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Results for "

Aggregated amyloid-beta

" in MedChemExpress (MCE) Product Catalog:

33

Inhibitors & Agonists

1

Fluorescent Dyes

8

Peptides

3

Inhibitory Antibodies

4

Natural
Products

1

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-101855
    Emrusolmin

    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-P9967
    Aducanumab

    BIIB037

    		 Amyloid-β Neurological Disease
    Aducanumab (BIIB037) is a human monoclonal antibody that selectively targets aggregated amyloid-beta (Aβ). Aducanumab shows blood-brain-barrier penetration, and can be used for Alzheimer's disease (AD) research .
    Aducanumab
  • HY-N7046
    Silybin B

    Silibinin B

    		 Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B
  • HY-N7368
    Hibifolin

    		Adenosine Deaminase Bacterial Caspase Infection Neurological Disease Inflammation/Immunology Cancer
    Hibifolin is a flavonol glycoside that can be isolated from Helicteres isora. Hibifolin is an inhibitor of adenosine deaminase (ADA) (Ki = 49.92 μM). Hibifolin protects neurons against β-amyloid-induced neurotoxicity. Hibifolin possesses a potent protective activity against cell death induced by aggregated Aβ. Hibifolin can abolish Aβ-induced caspase-3 and caspase-7 activation. Hibifolin induces Akt phosphorylation in cortical neurons. Hibifolin is also a natural sortase A (SrtA) inhibitor (IC50 = 31.2 μM) through direct binding to SrtA protein. Hibifolin attenuates the pathogenic behavior of Staphylococcus aureus including adhesion, invasion, and biofilm formation. Hibifolin improves the survival of pneumonia induced by Staphylococcus aureus in mouse model and alleviates pathological damage. Hibifolin shows a synergistic antibacterial effect with Cefotaxime (HY-A0088A) .
    Hibifolin
  • HY-P990109
    Aducanumab (Mouse IGG2a)

    		Amyloid-β Neurological Disease
    Aducanumab (Mouse IGG2a) is a monoclonal antibody that selectively targets aggregated amyloid-beta (Aβ). The variable region of Aducanumab (Mouse IGG2a) is consistent with that of Aducanumab (HY-P9967), while the constant region is of Mouse IGG2a sequence. Aducanumab (Mouse IGG2a) has strong selectivity for Aβ fibrils with EC50s of >1 μM and 0.2 nM for monomeric Aβ1-40 and fibrillar Aβ1-42, respectively. Aducanumab (Mouse IGG2a) can be used for Alzheimer's disease (AD) research .
    Aducanumab (Mouse IGG2a)
  • HY-P991480
    ONC-841

    		Transmembrane Glycoprotein Tau Protein Amyloid-β Neurological Disease Cancer
    ONC-841 is a blood-brain barrier-permeable, humanized monoclonal antibody targeting SIGLEC10. As an immune checkpoint inhibitor, ONC-841 restores the functions of immune effector cells such as T cells and enhances anti-tumor immune responses by blocking inhibitory signals mediated by SIGLEC10. ONC-841 restores the phagocytic and migratory activities of microglia, and promotes the phagocytosis of Amyloid-β and Tau protein aggregates by microglia. ONC-841 is applicable to research related to solid tumors and Alzheimer's disease .
    ONC-841
  • HY-P3688A
    β-Amyloid (1-38) TFA

    Aβ (1-38) TFA; Aβ38 TFA

    		 Amyloid-β Neurological Disease
    β-Amyloid (1-38) (Aβ (1-38)) TFA is a β-Amyloid (Aβ) peptide. β-Amyloid (1-38) TFA interferes with the conversion of Aβ(1-42) to a β-sheet-rich aggregate. β-Amyloid (1-38)TFA reverses the negative impact of Aβ(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an Aβ(1-42) phenotype in Caenorhabditis elegans .
    β-Amyloid (1-38) TFA
  • 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-150049
    γ-Secretase modulator 13

    		Amyloid-β Neurological Disease
    γ-Secretase modulator 13 (compound 4) is a gamma-secretase modulator (GSMs) that inhibits the production of the aggregated amyloid β-peptide Aβ42 with an IC50 value of 163 nM. γ-Secretase modulator 13 can be used in the study of Alzheimer's disease .
    γ-Secretase modulator 13
  • HY-P3688
    β-Amyloid (1-38)

    Aβ (1-38); Aβ38

    		 Amyloid-β Neurological Disease
    β-Amyloid (1-38) (Aβ (1-38)) is a β-Amyloid (Aβ) peptide. β-Amyloid (1-38) interferes with the conversion of Aβ(1-42) to a β-sheet-rich aggregate. β-Amyloid (1-38) reverses the negative impact of Aβ(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an Aβ(1-42) phenotype in Caenorhabditis elegans .
    β-Amyloid (1-38)
  • HY-177906
    h-FTAA

    		Fluorescent Dye Amyloid-β Neurological Disease
    h-FTAA is a luminescent conjugated oligothiophene (LCO) probe. h-FTAA can selectively bind to amyloid protein aggregates (such as Aβ 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 .
    h-FTAA
  • HY-176925
    α-Synuclein aggregate binder 2

    		α-synuclein Amyloid-β Neurological Disease
    α-Synuclein aggregate binder 2 (Compound 1) is a specific alpha-synuclein binder with a Ki of 1.6 nM. α-Synuclein aggregate binder 2 has a weak binding affinity for β-amyloid aggregates with a Ki of 295 nM. α-Synuclein aggregate binder 2 can be used as a tracer in Parkinson's disease .
    α-Synuclein aggregate binder 2
  • HY-174305
    Aβ42-IN-7

    		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-158204
    CNB-001

    		Lipoxygenase Amyloid-β Reactive Oxygen Species (ROS) Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology
    CNB-001 is a potent and orally active 5-lipoxygenase (5-LOX) inhibitor. CNB-001 can decreases 5-LOX expression and increase proteasome activity. CNB-001 can inhibit accumulation of soluble Amyloid-β and ubiquitinated aggregated proteins. CNB-001 can inhibit apoptosis, ROS production and stabilize mitochondrial membrane potential. CNB-001 can reduce insulin resistance and increase glucose uptake. CNB-001 also exhibits anti-ischemic, anti-inflammatory effects. CNB-001 can be used for the researches of inflammation, neurological and metabolic disease, such as Alzheimer's disease, stroke and diabetes .
    CNB-001
  • HY-P10037
    β Amyloid(17-28) human

    		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-P1474
    β-Amyloid (22-35)

    amyloid β-Protein (22-35)

    		 Amyloid-β Neurological Disease
    β-Amyloid 22-35 (Amyloid β-Protein 22-35), the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
    β-Amyloid (22-35)
  • HY-P1474A
    β-Amyloid (22-35) TFA

    amyloid β-Protein (22-35) TFA

    		 Amyloid-β Neurological Disease
    β-Amyloid 22-35 (Amyloid β-Protein 22-35) TFA, the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 TFA forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
    β-Amyloid (22-35) TFA
  • HY-P5906
    Citrullinated amyloid-β (1-40) peptide (human)

    Citrullinated Aβ (1-40); Citrullinated Aβ40

    		 Amyloid-β Neurological Disease
    Citrullinated amyloid-β (1-40) peptide (human) (Citrullinated Aβ (1-40)) is a modified form of β-Amyloid (1-40) (HY-P0265) with a citrullination at the Arg5 site. Citrullinated amyloid-β (1-40) peptide (human) exhibits increased transient formation of soluble oligomers and insoluble aggregates composed of distorted parallel β-sheets compared with unmodified β-Amyloid (1-40) .
    Citrullinated amyloid-β (1-40) peptide (human)
  • HY-151554
    SQ-3

    		Amyloid-β Others
    SQ-3 is a quinoline analogue, displays moderate selectivity for α-syn aggregates (Ki=39.3 nM) over β-amyloid (Aβ) aggregates (Ki=230 nM). [ 18F]SQ3 has basic properties as a lead compound for the development of a useful α-syn imaging probe .
    SQ-3
  • HY-D1684
    DCDAPH

    		Amyloid-β Neurological Disease
    DCDAPH (Compound 2c) is a novel smart NIRF probe for detection of β-amyloid (Aβ) plaques (λex/λem=597/665 nm in PBS). DCDAPH shows high affinity for Aβ aggregates (Ki=37 nM, Kd=27 nM). DCDAPH shows good blood brain barrier permeation and can meet most of the requirements for the detection of Aβ plaques both in vitro and in vivo .
    DCDAPH
  • HY-157382
    AChE-IN-51

    		Cholinesterase (ChE) Amyloid-β MMP Neurological Disease
    AChE-IN-51 (compound 8C) is an orally active, non-competitive inhibitor of AChE and BChE (IC50: 84 nM, 97 nM). It also inhibits MMP-2 and amyloid Aβ1-42 aggregates (IC50: 724 nM, 302 nM). AChE-IN-51 has low cytotoxicity and in silico predicted blood-brain barrier permeability. Can be used for research on diseases such as Alzheimer's disease (AD) .
    AChE-IN-51
  • HY-N7046R
    Silybin B (Standard)

    Silibinin B (Standard)

    		 Reference Standards JNK Amyloid-β p38 MAPK Apoptosis Neurological Disease Cancer
    Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B (Standard)
  • HY-N7046S
    Silybin B-d3

    Silibinin B-d3

    		 Isotope-Labeled Compounds Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B-d3 (Silibinin B-d3) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B-d3
  • HY-N7368R
    Hibifolin (Standard)

    		Reference Standards Adenosine Deaminase Bacterial Caspase Neurological Disease Inflammation/Immunology Cancer
    Hibifolin (Standard) is the analytical standard of Hibifolin. This product is intended for research and analytical applications. Hibifolin is a flavonol glycoside that can be isolated from Helicteres isora. Hibifolin is an inhibitor of adenosine deaminase (ADA) (Ki = 49.92 μM). Hibifolin protects neurons against β-amyloid-induced neurotoxicity. Hibifolin possesses a potent protective activity against cell death induced by aggregated Aβ. Hibifolin can abolish Aβ-induced caspase-3 and caspase-7 activation. Hibifolin induces Akt phosphorylation in cortical neurons. Hibifolin is also a natural sortase A (SrtA) inhibitor (IC50 = 31.2 μM) through direct binding to SrtA protein. Hibifolin attenuates the pathogenic behavior of Staphylococcus aureus including adhesion, invasion, and biofilm formation. Hibifolin improves the survival of pneumonia induced by Staphylococcus aureus in mouse model and alleviates pathological damage. Hibifolin shows a synergistic antibacterial effect with Cefotaxime (HY-A0088A) .
    Hibifolin (Standard)
  • HY-183660
    F-SLOH

    		Autophagy Amyloid-β Tau Protein Neurological Disease
    F-SLOH is a brain-penerant and orally active TFEB activator and amyloid-β inhibitor with an IC50 of 3.4 μM against amyloid-β. F-SLOH promotes nuclear translocation of TFEB, driving autophagy and lysosomal biogenesis. F-SLOH reduces amyloid-β oligomers and Tau aggregates via autophagy lysosomal degradation pathway. F-SLOH can be used for the research of Alzheimer’s disease .
    F-SLOH
  • HY-W569115
    JNJ-64326067

    		Tau Protein Neurological Disease
    JNJ-64326067 is an aggregated tau-binding agent with blood-brain barrier permeability, with a Ki of 2.4 nM. JNJ-64326067 selectively binds to aggregated tau protein but does not bind to aggregated β-amyloid protein, and shows no significant off-target binding to the tested receptors, ion channels, transporters, kinases or monoamine oxidases. JNJ-64326067 is applicable to the research of Alzheimer's disease .
    JNJ-64326067
  • HY-108010
    Aftobetin

    		Amyloid-β Neurological Disease
    Aftobetin is a non-invasive molecular probe used for the early diagnosis of Alzheimer's disease (AD). Aftobetin can specifically bind to the aggregated β-amyloid peptide (Aβ) in the lens of the eye, enabling the early diagnosis of AD through a rapid and painless detection method .
    Aftobetin
  • HY-182328
    BTA-EG6

    		Amyloid-β Neurological Disease
    BTA-EG6 is a brain-penetrant aggregated amyloid-β (Aβ) peptide binder with a Kd of 290 nM for Aβ1-42. BTA-EG6 binds to aggregated Aβ and forms protein-resistive coatings that block interactions between Aβ and catalase. BTA-EG6 protects neuroblastoma cells from Aβ-induced toxicity and oxidative stress, and inhibits Aβ-induced increases in cellular hydrogen peroxide (H2O2) levels. BTA-EG6 can be used for the research of alzheimer’s disease (AD) .
    BTA-EG6
  • HY-117521
    EVP-0015962

    		γ-secretase Amyloid-β Neurological Disease
    EVP-0015962 is an orally active, blood-brain barrier-permeable γ-secretase inhibitor with an IC50 of 3.9 μM. EVP-0015962 alters γ-secretase-mediated cleavage of amyloid precursor protein, reduces Aβ42 production and increases Aβ38 production. EVP-0015962 reduces Aβ aggregates, amyloid plaques and inflammatory markers in the brains of mice, and improves their cognitive impairment. EVP-0015962 can be used for the research of Alzheimer's disease .
    EVP-0015962
  • HY-150050
    gamma-secretase modulator 5

    		Amyloid-β Neurological Disease
    gamma-secretase modulator 5 (compound 22d) is a brain-penetrant gamma-secretase modulator (GSMs) that inhibits the production of the aggregated amyloid β-peptide Aβ42 with an IC50 value of 60 nM. gamma-secretase modulator 5 can be used in the study of Alzheimer's disease .
    gamma-secretase modulator 5
  • HY-169268
    Aβ-IN-10

    		Amyloid-β Neurological Disease
    Aβ-IN-10 (Compound Alz -5) is a bifunctional copper chelator and an inhibitor for beta-amyloid (Aβ), that interacts with Aβ aggregates and reduces the neurotoxicity. Aβ-IN-10 exhibits antioxidant efficacy, reveals moderate cytotoxicity with the presence of CuCl2 in SH-SY5Y and HepG2 with IC50 of 65.5, 31.2 μM. Aβ-IN-10 reduces the increase of cell stiffness caused by Aβ .
    Aβ-IN-10
  • HY-103442R
    CGP52411 (Standard)

    DAPH (Standard)

    		 Reference Standards EGFR Amyloid-β Neurological Disease Cancer
    CGP52411 (Standard) is the analytical standard of CGP52411 (HY-103442). This product is intended for research and analytical applications. 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 Ca2+ ions into neuronal cells, and dramatic inhibits and reverses the formation of β-amyloid (Aβ42) fibril aggregates associated with Alzheimer's disease .
    CGP52411 (Standard)
  • HY-101855R
    Emrusolmin (Standard)

    Anle138b (Standard)

    		 Reference Standards Amyloid-β 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 .
    Emrusolmin (Standard)

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