β amyloid (1 16)

β-Amyloid (1-16) is an amyloidogenic protein fragment with a sequence derived from β-amyloid. It exhibits the ability to bind to metal ions, indicating its involvement in metal-binding processes. β-Amyloid, a peptide, is responsible for the formation of amyloid plaques in the brains of individuals affected by Alzheimer's disease (AD).

β-Amyloid (1-16) rat 是β-淀粉样肽 (Abeta) 金属结合域的片段，含有三个与人类相异的氨基酸替代，因此在大鼠和小鼠中降低了 AD 样神经退行性变的易感性。

Donecopride is a partial agonist of the serotonin (5-HT) receptor subtype 5-HT4E(Ki= 8.5 nM) and an inhibitor of acetylcholinesterase (AChE; IC50= 16 nM).1It is selective for AChE over butyrylcholinesterase (BChE; IC50= 3,530 nM) but does bind to 5-HT2Band sigma-2 (σ2) receptors (Ki= 1.6 nM for both) in a panel of 42 neurotransmitter receptors and transporters. Donecopride induces release of soluble amyloid precursor protein-α (sAPP-α) in COS-7 cells transiently expressing 5-HT4with an EC50value of 11.3 nM. Oral administration of donecopride (1 mg/kg) reduces brain soluble and insoluble amyloid-β (1-42) levels and increases the time spent exploring the novel object in the novel object recognition (NOR) test in the 5XFAD transgenic mouse model of Alzheimer's disease. Donecopride (3 mg/kg, p.o.) prevents a reduction in spontaneous alternation behavior induced by intracerebroventricular administration of soluble Aβ42 (sAβ42) in the Y-maze in mice.2 1.Lecoutey, C., Hedou, D., Freret, T., et al.Design of donecopride, a dual serotonin subtype 4 receptor agonist/acetylcholinesterase inhibitor with potential interest for Alzheimer's disease treatmentProc. Natl. Acad. Sci. USA111(36)E3825-E3830(2014) 2.Rochais, C., Lecoutey, C., Hamidouche, K., et al.Donecopride, a Swiss army knife with potential against Alzheimer's diseaseBr. J. Pharmacol.177(9)1988-2005(2020)

AChE BChE-IN-9 (Compound 7a) is a potent orally active inhibitor of AChE and BChE, with IC50 values of 5.74 μM and 14.05 μM against hAChE and eqBChE, respectively. It also demonstrates effective antioxidant activity, with an IC50 value of 57.35 μM. Additionally, AChE BChE-IN-9 exhibits the ability to chelate iron and modulate the aggregation of amyloid β 1-42. Notably, AChE-IN-16 has the ability to cross the blood-brain barrier [1].

β-Amyloid peptide(16-20)，即 Amyloid-β(Abeta) 的氨基酸序列(KLVFF)部分，有效抑制 Abeta 原纤维形成，通过在 N 和 C 末端添加 RG- -GR-NH2 残基增强其溶解性。