Aβ aggregation-IN-4 reduces the neurotoxicity of β-amyloid protein (Aβ) and significantly decreases the levels of Aβ oligomeric complexes (Aβ-OCs), without affecting the overall levels of Aβ. It mitigates Aβ oligomerization and prevents oligomer-induced death of primary cortical neurons. Aβ aggregation-IN-4 is applicable in Alzheimer's disease (AD) research.

Aβ aggregation-IN-4 (0-2 μM, 24-48 hours) provides protection to MC65 cells, with an EC50 of 0.15 μM, and reduces intracellular Aβ oligomer levels in a dose-dependent manner. This cell-permeable compound saturates within MC65 cells in 2 hours, indicated by [14 C]Amyloid-β-IN-4, allowing rapid cellular entry. The binding affinity (K D) of Aβ aggregation-IN-4 is 5.05 nM for Aβ40 and 269 nM for Aβ42. At a concentration of 10 μM for 24 hours, it significantly lowers Aβ40 and Aβ42 oligomer density. Additionally, Aβ aggregation-IN-4 (50 nM, 48 hours) prevents the neurotoxicity of extracellular Aβ oligomers in primary cultures of neonatal mouse cortical neurons.