Gozes Illana, Morimoto Bruce H, Tiong Jacqueline, Fox Anthony, Sutherland Karole, Dangoor David, Holser-Cochav Miriam, Vered Karin, Newton Paul, Aisen Paul S, Matsuoka Yasuji, van Dyck Christopher H, Thal Leon
Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
CNS Drug Rev. 2005 Winter;11(4):353-68. doi: 10.1111/j.1527-3458.2005.tb00053.x.
Activity-dependent neuroprotective protein (ADNP) is essential for brain formation. Peptide activity scanning identified NAP (NAPVSIPQ) as a small active fragment of ADNP that provides neuroprotection at very low concentrations. In cell culture, NAP has demonstrated protection against toxicity associated with the beta-amyloid peptide, N-methyl-D-aspartate, electrical blockade, the envelope protein of the AIDS virus, dopamine, H2O2, nutrient starvation and zinc overload. NAP has also provided neuroprotection in animal models of apolipoprotein E deficiency, cholinergic toxicity, closed head injury, stroke, middle aged anxiety and cognitive dysfunction. NAP binds to tubulin and facilitates microtubule assembly leading to enhanced cellular survival that is associated with fundamental cytoskeletal elements. A liquid-chromatography, mass spectrometry assay demonstrated that NAP reaches the brain after either intravenous or intranasal administration. In a battery of toxicological tests including repeated dose toxicity in rats and dogs, cardiopulmonary tests in dogs, and functional behavioral assays in rats, no adverse side effects were observed with NAP concentrations that were approximately 500-fold higher than the biologically active dose. A Phase Ia clinical trial in the US assessed the tolerability and pharmacokinetics of intranasal administration of NAP in sequential ascending doses. The results supported the safety and tolerability of a single dose of NAP administered at up to 15 mg intranasally. Furthermore, dosing was recently completed for a second Phase I clinical trial in healthy adults and elderly volunteers with an intravenous formulation of NAP. NAP is poised for further clinical development targeting several indications, including Alzheimer's disease.
活性依赖的神经保护蛋白(ADNP)对大脑形成至关重要。肽活性扫描确定NAP(NAPVSIPQ)为ADNP的一个小活性片段,其在极低浓度下即可提供神经保护作用。在细胞培养中,NAP已证明可抵御与β-淀粉样肽、N-甲基-D-天冬氨酸、电阻滞、艾滋病病毒包膜蛋白、多巴胺、过氧化氢、营养饥饿和锌过载相关的毒性。NAP在载脂蛋白E缺乏、胆碱能毒性、闭合性颅脑损伤、中风、中年焦虑和认知功能障碍的动物模型中也提供了神经保护作用。NAP与微管蛋白结合并促进微管组装,从而导致与基本细胞骨架成分相关的细胞存活率提高。液相色谱-质谱分析表明,静脉注射或鼻内给药后NAP均可到达大脑。在一系列毒理学试验中,包括大鼠和犬的重复给药毒性试验、犬的心肺试验以及大鼠的功能行为试验,未观察到NAP浓度比生物活性剂量高约500倍时出现任何不良副作用。美国的一项Ia期临床试验评估了鼻内递增剂量给药的NAP的耐受性和药代动力学。结果支持鼻内给予单剂量高达15 mg的NAP的安全性和耐受性。此外,最近针对健康成年人和老年志愿者的NAP静脉制剂完成了第二项I期临床试验的给药。NAP有望针对包括阿尔茨海默病在内的多种适应症进行进一步的临床开发。