Aβ aggregation-IN-4 

Aβ aggregation-IN-4 can alleviate the neurotoxicity of amyloid-β protein (Aβ) and significantly reduce the level of oligomeric complexes of Aβ (Aβ-OCs). Aβ aggregation-IN-4 does not decrease the level of amyloid-β protein (Aβ). Aβ aggregation-IN-4 attenuates Aβ oligomerization and prevents oligomer-induced death of primary cortical neurons. Aβ aggregation-IN-4 can be used for the study of Alzheimer’s disease (AD)^[1].

Aβ aggregation-IN-4 (0-2 μM, 24-48 hours) can protect MC65 cells and reduce the level of intracellular Aβ oligomers in MC65 cells in a dose-dependent manner (EC₅₀=0.15 μM)^[1].
Aβ aggregation-IN-4 (0-14 hours) is a cell-permeable compound. [¹⁴C]Amyloid-β-IN-4 can reach a saturated concentration in MC65 cells within 2 hours and can enter the cells rapidly^[1].
The binding affinities (K_d) of Aβ aggregation-IN-4 to Aβ40 and Aβ42 are 5.05 nM and 269 nM, respectively^[1].
Aβ aggregation-IN-4 (10 μM, 24 hours) can significantly reduce the density of Aβ40 and Aβ42 oligomers^[1].
Aβ aggregation-IN-4 (50 nM, 48 hours) can block the neurotoxicity of extracellular Aβ oligomers in primary neuron cultures of the neonatal mouse cortex^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

393.44

C₂₁H₂₃N₅O₃

603113-07-1

[H][C@]12C[C@H](CCC1=CC3=C(O2)C=C(OC3=O)C)[C@@H](CN4C=NC(N)=C5C4=NC=N5)C

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• [1]. Maezawa I, et al. A novel tricyclic pyrone compound ameliorates cell death associated with intracellular amyloid-beta oligomeric complexes. J Neurochem. 2006 Jul;98(1):57-67.  [Content Brief]