20 Results for "

Aβ oligomer toxicity

" in MedChemExpress (MCE) Product Catalog:
Products (20)

20 Results for "Aβ oligomer toxicity" in MCE Product Catalog:

27
27 Publications Verification
Cat. No.: HY-P1363
Synonyms: Amyloid β-peptide (1-42) (human) TFA
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42) (Amyloid β-peptide (1-42), human TFA, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human TFA remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human TFA, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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27
27 Publications Verification
Cat. No.: HY-P1363A
CAS No.: 107761-42-2
Synonyms: Amyloid β-peptide (1-42) (human)
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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27
27 Publications Verification
Cat. No.: HY-P1363B
CAS No.: 107761-42-2
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42), human, HFIP-treated, a 42-amino acid peptide that has been treated with HFIP from β-Amyloid (1-42), human (HY-P1363A), is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human, HFIP-treated remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, HFIP-treated, after being dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4°C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37°C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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Cat. No.: HY-101855
CAS No.: 882697-00-9
Purity:  99.93%
Synonyms: Anle138b
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

Emrusolmin (Anle138b), an oligomeric aggregation inhibitor, blocks the formation of pathological aggregates of prion protein (PrPSc) and of α-synuclein (α-syn). Emrusolmin strongly inhibits oligomer accumulation, neuronal degeneration, and disease progression in vivo. Emrusolmin has low toxicity and an excellent oral bioavailability and blood-brain-barrier penetration. Emrusolmin blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology .
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Cat. No.: HY-W143216
CAS No.: 531-57-7
Synonyms: Monomethylthionine
Target:  

Amyloid-β Tau Protein HSP

Research Areas:  

Neurological Disease

Azure C (Monomethylthionine) acts as a tau oligomer inhibitor and Aβ42 oligomerization inhibitor. Azure C regulates hsp70 ATPase activity, thereby mediating the clearance of tau protein. Azure C reduces the levels of toxic tau oligomers by promoting the formation of non-toxic tau aggregates, rescues neuroblastoma cells from tau oligomer-induced toxicity, and binds to and inhibits Aβ42 oligomerization. Azure C is generated via continuous oxidation of methylene blue or azure B through a horseradish peroxidase-mediated reaction. Azure C can be used in research related to tauopathies, including Alzheimer's disease .
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Cat. No.: HY-W010041
CAS No.: 488-59-5
Scyllo-Inositol is an inhibitor that targets the aggregation of misfolded proteins (such as α-synuclein and Amyloid-β), is orally effective, and can cross the blood-brain barrier. Scyllo-Inositol can selectively bind to and stabilize non-toxic oligomers, preventing them from converting into toxic fibers, exerting protein homeostasis regulation and neuroprotective activity. Scyllo-Inositol binds to the hydrophobic region of pathogenic proteins, inhibits protein aggregation, and promotes lysosome- and proteasome-mediated degradation pathways, thereby reducing neurotoxicity. Scyllo-Inositol can be used in the study of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Huntington's disease .
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Cat. No.: HY-P10578
CAS No.: 906357-94-6
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

SEN 304 is an Aβ aggregation inhibitor. SEN 304 can bind directly to Aβ(1-42), delay β-sheet formation and promote aggregation of toxic oligomers into a nontoxic form. SEN 304 can be used for research of Alzheimer’s disease .
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Cat. No.: HY-177906
CAS No.: 1352477-26-9
Research Areas:  

Neurological Disease

h-FTAA is a luminescent conjugated oligothiophene (LCO) probe. h-FTAA can selectively bind to amyloid protein aggregates (such as plaques) and distinguish different conformations of the protein aggregates through changes in fluorescence signals. h-FTAA significantly reduces the neurotoxicity of Aβ1-42 and the Arctic mutant Aβ (AβArc), thereby protecting SH-SY5Y neuroblastoma cells. h-FTAA can be used to dynamically track the formation and maturation process of Aβ plaques .
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Cat. No.: HY-174305
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

Aβ42-IN-7 (Compound CT-01) is a brain-penetrant and selective amyloid-β42 (Aβ42) inhibitor. Aβ42-IN-7 inhibits Aβ42’s assembly into neurotoxic soluble oligomers and extracellular fibrillary aggregates. Aβ42-IN-7 exerts neuroprotective effects by reducing amyloid-mediated neuronal toxicity. Aβ42-IN-7 can be used in research on Alzheimer’s disease (AD) .
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Cat. No.: HY-P1363S1
β-Amyloid (1-42), human, Ala( 13C3, 15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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Cat. No.: HY-N6640
CAS No.: 19536-25-5
Synonyms: 20-Hydroxyeedysone 2-acetate
2-O-Acetyl-20-hydroxyecdysone, an ecdysterones in insects and terrestrial plants, inhibits amyloid-β42 (Aβ42)-induced cytotoxicity. 2-O-Acetyl-20-hydroxyecdysone could decrease Aβ oligomer formation through promotion of fibrogenesis, transforming Aβ oligomers to the low-toxicity fibrils .
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Cat. No.: HY-168052
Research Areas:  

Neurological Disease

hAChE-IN-9 (compound 7i) is a selective inhibitor of human acetylcholinesterase (hAChE) with IC50 of 0.05 μM and 2.85 μM for AChE and BChE, respectively. hAChE-IN-9 modulates toxic Aβ oligomer forms into non-toxic ones and has antioxidant and neuroprotective effects against Aβ-induced toxicity. hAChE-IN-9 can be used for the study of Alzheimer's disease .
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Cat. No.: HY-13325
CAS No.: 71939-12-3
Research Areas:  

Neurological Disease

Aβ aggregation modulator-1 is a stimulator of amyloid-β (Aβ) fibrillogenesis. Aβ aggregation modulator-1 binds hydrophobic residues in Aβ peptides and stabilizes β-sheet-rich protofibrils and fibrils. Aβ aggregation modulator-1 accelerates Aβ polymerization and reduces concentrations of small, toxic Aβ oligomers in heterogeneous aggregation reactions. Aβ aggregation modulator-1 suppresses long-term potentiation (LTP) inhibition by Aβ oligomers in hippocampal brain slices. Aβ aggregation modulator-1 can be used for the study of Alzheimer's disease (AD) .
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Cat. No.: HY-P5368
CAS No.: 1802084-26-9
Target:  

Inhibitory Antibodies

Research Areas:  

Others

[Arg6]-β-Amyloid (1-40), england mutation is a biological active peptide. (Several mutations in the beta amyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds. Among them, the English mutation, with His at position 6 replaced with Arg, was reported to accelerate the kinetics of oligomers formation which act as fibril seeds and are more toxic to cultured neuronal cells.)
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Cat. No.: HY-P991073

Target:  

Amyloid-β

Research Areas:  

Neurological Disease

MEDI-1814 is a fully human IgG1 antibody that targets the C terminus of Aβ42. MEDI-1814 binds to and sweeps away the circulated Aβ peptides, hence, restricting them from aggregating into toxic oligomers. MEDI-1814 can be used for the study of Alzheimer's diseases. The isotype control for MEDI-1814 can refer to Human IgG1 kappa, Isotype Control (HY-P99001) .
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Cat. No.: HY-118243
CAS No.: 1089681-42-4
Target:  

Amyloid-β

Research Areas:  

Others

KMS88009 is a potent small molecule that directly interferes with the formation of amyloid-β oligomers, thereby preserving cognitive behavior when used preventively and reversing cognitive behavior decline when used therapeutically. Oral administration of KMS88009 around the onset of Alzheimer's disease symptoms significantly reduced the assembly of amyloid-β oligomers and improved cognitive behavior in the APP/PS1 double transgenic mouse model. This unique dual mode of action suggests that KMS88009 may be a powerful therapeutic candidate for the treatment of Alzheimer's disease. In an evaluation, the physicochemical properties, pharmacokinetics and toxicity of this anti-amyloidogenic small molecule KMS88009 were studied, as well as post-mortem analysis of APP/PS1 TG mice after behavioral testing.
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Cat. No.: HY-W010041R
CAS No.: 488-59-5
Scyllo-Inositol is an inhibitor that targets the aggregation of misfolded proteins (such as α-synuclein and Amyloid-β), is orally effective, and can cross the blood-brain barrier. Scyllo-Inositol can selectively bind to and stabilize non-toxic oligomers, preventing them from converting into toxic fibers, exerting protein homeostasis regulation and neuroprotective activity. Scyllo-Inositol binds to the hydrophobic region of pathogenic proteins, inhibits protein aggregation, and promotes lysosome- and proteasome-mediated degradation pathways, thereby reducing neurotoxicity. Scyllo-Inositol can be used in the study of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Huntington's disease .
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Cat. No.: HY-W707693
CAS No.: 115268-26-3
Scyllo-Inositol-d6 is the deuterium labeled Scyllo-Inositol (HY-W010041). Scyllo-Inositol is an inhibitor that targets the aggregation of misfolded proteins (such as α-synuclein and Amyloid-β), is orally effective, and can cross the blood-brain barrier. Scyllo-Inositol can selectively bind to and stabilize non-toxic oligomers, preventing them from converting into toxic fibers, exerting protein homeostasis regulation and neuroprotective activity. Scyllo-Inositol binds to the hydrophobic region of pathogenic proteins, inhibits protein aggregation, and promotes lysosome- and proteasome-mediated degradation pathways, thereby reducing neurotoxicity. Scyllo-Inositol can be used in the study of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Huntington's disease .
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Cat. No.: HY-114613
CAS No.: 1123071-24-8
D-Trp-Aib is a dipeptide and amyloid-β inhibitor with a Kd of 29.6 nM. D-Trp-Aib triggers formation of non-toxic, non-β-sheet, amorphous amyloid β clusters from misfolded amyloid β monomers and toxic amyloid β oligomers, and reduces toxic amyloid β1-42 deposits. D-Trp-Aib inhibits amyloid fibril formation of α‑synuclein, IAPP and calcitonin. D-Trp-Aib can be used for the research of Alzheimer's disease .
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Cat. No.: HY-101855R
CAS No.: 882697-00-9
Synonyms: Anle138b (Standard)
Research Areas:  

Neurological Disease

Emrusolmin (Standard) (Anle138b (Standard)) is the analytical standard of Emrusolmin (HY-101855). This product is intended for research and analytical applications. Emrusolmin (Anle138b), an oligomeric aggregation inhibitor, blocks the formation of pathological aggregates of prion protein (PrPSc) and of α-synuclein (α-syn). Emrusolmin strongly inhibits oligomer accumulation, neuronal degeneration, and disease progression in vivo. Emrusolmin has low toxicity and an excellent oral bioavailability and blood-brain-barrier penetration. Emrusolmin blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology .
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