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Amyloid-β (Aβ) research compounds include Aβ peptides and modulators of Aβ production, aggregation and signaling. Aβ was first purified from cerebrovascular amyloid in Alzheimer's disease and characterized in 1984. The peptide is cleaved from the amyloid precursor protein (APP), whose cloning in 1987 revealed a structure resembling a cell-surface receptor. The amyloid hypothesis proposes that Aβ accumulation drives Alzheimer's disease pathogenesis, and it frames much current research. The category includes Amyloid b-Peptide (1-42) (human) for aggregation and toxicity studies. γ-Secretase inhibitors such as avagacestat and RO4929097 reduce Aβ formation. FPS-ZM1 blocks the receptor for advanced glycation end products (RAGE), which binds Aβ.
Synonyms: PKC Activator V
alpha-Amyloid Precursor Protein Modulator is a cell-permeable benzolactam derived PKC activator (Ki = 11.9 nM for PKCα) that efficiently enhances non-amyloidogenic α-processing of amyloid precursor protein (APP) even at 100 nM in human fibroblas.
Synonyms: Dimebone; Latrepirdine
Dimebon dihydrochloride is a non-selective antihistamine that displays cognitive enhancing abilities.
Amyloid b-Peptide (10-20) (human), soluble amyloid b-peptide fragment that is a substrate for gelatinase A/type IV collagenase/MMP-2 and APP secretase; cleaved between Lys16 and Leu17.
Colivelin TFA is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro. Colivelin TFA exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease. Colivelin TFA has the potential for the treatment of alzheimer's disease and ischemic brain injury.
Colivelin is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro. Colivelin exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease. Colivelin has the potential for the treatment of alzheimer's disease and ischemic brain injury
TFEB Activator 3 is a potent activator of TFEB, enhancing its nuclear translocation and promoting lysosome biogenesis. Demonstrated effects include a 44% increase in nuclear translocation at 10 µM after 3 hours and up to 97% at 30 µM under the same conditions. This compound is significant for research into Alzheimer’s disease, as it effectively crosses the blood-brain barrier, making it a valuable tool for studies on neurodegeneration and cellular clearance mechanisms.
Synonyms: GroPEtn sodium
Glycerophosphorylethanolamine sodium is an active phosphodiester metabolite of phosphatidylethanolamine that functions as an Aβ1-40 aggregation activator. This compound promotes the aggregation of amyloid β-protein (Aβ1-40) in vitro, facilitating studies related to amyloid plaque formation. Glycerophosphorylethanolamine sodium is particularly relevant for research in neurodegenerative diseases, including Alzheimer’s disease.
Mca-SEVKMDAEFRK(Dnp)RR-NH2 is a substrate specifically designed for thimet oligopeptidase (TOP), featuring the beta-secretase cleavage site of the wild-type amyloid precursor protein (APP). This compound plays a crucial role in elucidating the processing of APP and the pathways leading to Alzheimer's disease. It serves as a valuable tool for researchers investigating amyloid pathology and related neurodegenerative processes.
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Aβ aggregation modulator-1 is a stimulator of amyloid-β (Aβ) fibrillogenesis, targeting the stabilization of β-sheet-rich protofibrils and fibrils by binding to hydrophobic residues in Aβ peptides. This compound accelerates Aβ polymerization while decreasing the concentration of small, toxic Aβ oligomers in heterogeneous aggregation reactions. Additionally, Aβ aggregation modulator-1 mitigates the inhibition of long-term potentiation (LTP) caused by Aβ oligomers in hippocampal brain slices. This reagent is valuable for researching Alzheimer's disease (AD) and its underlying mechanisms.
