetic) target encoded by the parasite's genome.
血吸虫病每年危及超过 2 亿人的生命,主要通过一种单一类型的化疗药物吡喹酮(PZQ)进行控制。开发 PZQ 替代品(以应对 PZQ 不敏感/耐药性的威胁)或组合疗法(以促进杀死 PZQ 不敏感的幼体血吸虫)将有助于未来维持这种控制策略。在这里,我们重新分类了曼氏血吸虫中的两组可药物治疗的表观遗传靶标,即组蛋白甲基转移酶(HMTs)和组蛋白去甲基化酶(HDMs)。在这些靶标中,选择了曼氏血吸虫赖氨酸特异性去甲基酶 1(SmLSD1,Smp_150560)的同源物进行进一步分析。SmLSD1 的同源建模和超过四千种潜在抑制剂的计算机对接鉴定了七个(L1-L7),它们与人类 LSD1 相比,对 SmLSD1 靶口袋的结合更有利;这七个中的六个(L1-L6)加上 L7 的三个结构类似物(L8-L10)随后在 Roboworm 驱肠虫药物发现平台上针对毛蚴进行了筛选。最有效的化合物(L10-吡柔比星>L8-盐酸柔红霉素)随后针对幼体(3 周龄)和成熟(7 周龄)血吸虫阶段进行了测试,发现它们阻碍了运动,抑制了产卵并影响了表皮表面。与替代的人细胞系(HepG2)相比,观察到最有效化合物 L10 具有适度的选择性窗口(对毛蚴的选择性指数为 11,对幼体为 9,对成虫为 1.5)。最后,SmLSD1 的 RNA 干扰再现了在 L10 和 L8 存在下共同培养的血吸虫的产卵缺陷。这些初步结果表明 SmLSD1 是一种有吸引力的新血吸虫病靶点;然而,识别更有效和选择性的 SmLSD1 化合物是至关重要的。尽管如此,本文所述的方法强调了一种选择和筛选新型/再定位抗血吸虫药物的跨学科策略,该策略可应用于寄生虫基因组编码的任何可药物治疗的(表观遗传)靶标。