Department of Lead Discovery Research, New Drug Research Division, Otsuka Pharmaceutical Co., Ltd., 463-10 Kagasuno Kawauchi-cho, Tokushima, 771-0192, Japan.
Department of CNS Research, New Drug Research Division, Otsuka Pharmaceutical Co., Ltd., 463-10 Kagasuno Kawauchi-cho, Tokushima, 771-0192, Japan.
Nat Commun. 2019 May 15;10(1):2172. doi: 10.1038/s41467-019-09911-6.
Inducing mitochondrial uncoupling (mUncoupling) is an attractive therapeutic strategy for treating metabolic diseases because it leads to calorie-wasting by reducing the efficiency of oxidative phosphorylation (OXPHOS) in mitochondria. Here we report a safe mUncoupler, OPC-163493, which has unique pharmacokinetic characteristics. OPC-163493 shows a good bioavailability upon oral administration and primarily distributed to specific organs: the liver and kidneys, avoiding systemic toxicities. It exhibits insulin-independent antidiabetic effects in multiple animal models of type I and type II diabetes and antisteatotic effects in fatty liver models. These beneficial effects can be explained by the improvement of glucose metabolism and enhancement of energy expenditure by OPC-163493 in the liver. Moreover, OPC-163493 treatment lowered blood pressure, extended survival, and improved renal function in the rat model of stroke/hypertension, possibly by enhancing NO bioavailability in blood vessels and reducing mitochondrial ROS production. OPC-163493 is a liver-localized/targeted mUncoupler that ameliorates various complications of diabetes.
诱导线粒体解偶联(mUncoupling)是治疗代谢疾病的一种有吸引力的治疗策略,因为它通过降低线粒体氧化磷酸化(OXPHOS)的效率导致热量消耗。在这里,我们报告了一种安全的 mUncoupler,OPC-163493,它具有独特的药代动力学特征。OPC-163493 经口服给药具有良好的生物利用度,主要分布于特定器官:肝脏和肾脏,避免了全身毒性。它在 I 型和 II 型糖尿病的多种动物模型中表现出胰岛素非依赖性的抗糖尿病作用,并在脂肪肝模型中表现出抗脂肪变性作用。这些有益的效果可以通过 OPC-163493 在肝脏中改善葡萄糖代谢和增强能量消耗来解释。此外,OPC-163493 治疗降低了中风/高血压大鼠模型的血压、延长了生存时间并改善了肾功能,这可能是通过增强血管中 NO 的生物利用度和减少线粒体 ROS 的产生。OPC-163493 是一种肝脏定位/靶向的 mUncoupler,可改善糖尿病的各种并发症。