Buck Institute for Research on Aging, Novato, CA, 94945, USA.
Department of Dairy Science, University of Wisconsin-Madison, Madison, WI, 53706, USA.
Nat Commun. 2019 Jul 19;10(1):3194. doi: 10.1038/s41467-019-11174-0.
Rapamycin, an inhibitor of mechanistic Target Of Rapamycin Complex 1 (mTORC1), extends lifespan and shows strong potential for the treatment of age-related diseases. However, rapamycin exerts metabolic and immunological side effects mediated by off-target inhibition of a second mTOR-containing complex, mTOR complex 2. Here, we report the identification of DL001, a FKBP12-dependent rapamycin analog 40x more selective for mTORC1 than rapamycin. DL001 inhibits mTORC1 in cell culture lines and in vivo in C57BL/6J mice, in which DL001 inhibits mTORC1 signaling without impairing glucose homeostasis and with substantially reduced or no side effects on lipid metabolism and the immune system. In cells, DL001 efficiently represses elevated mTORC1 activity and restores normal gene expression to cells lacking a functional tuberous sclerosis complex. Our results demonstrate that highly selective pharmacological inhibition of mTORC1 can be achieved in vivo, and that selective inhibition of mTORC1 significantly reduces the side effects associated with conventional rapalogs.
雷帕霉素是一种机械靶蛋白雷帕霉素复合物 1(mTORC1)抑制剂,它可以延长寿命,并显示出治疗与年龄相关疾病的巨大潜力。然而,雷帕霉素通过对第二种含有 mTOR 的复合物 mTOR 复合物 2 的非靶标抑制,产生代谢和免疫方面的副作用。在这里,我们报告了 DL001 的鉴定,它是一种 FKBP12 依赖性雷帕霉素类似物,对 mTORC1 的选择性比雷帕霉素高 40 倍。DL001 在细胞培养系和 C57BL/6J 小鼠体内抑制 mTORC1,在小鼠体内,DL001 抑制 mTORC1 信号而不损害葡萄糖稳态,并且对脂质代谢和免疫系统的副作用大大降低或没有。在细胞中,DL001 能有效地抑制升高的 mTORC1 活性,并使缺乏功能结节性硬化复合物的细胞恢复正常的基因表达。我们的研究结果表明,在体内可以实现对 mTORC1 的高度选择性药理学抑制,而对 mTORC1 的选择性抑制显著降低了与传统雷帕霉素相关的副作用。