Kamal Mohammad A, Qu Xianqin, Yu Qian-Sheng, Tweedie David, Holloway Harold W, Li Yazhou, Tan Yi, Greig Nigel H
Department of Medical and Molecular BioSciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
J Neural Transm (Vienna). 2008 Jun;115(6):889-98. doi: 10.1007/s00702-008-0022-y. Epub 2008 Jan 31.
Synaptic loss, particularly related to the forebrain cholinergic system, is considered to be an early event that leads to Alzheimer's disease (AD) and has led to the development of acetylcholinesterase inhibitors (AChE-Is) as the mainstay of treatment for several degenerative disorders that culminate in dementia. The primary dose-limiting toxicities of all clinically available AChE-Is are, similar to useful actions on cognition, cholinergically mediated and they ultimately limit the value of this drug class in achieving anything but symptomatic improvements. In addition, AChE levels in brain areas associated with AD decline with disease progression, which likely ultimately limits the therapeutic utility of this drug class. New research indicates that selective inhibition of butyrylcholinesterase (BuChE), a closely related enzyme that is markedly elevated in AD brain, increases acetylcholine (ACh) and augments cognition in rodents free of the characteristic undesirable actions of AChE-Is. BuChE inhibition hence represents an innovative treatment approach for AD, and agents are currently being synthesized to optimally achieve this. The novel compound, tetrahydrofurobenzofuran cymserine (THFBFC), is derived from our effort to produce a potent and BuChE-selective inhibitor as a candidate to test the hypothesis that BuChE-Is would be efficacious and better tolerated than AChE-Is in AD. Herein, we applied innovative enzyme kinetic analyses to characterize the quantitative interaction of THFBFC with human BuChE. These provided values for the agent's IC(50), together with specific new kinetic constants, such as K (T50), K (T1/2), R (I), (o)K (RT), (o)P(max), K(PT) and PT(1/2), to aid define target concentrations for clinical translation. Additional classical kinetic parameters, including K(i), K(m)or K(s), k(cat) or V(max) and V (mi) were also determined. THFBFC proved to be a potent competitive inhibitor of human BuChE and, like its isomer dihydrobenzodioxepine cymserine, is a potentially interesting AD drug candidate.
突触丧失,尤其是与前脑胆碱能系统相关的突触丧失,被认为是导致阿尔茨海默病(AD)的早期事件,这也促使了乙酰胆碱酯酶抑制剂(AChE-Is)的研发,成为治疗最终导致痴呆的几种退行性疾病的主要手段。所有临床可用的AChE-Is的主要剂量限制毒性,与它们对认知的有益作用类似,是由胆碱能介导的,并且最终限制了这类药物除了产生症状改善之外的价值。此外,与AD相关的脑区中的AChE水平会随着疾病进展而下降,这可能最终限制了这类药物的治疗效用。新的研究表明,选择性抑制丁酰胆碱酯酶(BuChE),一种在AD脑中显著升高的密切相关酶,可增加乙酰胆碱(ACh)并增强啮齿动物的认知能力,且没有AChE-Is的典型不良作用。因此,抑制BuChE代表了一种针对AD的创新治疗方法,目前正在合成相关药物以最佳地实现这一目标。新型化合物四氢呋喃苯并呋喃西姆斯林(THFBFC),源自我们生产一种强效且对BuChE具有选择性的抑制剂的努力,以此作为测试以下假设的候选药物:在AD中,BuChE抑制剂比AChE抑制剂更有效且耐受性更好。在此,我们应用创新的酶动力学分析来表征THFBFC与人类BuChE的定量相互作用。这些分析提供了该药物的半数抑制浓度(IC50)值,以及特定的新动力学常数,如K(T50)、K(T1/2)、R(I)、(o)K(RT)、(o)P(max)、K(PT)和PT(1/2),以帮助确定临床转化的目标浓度。还测定了其他经典动力学参数,包括抑制常数(Ki)、米氏常数(Km)或底物常数(Ks)、催化常数(kcat)或最大反应速度(Vmax)以及初始速度(Vmi)。THFBFC被证明是人类BuChE的强效竞争性抑制剂,并且与其异构体二氢苯并二恶英西姆斯林一样,是一种潜在有趣的AD候选药物。