Abstract：
Recently, the roles of inflammation and insulin resistance in neurodegeneration have become better appreciated. NE3107, an oral small molecule, blood-brain permeable anti-inflammatory insulin sensitizer that binds extracellular signal-regulated kinase, has been shown to selectively inhibit inflammation-driven ERK- and NF-κB-stimulated inflammatory mediators, including TNF-α, without inhibiting their homeostatic functions. We describe the rationale and design of NM101, the first randomized, multicenter Phase III clinical study to examine the safety and efficacy of 30 week treatment with NE3107 versus placebo in elderly adults with mild-to-moderate Alzheimer\'s disease. Patients (316) will be randomized in a 1:1 ratio. The co-primary end points measure cognitive function (ADAS Cog12), and functional and behavioral characteristics (ADCS CGIC). Trial registration number: NCT04669028 (Clinicaltrials.gov).
Lay abstract Diabetes and other inflammatory diseases increase the risk of Alzheimer’s disease. Insulin controls energy use in both the body and the brain. NE3107 is an oral pharmaceutical that has been shown to decrease inflammation and to improve insulin function in animals and in human subjects. We have designed a Phase III clinical trial to test the safety and activity of NE3107 in 316 elderly adults with Alzheimer’s disease, compared with a placebo capsule. After 30 weeks, assessments will be made to look for benefits in cognition, function and behavior compared with the control group.
Lay abstract Diabetes and other inflammatory diseases increase the risk of Alzheimer’s disease. Insulin controls energy use in both the body and the brain. NE3107 is an oral pharmaceutical that has been shown to decrease inflammation and to improve insulin function in animals and in human subjects. We have designed a Phase III clinical trial to test the safety and activity of NE3107 in 316 elderly adults with Alzheimer’s disease, compared with a placebo capsule. After 30 weeks, assessments will be made to look for benefits in cognition, function and behavior compared with the control group.
摘要：
最近,炎症和胰岛素抵抗在神经变性中的作用已得到更好的理解。NE3107，一种口服小分子，血脑通透性抗炎胰岛素增敏剂结合细胞外信号调节激酶,已显示选择性抑制炎症驱动的ERK和NF-κB刺激的炎症介质，包括TNF-α,而不抑制它们的稳态功能。我们描述了第一个随机的NM101的基本原理和设计，多中心III期临床研究，旨在研究NE3107与安慰剂治疗30周的安全性和有效性。患者(316)将以1:1的比例随机化。共同主要终点测量认知功能(ADASCog12)，以及功能和行为特征(ADCSCGIC)。试验注册号：NCT04669028(Clinicaltrials.gov)。
Layabstract糖尿病和其他炎症性疾病增加阿尔茨海默病的风险。胰岛素控制身体和大脑的能量使用。NE3107是一种口服药物，已被证明可以减轻动物和人类受试者的炎症并改善胰岛素功能。我们设计了一项III期临床试验，以测试NE3107在316名患有阿尔茨海默病的老年人中的安全性和活性，与安慰剂胶囊相比。30周后,将进行评估以寻找认知方面的益处，功能和行为与对照组的比较。
Layabstract糖尿病和其他炎症性疾病增加阿尔茨海默病的风险。胰岛素控制身体和大脑的能量使用。NE3107是一种口服药物，已被证明可以减轻动物和人类受试者的炎症并改善胰岛素功能。我们设计了一项III期临床试验，以测试NE3107在316名患有阿尔茨海默病的老年人中的安全性和活性，与安慰剂胶囊相比。30周后,将进行评估以寻找认知方面的益处，功能和行为与对照组的比较。
