Neuroscience Drug Discovery Unit, Research, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Discovery Biology, Discovery Science, Axcelead Drug Discovery Partners, Inc., Fujisawa, Kanagawa, Japan.
J Neurochem. 2021 Nov;159(3):543-553. doi: 10.1111/jnc.15492. Epub 2021 Aug 31.
Gaucher disease (GD), the most common lysosomal storage disorders, is caused by GBA gene mutations resulting in glycosphingolipids accumulations in various tissues, such as the brain. While suppressing glycosphingolipid accumulation is the central strategy for treating peripheral symptoms of GD, there is no effective treatment for the central nervous system symptoms. As glycosphingolipid biosynthesis starts from ceramide glycosylation by glucosylceramide synthase (GCS), inhibiting GCS in the brain is a promising strategy for neurological GD. Herein, we discovered T-036, a potent and brain-penetrant GCS inhibitor with a unique chemical structure and binding property. T-036 does not harbor an aliphatic amine moiety and has a noncompetitive inhibition mode to the substrates, unlike other known inhibitors. T-036 exhibited sufficient exposure and a significant reduction of glucosylsphingolipids in the plasma and brain of the GD mouse model. Therefore, T-036 could be a promising lead molecule for treating central nervous system symptoms of GD.
戈谢病(GD)是最常见的溶酶体贮积症,由 GBA 基因突变引起,导致糖脂在各种组织中积累,如大脑。虽然抑制糖脂积累是治疗 GD 外周症状的核心策略,但对中枢神经系统症状尚无有效治疗方法。由于糖脂的生物合成始于葡萄糖脑苷脂合成酶(GCS)对神经酰胺的糖基化,因此抑制大脑中的 GCS 是治疗神经 GD 的一种很有前途的策略。在此,我们发现了 T-036,一种具有独特化学结构和结合特性的强效、可穿透血脑屏障的 GCS 抑制剂。与其他已知抑制剂不同,T-036 不含脂肪族胺部分,且对底物具有非竞争性抑制模式。T-036 在 GD 小鼠模型的血浆和大脑中表现出足够的暴露量和显著降低的葡萄糖神经酰胺水平。因此,T-036 可能成为治疗 GD 中枢神经系统症状的有前途的先导化合物。