β-Sheet Breaker Peptide iAβ5

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]. In Vitro:β-Sheet Breaker Peptide iAβ5 (1.5 μg/μL; 7 days) incubates with Aβ1-42 (0.5 μg/μL) for 7 days, inhibits amyloid βprotein fibrillogenesis, disassembles preformed fibrils in vitro and prevents neuronal death induced by fibrils in cell culture^[1].
β-Sheet Breaker Peptide iAβ5 (60 μM; 48 h) shows insignificant cytotoxicity in human neuroblastoma (IMR-32) cell treated with 50 μM aggregated Aβ1-42 for 2 days^[1].
In Vivo:β-Sheet Breaker Peptide iAβ5 (100 nmol/rat; Intra-amygdala injection; 7 days) coinjected with Aβ1-42 (5 nmol) into in the rat amygdala, blocks Aβ1-42 neurotoxicity in tissue culture, and amyloid fibril formation in the rat model^[1].
β-Sheet Breaker Peptide iAβ5 (100 nmol/rat, 200 nmol/rat; Intra-amygdaloid injection; 7 days) followed by Aβ1-42 (5 nmol), induces disassembly of pre-existing Aβ fibrils in vivo, and leads to a reversal or prevention of Aβ-induced histopathological changes in rat model^[2].