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amyloid deposits

" in MedChemExpress (MCE) Product Catalog:

8

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9

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Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-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 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-139066

    Trichosanic acid

    TNF Receptor GLUT Proteasome Tau Protein PKC Neurological Disease Metabolic Disease Inflammation/Immunology
    Punicic acid is a bioactive compound of pomegranate seed oil. Punicic acid is an isomer of conjugated α-linolenic acid and ω-5 polyunsaturated fatty acids. Punicic acid has anti-inflammatory and antioxidant activities and can inhibit the expression of inflammatory mediators such as tumor necrosis factor α (TNF-α). Punicic acid can also reduce the formation of β-amyloid deposits and hyperphosphorylation of tau by increasing the expression of GLUT4 protein and inhibiting the overactivation of calpain, and is used to prevent and treat neurodegenerative diseases. In addition, punicic acid also has breast cancer inhibitor properties that depend on lipid peroxidation and PKC pathways .
    Punicic acid
  • 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-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)

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