Amyloid-β (Aβ) denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer's disease as the main component of theamyloid plaques found in the brains of Alzheimer patients. The peptides result from the amyloid precursor protein (APP), which is being cut by certain enzymes to yield Aβ. Amyloid-β molecules can aggregate to form flexible soluble oligomers which may exist in several forms. Amyloid-β peptide is due to overproduction of Aβ and/or the failure of clearance mechanisms. Amyloid-β self-aggregates into oligomers, which can be of various sizes, and forms diffuse and neuritic plaques in the parenchyma and blood vessels. Amyloid-β oligomers and plaques are potent synaptotoxins, block proteasome function, inhibit mitochondrial activity, alter intracellular Ca2+levels and stimulate inflammatory processes. Loss of the normal physiological functions of Aβ is also thought to contribute to neuronal dysfunction.
|Cat. No.||Product Name||CAS No.||Information|
GSK-3039294 is an orally available small molecule inhibitor of serum amyloid P component (SAP) binding to amyloid fibrils for the depletion of serum amyloid-P (SAP) component from the circulation.
TRX-0237 Methylate (Hydromethylthionine, Methylene blue) is a Tau aggregation inhibitor (TAI) with Ki of 0.12 uM for intracellular TAI activity; disrupts paired helical filaments (PHFs) isolated from AD brain tissues at 0.16 uM, delays cellular senescence and enhances key mitochondrial biochemical pathways; demonstrates activities in clinical trials in Alzheimer's disease (AD) with drugs targeting β-amyloid accumulation in the brain.
FPS-ZM1 is a high-affinity RAGE-specific inhibitor; blocks Aβ binding to the V domain of RAGE and inhibits Aβ40- and Aβ42-induced cellular stress in RAGE-expressing cells in vitro and in the mouse brain in vivo.
ARN-2966 is a potent, BBB penetrant post-transcriptional modulator of APP expression in transfected CHO cells that produce amyloid precursor protein (APP); reduces expression of APP with resultant lower production of Aβ; improves the memory and reduces Aβ in AD transgenic mice; orally active.
Miridesap (Ro 638695;GSK-2315698;CPHPC) is a competitive inhibitor of serum amyloid P component (SAP) binding to amyloid fibrils; crosslinks and dimerizes SAP molecules, leading to their very rapid clearance by the liver, and thus produces a marked depletion of circulating human SAP; Miridesap is a novel therapeutic approach to both systemic amyloidosis and diseases associated with local amyloid, including Alzheimer's disease and type 2 diabetes.
Aβ polymerization stimulator O4
Aβ polymerization stimulator O4 is an orcein-related small molecule can drive polymerization of amyloid-β (Aβ); directly binds to hydrophobic amino acid residues in Aβ peptides and stabilizes the self-assembly of seeding-competent, β-sheet-rich protofibrils and fibrils, efficiently decreases the concentration of small, toxic Aβ oligomers in complex, heterogeneous aggregation reactions; suppresses inhibition of long-term potentiation by Aβ oligomers in hippocampal brain slices.
CID 9998128 is a potential multi-target drug for the Alzheimer's disease (AD), inhibits the Aβ42 amyloid fibrillization and is capable to clear Aβ42 fibrils; strongly binds to both amyloid beta 42 (Aβ42) fibrils and β-secretase and the van der Waals interaction is dominating over the electrostatic interaction in binding affinity.
SEN1269 is a novel potent Aβ aggregation inhibitor that binds to monomeric Aβ1-42 with Kd of 4.4 uM, protects neuronal cell lines against an Aβ1-42 insult with IC50 of 15 uM; produces a concentration-related blockade of Aβ(1-42) aggregation and protects neuronal cell lines exposed to Aβ(1-42); alleviates deficits in hippocampal LTP induced by Aβ(1-42) and cell-derived Aβ oligomers; reduces Aβ-induced neurotoxicity and shows neuroprotective in behavioural models of memory relevant to Aβ-induced neurodegeneration.
TDI-2760 si a small molecule Aβ-aggregation inhibitor that not only shows a strong inhibitory efficacy toward the Aβ-fibrinogen interaction (IC50=1.67 uM) but also retains potency toward the Aβ42 aggregation inhibition process; restores the Aβ42-induced decrease in fibrin clot turbidity without affecting normal clotting in an in vitro clotting assay, effectively inhibits Aβ42 fibrillization and modulates Aβ42-induced contact system activation.
BNC-1 is a small molecule modulator of Amyloid pathology by promoting phosphorylation and activation of Elk-1, a transcriptional repressor of presenilin-1 but not presenilin-2; increases levels of synaptophysin and synapsin, markers of synaptic integrity, but does not adversely impact presenilin-2 or processing of Notch-1, significantly decreases amyloid burden and improves markers of synaptic integrity in a well-established mouse model of amyloid deposition.
No.1378 West Wenyi Road, Yuhang District, HangZhou, Zhejiang, China