(Pro18,Asp21)-Amyloid β-Protein (17-21) trifluoroacetate salt

β-Sheet Breaker Peptide iAβ5 is a potent degrader of cerebral amyloid-beta (Abeta). Abeta deposition is associatied with the Alzheimer disease (AD), due to its related toxicity linked to its beta-sheet conformation and/or aggregation. β-Sheet Breaker Peptide iAβ5 reproducibly induces in vivo disassembly of fibrillar amyloid deposits. Thus, β-Sheet Breaker Peptide iAβ5 prevents and/or reverses neuronal shrinkage caused by Abeta, and reduces the extent of interleukin-1beta positive microglia-like cells that surround the Abeta deposits. β-Sheet Breaker Peptide iAβ5 reduces the size and/or number of cerebral amyloid plaques in AD. β-Sheet Breaker Peptide iAβ5 labeled by hydrophobic benzyl alcohol (HBA) tag, can be used for quantitative assay by showing vivid blue color under acidic conditions[1][2][3].

Research Areas >> Neurological Disease

β-Sheet Breaker Peptide iAβ5 (1.5 μg/μL；7 天) 与 Aβ1-42 (0.5 μg/μL) 孵育 7 天，抑制淀粉样蛋白 β 蛋白原纤维形成，在体外分解预先形成的原纤维，并防止细胞培养中原纤维诱导的神经元死亡[1]。 β-Sheet Breaker Peptide iAβ5 (60 μM；48 小时) 在用 50 μM 聚集的 Aβ1-42 处理 2 天的人神经母细胞瘤 (IMR-32) 细胞中显示出不显着的细胞毒性[1]。

β-Sheet Breaker Peptide iAβ5 (100 nmol/大鼠；杏仁核内注射；7 天) 与 Aβ1-42 (5 nmol) 共同注射到大鼠杏仁核中，阻断组织培养中的 Aβ1-42 神经毒性，以及大鼠模型中淀粉样原纤维的形成[1]。 β-Sheet Breaker Peptide iAβ5 (100 nmol/大鼠，200 nmol/大鼠；杏仁核内注射；7 天) 在 Aβ1-42 (5 nmol) 处理后注射，诱导体内预先存在的 Aβ 原纤维的分解，并导致逆转或预防 Aβ 诱导的大鼠模型组织病理学改变[2]。

[1]. Soto C, et al. Beta-sheet breaker peptides inhibit fibrillogenesis in a rat brain model of amyloidosis: implications for Alzheimer's therapy. Nat Med. 1998 Jul;4(7):822-6.  

[2]. Sigurdsson EM, et al. In vivo reversal of amyloid-beta lesions in rat brain. J Neuropathol Exp Neurol. 2000 Jan;59(1):11-7.  

[3]. Okada Y, et al. Acid-Triggered Colorimetric Hydrophobic Benzyl Alcohols for Soluble Tag-Assisted Liquid-Phase Synthesis. Org Lett. 2015 Sep 4;17(17):4264-7.