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Results for "

amyloid deposits

" in MedChemExpress (MCE) Product Catalog:

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9

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P4882

    Amyloid-β Neurological Disease
    (Pyr3)-Amyloid β-Protein (3-42) is the predominant amyloid β-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloid β-Protein (3-42) is suggested to accumulate in the brain and to trigger the formation of insoluble amyloid β-peptide deposits .
    (Pyr3)-Amyloid β-Protein (3-42)
  • HY-P4882A

    Amyloid-β Neurological Disease
    (Pyr3)-Amyloid β-Protein (3-42) TFA is the predominant amyloid β-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloid β-Protein (3-42) TFA is suggested to accumulate in the brain and to trigger the formation of insoluble amyloid β-peptide deposits .
    (Pyr3)-Amyloid β-Protein (3-42) (TFA)
  • HY-N12840

    Others Metabolic Disease
    Logmalicid B is an iridoid glycoside compound that can be isolated from Cornus officinalis and can be used in diabetes research .
    Logmalicid B
  • HY-P3858

    Amyloid-β Neurological Disease
    (D-Asp1)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .
    (D-Asp1)-Amyloid β-Protein (1-42)
  • HY-P3845

    Amyloid-β Neurological Disease
    (Gly22)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease. Mutation of Glu22 to Gly22 in Aβ can increase aggregation .
    (Gly22)-Amyloid β-Protein (1-42)
  • HY-P3846

    Amyloid-β Neurological Disease
    (Glu20)-Amyloid β-Protein (1-42) is a slower fibrillizing variant of amyloid β-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .
    (Glu20)-Amyloid β-Protein (1-42)
  • HY-P1387
    β-Amyloid (1-40) (rat)
    1 Publications Verification

    Amyloid-β Apoptosis Neurological Disease
    β-Amyloid (1-40) (rat) is a rat form of the amyloid β-peptide, which accumulates as an insoluble extracellular deposit around neurons, giving rise to the senile plaques associated with Alzheimer's disease (AD). β-Amyloid (1-40) (rat) increases 45Ca 2+ influx, induces neurodegeneration in the rat hippocampal neurons of the CA1 subfield. β-Amyloid (1-40) (rat) induces apoptosis. β-Amyloid (1-40) (rat) can be used for the research of Alzheimer's disease .
    β-Amyloid (1-40) (rat)
  • HY-P1047

    [Pro18, Asp21] β-amyloid (17-21)

    Amyloid-β Neurological Disease
    β-Sheet Breaker Peptide iAβ5 is a potent degrader of cerebral amyloid-beta (Abeta). Abeta deposition is associatied with the Alzheimer disease (AD), due to its related toxicity linked to its beta-sheet conformation and/or aggregation. β-Sheet Breaker Peptide iAβ5 reproducibly induces in vivo disassembly of fibrillar amyloid deposits. Thus, β-Sheet Breaker Peptide iAβ5 prevents and/or reverses neuronal shrinkage caused by Abeta, and reduces the extent of interleukin-1beta positive microglia-like cells that surround the Abeta deposits. β-Sheet Breaker Peptide iAβ5 reduces the size and/or number of cerebral amyloid plaques in AD. β-Sheet Breaker Peptide iAβ5 labeled by hydrophobic benzyl alcohol (HBA) tag, can be used for quantitative assay by showing vivid blue color under acidic conditions .
    β-Sheet Breaker Peptide iAβ5

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