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amyloid toxicity

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32

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-148495

    Amyloid-β Neurological Disease
    Carnosine conjugated hyalyronate is a hyaluronic acid derivative functionalized with the dipeptide carnosine (Carnosine, Car) and has the ability to resist amyloid aggregation. Carnosine conjugated hyalyronate dissolves amyloid fibrils and reduces Aβ-induced toxicity in vitro. The effectiveness of Carnosine conjugated hyalyronate against amyloid aggregation is directly proportional to the Carnosine loading .
    Carnosine conjugated hyalyronate
  • HY-P0198A
    Neuropeptide Y (human,rat,mouse) TFA
    2 Publications Verification

    Neuropeptide Y Receptor Neurological Disease Endocrinology
    Neuropeptide Y (human) TFA is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.
    Neuropeptide Y (human,rat,mouse) TFA
  • HY-P0198
    Neuropeptide Y (human,rat,mouse)
    2 Publications Verification

    Neuropeptide Y (29-64), amide

    Neuropeptide Y Receptor Neurological Disease Endocrinology
    Neuropeptide Y (human,rat,mouse) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.
    Neuropeptide Y (human,rat,mouse)
  • HY-P1363S1

    Isotope-Labeled Compounds Amyloid-β Neurological Disease
    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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human, Ala(13C3,15N) TFA
  • HY-P3340

    iGluR Neurological Disease
    Leptin (116-130) is a bioactive leptin fragment. Leptin (116-130) promotes AMPA receptor trafficking to synapses and facilitate activity-dependent hippocampal synaptic plasticity. Leptin (116-130) prevents hippocampal synaptic disruption and neuronal cell death in models of amyloid toxicity. Leptin (116-130) has the potential for the research of Alzheimer's disease (AD) .
    Leptin (116-130)
  • HY-P10037

    Amyloid-β Neurological Disease
    β Amyloid(17-28) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid(17-28) human enhances aggregation of full-length β Amyloid40, producing toxic aggregates in Alzheimer's disease (AD) .
    β Amyloid(17-28) human
  • HY-P3793

    Amyloid-β Neurological Disease
    Amyloid β-Protein (33-42) TFA is the residues 33-42 fragment of the β-amyloid protein. Amyloid β-Protein (33-42) TFA inhibits Aβ42-induced toxicity .
    Amyloid β-Protein (33-42) (TFA)
  • HY-P1378A

    Amyloid-β Neurological Disease
    β-Amyloid (1-43)(human) TFA is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) TFA shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) TFA could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
    β-Amyloid (1-43)(human) TFA
  • HY-P1378

    Amyloid-β Neurological Disease
    β-Amyloid (1-43)(human) is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
    β-Amyloid (1-43)(human)
  • HY-136480

    Amyloid-β Neurological Disease
    Chrysamine G, a carboxylic acid analogue of Congo Red, can be used as a probe of amyloid deposition in Alzheimer's disease. Chrysamine G also can inhibit Aβ-induced toxicity in PC12 cells .
    Chrysamine G
  • HY-107790
    5-Methoxyflavone
    1 Publications Verification

    DNA/RNA Synthesis Neurological Disease
    5-Methoxyflavone, belonged to Flavonoid family, is a DNA polymerase-beta inhibitor and neuroprotective agent against beta-amyloid toxicity. possess central nervous system (CNS) depressant effect mediated through the ionotropic GABAA receptors.
    5-Methoxyflavone
  • HY-P1363
    β-Amyloid (1-42), human TFA
    Maximum Cited Publications
    16 Publications Verification

    amyloid β-peptide (1-42) (human) TFA

    Amyloid-β 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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human TFA
  • HY-P1363A
    β-Amyloid (1-42), human
    Maximum Cited Publications
    16 Publications Verification

    amyloid β-peptide (1-42) (human)

    Amyloid-β 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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human
  • HY-P1363B
    β-Amyloid (1-42), human, HFIP-treated
    Maximum Cited Publications
    16 Publications Verification

    Amyloid-β 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 .
    β-Amyloid (1-42), human, HFIP-treated
  • HY-P0198B

    Neuropeptide Y Receptor Neurological Disease Metabolic Disease
    [D-Arg25]-Neuropeptide Y (human) ([D-Arg25] NPY) is a Y1 receptor selective agonist. Neuropeptide Y (human) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity .
    [D-Arg25]-Neuropeptide Y (human)
  • HY-107509

    mGluR Neurological Disease
    LY2389575 hydrochloride is a selective and noncompetitive mGlu3 negative allosteric modulator (NAM), with an IC50 value of 190 nM. LY2389575 hydrochloride induces an increase in Mrc1 levels. LY2389575 hydrochloride also independently amplifies Amyloid beta (Aβ) toxicity and can be used in study of Alzheimer's disease .
    LY2389575 hydrochloride
  • HY-P991413

    Trk Receptor Neurological Disease
    ZEB85 is a human monoclonal antibody (mAb) targeting TrkB. ZEB85 activates TrkB and its downstream signaling cascades and increases neuronal activity. ZEB85 prevents β-amyloid toxicity in cultured hippocampal neurons. ZEB85 can be used in Alzheimer's disease (AD) research .
    ZEB85
  • HY-103442
    CGP52411
    1 Publications Verification

    DAPH

    EGFR Amyloid-β Neurological Disease Cancer
    CGP52411 (DAPH) is a high selective, potent, orally active and ATP-competitive EGFR inhibitor with an IC50 of 0.3 μM. CGP52411 blocks the toxic influx of Ca 2+ ions into neuronal cells, and dramatic inhibits and reverses the formation of β-amyloid (Aβ42) fibril aggregates associated with Alzheimer's disease .
    CGP52411
  • HY-113950

    Transthyretin (TTR) Neurological Disease
    Dichlorophenyl-ABA is an inhibitor of transthyretin (TTR) amyloid fibril formation, inhibiting aggregate formation in more than 80% in TTR L55P-expressing cells .
    Dichlorophenyl-ABA
  • HY-174305

    Amyloid-β 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) .
    Aβ42-IN-7
  • HY-N6640

    20-Hydroxyeedysone 2-acetate

    Amyloid-β Neurological Disease
    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 .
    2-O-Acetyl-20-hydroxyecdysone
  • HY-W010041R

    α-synuclein Amyloid-β Neurological Disease
    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 .
    Scyllo-Inositol (Standard)
  • HY-W010041

    α-synuclein Amyloid-β Neurological Disease
    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 .
    Scyllo-Inositol
  • HY-116753

    Amyloid-β Tau Protein Neurological Disease
    (-)Clausenamide is an active alkaloid isolated from the leaves of Clausena lansium (Lour.) Skeels, and improves cognitive function in both normal physiological and pathological conditions. (-)Clausenamide inhibits β-amyloid (Aβ) toxicity, blocking neurofibrillary tangle formation by inhibiting the phosphorylation of tau protein. (-)Clausenamide exerts a significant neuroprotective activity against Aβ25-35. (-)Clausenamide can be used for researching Alzheimer's disease (AD) .
    (-)Clausenamide
  • HY-101855

    Anle138b

    Amyloid-β 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 .
    Emrusolmin
  • HY-118243

    Amyloid-β 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.
    KMS88009
  • HY-P1047

    [Pro18, Asp21] β-amyloid (17-21)

    Amyloid-β Neurological Disease
    β-Sheet Breaker Peptide iAβ5 is an effective brain amyloid-β (Abeta) degrader. Abeta deposits are associated with Alzheimer's disease (AD), and the related toxicity arises from its β-sheet conformation and aggregation. β-Sheet Breaker Peptide iAβ5 can repeatedly induce the degradation of fibrillary amyloid deposits in vivo. Therefore, β-Sheet Breaker Peptide iAβ5 can prevent and/or reverse neuronal contraction caused by Abeta and reduce the range of interleukin IL-1beta positive microglial-like cells around Abeta deposits. β-Sheet Breaker Peptide iAβ5 can reduce the size and/or number of brain amyloid plaques in AD. β-Sheet Breaker Peptide iAβ5 is labeled with a hydrophobic benzyl alcohol (HBA) tag and shows a bright blue color under acidic conditions, which can be used for quantitative determination.
    β-Sheet Breaker Peptide iAβ5
  • HY-W707693

    Isotope-Labeled Compounds Amyloid-β α-synuclein Neurological Disease
    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 .
    Scyllo-Inositol-d6
  • HY-13325

    Drug Derivative Amyloid-β Neurological Disease
    Aβ aggregation modulator-1 is a stimulator of amyloid-β () fibrillogenesis. Aβ aggregation modulator-1 binds hydrophobic residues in peptides and stabilizes β-sheet-rich protofibrils and fibrils. Aβ aggregation modulator-1 accelerates polymerization and reduces concentrations of small, toxic oligomers in heterogeneous aggregation reactions. Aβ aggregation modulator-1 suppresses long-term potentiation (LTP) inhibition by oligomers in hippocampal brain slices. Aβ aggregation modulator-1 can be used for the study of Alzheimer's disease (AD) .
    Aβ aggregation modulator-1
  • HY-146483

    Amyloid-β Neurological Disease Inflammation/Immunology
    Anti-Aβ agent 1A (compound M15) has potent activity against amyloid-β. Anti-Aβ agent 1A possesses can significantly inhibit LPS-induced levels of IL-1β, IL-6 and TNF-α, and reduces the apoptosis of SH-SY5Y induced by H2O2 through mitochondria pathway. Anti-Aβ agent 1A possesses antioxidant, anti-inflammatory, anti-Aβ toxicity and neuroprotective activities. Anti-Aβ agent 1A can be used for researching Alzheimer’s disease (AD) .
    Anti-Aβ agent 1A
  • HY-175523

    Monoamine Oxidase Cholinesterase (ChE) Amyloid-β Neurological Disease
    MAO-B-IN-48 is a selective MAO-B inhibitor (IC50 = 0.09 μM, Ki = 0.02 μM). MAO-B-IN-48 exhibits inhibitory activity against hBChE (IC50 = 1.10 μM, Ki = 0.43 μM) and AChE (IC50 = 0.56 μM, Ki = 0.14 μM). MAO-B-IN-48 suppresses self-induced aggregation of toxic β-amyloid peptides and exerts antioxidant activity, including DPPH radical scavenging, CUPRAC copper ion reduction, and superoxide anion scavenging. MAO-B-IN-48 can be used for the study of Alzheimer's disease (AD) .
    MAO-B-IN-48
  • HY-124832
    δ-Secretase inhibitor 11
    1 Publications Verification

    Caspase Amyloid-β Neurological Disease
    δ-Secretase inhibitor 11 (compound 11) is an orally active, potent, BBB-penetrated, non-toxic, selective and specific δ-secretase inhibitor, with an IC50 of 0.7 μM. δ-Secretase inhibitor 11 interacts with both the active site and allosteric site of δ-secretase. δ-Secretase inhibitor 11 attenuates tau and APP (amyloid precursor protein) cleavage. δ-Secretase inhibitor 11 ameliorates synaptic dysfunction and cognitive impairments in tau P301S and 5XFAD transgenic mouse models. δ-Secretase inhibitor 11 can be used for Alzheimer's disease research .
    δ-Secretase inhibitor 11

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