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Results for "

amyloid toxicity

" in MedChemExpress (MCE) Product Catalog:

22

Inhibitors & Agonists

13

Peptides

3

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-W010041

    Amyloid-β Endogenous Metabolite Neurological Disease
    Scyllo-Inositol, an amyloid inhibitor, potentialy inhibits α-synuclein aggregation. Scyllo-Inositol stabilizes a non-fibrillar non-toxic form of amyloid-β peptide (Aβ42) in vitro, reverses cognitive deficits, and reduces synaptic toxicity and lowers amyloid plaques in an Alzheimer's disease mouse model .
    Scyllo-Inositol
  • 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
    1 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)
    1 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-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-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-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-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

    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-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-103442

    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-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-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-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-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-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-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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