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amyloid aggregation

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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-N0373
    Licochalcone B
    10+ Cited Publications

    		 Amyloid-β Apoptosis NOD-like Receptor (NLR) Neurological Disease
    Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloid β (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
    Licochalcone B
  • HY-113283
    Homogentisic acid

    		Amyloid-β Natriuretic Peptide Receptor (NPR) α-synuclein Transthyretin (TTR) Claudin Neurological Disease Metabolic Disease Cancer
    Homogentisic acid is an orally active, blood-brain barrier-permeable amyloidogenic compound that functions as both an amyloid component and a pigment precursor. Accumulation of homogentisic acid downregulates tight junction proteins (such as claudin-5, occludin, ZO-1) and impairs blood-brain barrier integrity. Homogentisic acid and its oxidation product benzoquinone acetic acid not only induce the aggregation and fibrosis of multiple proteins (such as Aβ1-42, α-synuclein, SAA, Transthyretin (TTR), atrial natriuretic peptide), but also trigger oxidative stress, damage to the Wnt/β-catenin pathway, and neurotoxicity, leading to ochronosis pigment deposition and synaptic dysfunction. At specific concentrations, homogentisic acid exerts no cytotoxicity or genotoxicity on human peripheral blood lymphocytes, and even counteracts the genotoxicity induced by Irinotecan (HY-16562). Homogentisic acid serves as an important tool molecule for investigating the mechanisms of diseases including ochronosis, secondary amyloidosis, Alzheimer's disease, and colorectal cancer .
    Homogentisic acid
  • HY-117259
    Valiltramiprosate
    1 Publications Verification

    ALZ-801

    		 Amyloid-β Neurological Disease
    ALZ-801 is a potent and orally available small-molecule β-amyloid (Aβ) anti-oligomer and aggregation inhibitor, valine-conjugated proagent of Tramiprosate with substantially improved PK properties and gastrointestinal tolerability compared with the parent compound . ALZ-801 is an advanced and markedly improved candidate for the treatment of alzheimer’s disease .
    Valiltramiprosate
  • HY-P2358
    PSMα3

    		NF-κB p38 MAPK Infection Inflammation/Immunology
    PSMα3 is an inhibitor of NF-κB p65 and p38 MAPK. PSMα3 forms membrane pores and binds to residues of human insulin B chain to inhibit insulin aggregation. PSMα3 forms α-type amyloid-like fibrils to exert cytotoxic effects, and acts as a functional amyloid virulence determinant of Staphylococcus aureus. PSMα3 is applicable to research related to spondyloarthritis, rheumatoid arthritis, insulin-derived amyloidosis, and Staphylococcus aureus infection .
    PSMα3
  • 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-W010041
    Scyllo-Inositol

    		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-125616
    Biotinoyl tripeptide-1

    Biotinyl-GHK; Bio-GHK

    		 Amyloid-β Reactive Oxygen Species (ROS) Neurological Disease
    Biotinoyl tripeptide-1 (Biotinyl-GHK) is a biotinylating reagent linked to a GHK (glycyl-L-histidyl-L-lysine) tripeptide. Biotin tripeptide-1 is a bioactive peptide with hair care (improves the appearance and feel of hair) and hair growth effects. Biotinoyl tripeptide-1 has a certain affinity for streptavidin. Biotinoyl tripeptide-1 inhibits the production of ROS and has antioxidant effects. Biotinoyl tripeptide-1 reduces the production of carbonylated amyloid-β (Aβ) and inhibits Aβ aggregation. Biotinoyl tripeptide-1 can be used in the study of neurodegenerative diseases .
    Biotinoyl tripeptide-1
  • HY-NP009
    α-Lactalbumin

    		Bacterial Infection Neurological Disease
    α-Lactalbumin is a globular whey protein that exists in milk. α-Lactalbumin binds Ca 2+, Mg 2+, Mn 2+, Na +, K + and Zn 2+ ions; among these, Ca 2+ binding enhances protein stability, while Zn 2+ binding reduces stability and induces aggregation. α-Lactalbumin forms amyloid fibrils, amorphous aggregates, nanoparticles and nanotubes depending on external conditions. α-Lactalbumin exhibits bactericidal and antiviral activities. α-Lactalbumin has anxiolytic and antidepressant activities, and its effects are enhanced under stress conditions .
    α-Lactalbumin
  • HY-124876
    SynuClean-D
    1 Publications Verification

    SC-D

    		 α-synuclein Neurological Disease
    SynuClean-D (SC-D) is an inhibitor of α-synuclein aggregation, disrupts mature amyloid fibrils, prevents fibril propagation, and abolishes the degeneration of dopaminergic neurons in an animal model of Parkinson’s disease .
    SynuClean-D
  • HY-153430
    Aβ/tau aggregation-IN-3

    		Amyloid-β Neurological Disease
    Aβ/tau aggregation-IN-3 is a potent amyloid protein aggregation inhibitor with an IC50 of 0.85 μM by Aβ-Thioflavin T (Aβ-ThT) functional aggregation assay. Aβ/tau aggregation-IN-3 has anti-amyloid activity .
    Aβ/tau aggregation-IN-3
  • HY-128849
    Eprodisate (70% in water)

    		Amyloid-β Inflammation/Immunology
    Eprodisate (70% in water) is an amyloid inhibitor that interferes with the interaction between amyloidogenic proteins and glycosaminoglycans, thereby inhibiting the aggregation of amyloid fibrils and the deposition of fibrils in tissues. Eprodisate (70% in water) slows the progression of renal disease associated with AA amyloidosis and may be useful for other types of amyloidosis .
    Eprodisate (70% in water)
  • HY-P1047
    β-Sheet Breaker Peptide iAβ5

    [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-136500
    Prostaglandin H2

    PGH2

    		 Endogenous Metabolite Amyloid-β Neurological Disease Inflammation/Immunology
    Prostaglandin H2 (PGH2) is an endothelium-derived contracting factor. Prostaglandin H2 can cause vasoconstriction. Prostaglandin H2 is the common precursor of all PGs and is produced by several cells that express cyclooxygen-ases. Prostaglandin H2 can activate PGD2 receptors CRTH2 and DP via interacting directly with the receptors and/or by giving rise to PGD2 after catalytic conversion by plasma proteins. Prostaglandin H2 can induce eosinophils migration and inhibit platelet aggregation. Prostaglandin H2 can accelerate the formation of dimers and higher oligomers of amyloid β1-42. Prostaglandin H2 can be used for the researches of inflammation and neurological disease, such as Alzheimer disease .
    Prostaglandin H2
  • HY-W117986
    Aβ aggregation-IN-1

    		Amyloid-β Reactive Oxygen Species (ROS) Caspase Neurological Disease
    Aβ aggregation-IN-1 (Compound 1b) is a β-amyloid aggregation inhibitor/depolymerizer, with IC50 values of 3.92 μM and 7.19 μM, respectively. Aβ aggregation-IN-1 inhibits the activation of preformed β-amyloid fibrils, reactive oxygen species (ROS) and Caspase-3. Aβ aggregation-IN-1 can be used in research related to Alzheimer's disease .
    Aβ aggregation-IN-1
  • HY-P1378A
    β-Amyloid (1-43)(human) TFA

    		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-163830
    Pegasus

    DAD9

    		 Dopamine Receptor Neurological Disease
    Pegasus (DAD9) is a potent dopamine receptor agonist. Pegasus shows antioxidant and anti-inflammatory properties. Pegasus inhibits α-Syn amyloid aggregation. Pegasus has the potential for the research of Parkinson’s disease .
    Pegasus
  • HY-B1588
    Carbenoxolone

    		Amyloid-β Gap Junction Protein Neurological Disease Metabolic Disease
    Carbenoxolone is a blood-brain barrier-permeable Pannexin1 inhibitor, gap junction (Gap junction) blocker, and β-amyloid 42 inhibitor. Carbenoxolone modulates voltage-gated currents of wild-type and mutant Panx1, and inhibits stimulus-activated Panx1 channel function. Carbenoxolone interacts with stable residues of β-amyloid 42 peptides, fibrils and oligomers, thereby inhibiting their aggregation. Carbenoxolone alleviates liver fibrosis. Carbenoxolone exerts neuroprotective and nootropic effects. Carbenoxolone can be used in studies related to Alzheimer's disease and liver fibrosis .
    Carbenoxolone
  • HY-159083
    DN5355

    		Amyloid-β Neurological Disease
    DN5355 is a small molecule compound that targets amyloid β protein (Aβ) and hyperphosphorylated tau protein. DN5355 can inhibit the aggregation of Aβ and tau protein and disaggregate the formed Aβ and tau protein fibers. DN5355 can be used in the study of Alzheimer's disease .
    DN5355
  • HY-W004287
    Methyl tridecanoate

    		Amyloid-β Cholinesterase (ChE) Parasite Infection Neurological Disease
    Methyl tridecanoate is a fatty acid methyl ester. Methyl tridecanoate exhibits an IC50 of 3.26 μM and a Ki of 2.30 μM against AsOBP21f in Anopheles sinensis. Methyl tridecanoate induces electroantennographic responses in female Anopheles sinensis. Methyl tridecanoate shows a dose-dependent attractive effect on Anopheles sinensis. Methyl tridecanoate weakly inhibits β-amyloid aggregation and AChE activity. Methyl tridecanoate can be used in the research of malaria and Alzheimer's disease .
    Methyl tridecanoate
  • HY-P4886A
    Amyloid β-Protein (3-42) TFA

    		Amyloid-β Neurological Disease
    Amyloid β-Protein (3-42) TFA is a precursor of Pyr peptide. Pyroglutamic acid-modified Aβ (pEAβ) (3-42) is the core of the amyloid plaque in Alzheimer's disease. pEAβ (3-42) accelerates the aggregation of Aβ(1-42), while Aβ(1-42) significantly slows down the primary and secondary nucleation of pEAβ(3-42).
    Amyloid β-Protein (3-42) TFA
  • HY-148495
    Carnosine conjugated hyalyronate

    		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 Aβ 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-P1378
    β-Amyloid (1-43)(human)

    		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-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-P4886
    Amyloid β-Protein (3-42)

    		Amyloid-β Neurological Disease
    Amyloid β-Protein (3-42) is the precursor of Pyr peptide. Pyroglutamate-modified Aβ (pEAβ) (3-42) is the core of the amyloid template block in Alzheimer's disease. pEAβ(3-42) accelerated the aggregation of Aβ(1-42), while Aβ(1-42) significantly slowed the primary and secondary nucleation of pEAβ(3-42) .
    Amyloid β-Protein (3-42)
  • HY-177854
    Aβ aggregation-IN-4

    		Amyloid-β Neurological Disease
    Aβ aggregation-IN-4 can alleviate the neurotoxicity of amyloid-β protein (Aβ) and significantly reduce the level of oligomeric complexes of Aβ (Aβ-OCs). Aβ aggregation-IN-4 does not decrease the level of amyloid-β protein (Aβ). Aβ aggregation-IN-4 attenuates Aβ oligomerization and prevents oligomer-induced death of primary cortical neurons. Aβ aggregation-IN-4 can be used for the study of Alzheimer’s disease (AD) .
    Aβ aggregation-IN-4
  • HY-P3846
    (Glu20)-Amyloid β-Protein (1-42)

    		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-P1051
    β-Amyloid (12-28)

    amyloid β-Protein (12-28)

    		 Amyloid-β Neurological Disease
    β-Amyloid (12-28) (Amyloid β-Protein (12-28)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) shows aggregation properties. β-Amyloid (12-28) has the potential for Alzheimer’s disease research .
    β-Amyloid (12-28)
  • HY-P5968A
    [Ala28]-β Amyloid(25-35) TFA

    β(25-35)KA TFA

    		 Amyloid-β Neurological Disease
    [Ala28]-β Amyloid(25-35) (β(25-35)KA) TFA is an electrically neutral mutant peptide of Aβ(25-35) that accelerates the aggregation of Firefly Luciferase .
    [Ala28]-β Amyloid(25-35) TFA
  • HY-P1388F
    FITC-Ahx-β-Amyloid (1-42), (rat/mouse) tris

    FITC-Ahx-amyloid β-peptide (1-42) (rat/mouse) tris

    		 Amyloid-β Neurological Disease
    FITC-Ahx-β-Amyloid (1-42), (rat/mouse) (tris) is a fluorescently labeled (FITC) form of β-Amyloid (1-42), (rat/mouse) (HY-P1388), which can be used in Alzheimer's disease-related research, such as aggregation, fiber formation, cellular uptake or imaging experiments. This product is provided in the form of Tris salt.
    FITC-Ahx-β-Amyloid (1-42), (rat/mouse) tris
  • HY-134894A
    Glycerophosphorylethanolamine sodium

    GroPEtn sodium

    		 Amyloid-β Neurological Disease
    Glycerophosphorylethanolamine (GroPEtn) sodium is an active phosphodiester metabolite of Phosphatidylethanolamine. Glycerophosphorylethanolamine sodium promotes the aggregation of amyloid β-protein (Aβ (1-40)) in vitro. Glycerophosphorylethanolamine sodium can be used in the field of neurodegenerative diseases, such as Alzheimer’s disease research .
    Glycerophosphorylethanolamine sodium
  • HY-N2898
    Artanin

    		Cholinesterase (ChE) Neurological Disease
    Artanin is a coumarin, has biological activities related to Alzheimer’s disease. Artanin exerts function including AChE inhibitory and AChE- and self-induced amyloid beta (Aβ) aggregation inhibitory activities, with IC50s of 51 μM, 98 μM, and 124 μM, respectively .
    Artanin
  • HY-179167
    K2V-9

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    K2V-9 is an AChE and MAO-B inhibitor with IC50 values of 1.72 μM and 0.950 μM against AChE and MAO-B, respectively. K2V-9 inhibits amyloid β self-aggregation and reduces ROS. K2V-9 has neuroprotective effects .
    K2V-9
  • HY-146142
    AChE/BuChE-IN-2

    		Cholinesterase (ChE) Amyloid-β Neurological Disease
    AChE/BuChE-IN-2 (Compound 5f) is an orally active AChE and BuChE inhibitor with IC50 values of 0.72 μM and 0.16 μM, respectively. AChE/BuChE-IN-2 shows a non-competitive inhibition with AChE and shows potent self-induced β-amyloid (Aβ) aggregation inhibition with an IC50 of 62.52 μM. AChE/BuChE-IN-2 can cross the BBB .
    AChE/BuChE-IN-2
  • HY-153417
    Anti-amyloid agent-1

    		Amyloid-β Neurological Disease
    Anti-amyloid agent-1 (ex1140) is a potent anti-amyloid compound and inhibits amyloid aggregation, provides a useful method for amyloidosis research .
    Anti-amyloid agent-1
  • HY-112636
    Astrophloxine

    		Amyloid-β Others
    Astrophloxine is a fluorescent imaging probe capable of targeting antiparallel dimers. Astrophloxine can be used to detect aggregated Aβ in brain tissue and cerebrospinal fluid samples of Alzheimer's disease (AD) mice .
    Astrophloxine
  • HY-N8693
    Withanoside IV

    		COX Amyloid-β Sirtuin Reactive Oxygen Species (ROS) Apoptosis SARS-CoV Infection Neurological Disease
    Withanoside IV is an orally active, blood-brain barrier-permeable withanolide derivative. Withanoside IV specifically binds to the Sudlow I site of HSA, induces secondary structural changes in HSA, and forms stable HSA complexes. Withanoside IV inhibits the enzymatic activity of COX-2. Withanoside IV induces axonal regeneration, peripheral nervous system myelination and increased axonal density in spinal cord tissue, reduces reactive gliosis-related changes, and improves hindlimb motor function. Withanoside IV binds to amyloid-β 1-42 to inhibit its aggregation, induces neurite outgrowth and synapse reconstruction, repairs damaged axons and dendrites, enhances mitochondrial biogenesis, exerts neuroprotective effects via the BDNF and SIRT1 signaling pathways, reduces ROS production and neuronal apoptosis, and ameliorates memory deficits. Withanoside IV inhibits the activity of the SARS-CoV-2 main protease. Withanoside IV can be used in research related to spinal cord injury, Alzheimer's disease, and coronavirus disease 2019 (COVID-19) .
    Withanoside IV
  • HY-144775
    AChE-IN-10

    		Cholinesterase (ChE) Neurological Disease
    AChE-IN-10 (Compound 24r) is a potent inhibitor of AChE (IC50 = 2.4 nM). AChE-IN-10 potently inhibits AChE, reduces tau phosphorylation at S396 residue, provides neuroprotection by rescuing neuronal morphology and increasing cell viability. AChE-IN-10 is also found to reduce amyloid aggregation in the presence of AChE .
    AChE-IN-10
  • HY-146347
    MAO-B-IN-10

    		Monoamine Oxidase Amyloid-β Neurological Disease
    MAO-B-IN-10 (compound 4f) is a potent, selective, BBB-penetrated MAO-B (monoamine oxidase-B) inhibitor, with IC50 of 5.3 μM. MAO-B-IN-10 can inhibit (58.2%) and disaggregate (43.3%) self-mediated Aβ (amyloid β) aggregation. MAO-B-IN-10 can be use for Alzheimer’s disease research .
    MAO-B-IN-10
  • 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-153431
    TRV-1387

    		Tau Protein Amyloid-β Neurological Disease
    TRV-1387 is a benzofurazan that inhibits the aggregation of tau and amyloid-β .
    TRV-1387
  • HY-147820
    AY1511

    		Amyloid-β Neurological Disease
    AY1511 is an amyloid β (Aβ) aggregation inhibitor with low cytotoxicity .
    AY1511
  • HY-P3845
    (Gly22)-Amyloid β-Protein (1-42)

    		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-P5968
    [Ala28]-β Amyloid(25-35)

    β(25-35)KA

    		 Amyloid-β Neurological Disease
    [Ala28]-β Amyloid(25-35) (β(25-35)KA) is an electrically neutral mutant peptide of Aβ(25-35) that accelerates the aggregation of Firefly Luciferase .
    [Ala28]-β Amyloid(25-35)
  • HY-P1051A
    β-Amyloid (12-28) TFA

    amyloid β-Protein (12-28) TFA; amyloid Beta-Peptide (12-28) (human) TFA; β-amyloid protein fragment(12-28) TFA

    		 Amyloid-β Neurological Disease
    β-Amyloid (12-28) (TFA) (Amyloid β-Protein (12-28) (TFA)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) (TFA) shows aggregation properties. β-Amyloid (12-28) (TFA) has the potential for Alzheimer’s disease research .
    β-Amyloid (12-28) TFA
  • HY-163441
    BChE-IN-31

    		Cholinesterase (ChE) Neurological Disease
    BChE-IN-31 (Compound 14d) is a selective BChE inhibitor with an IC50 of 65 nM. BChE-IN-31 inhibits the self-induced aggregation of neurotoxic amyloid-β (Aβ) peptide .
    BChE-IN-31
  • HY-W004287S
    Methyl tridecanoate-d25

    		Isotope-Labeled Compounds Amyloid-β Cholinesterase (ChE) Neurological Disease
    Methyl tridecanoate-d25 is the deuterium labeled Methyl tridecanoate. Methyl tridecanoate moderately inhibits β-amyloid aggregation. Methyl tridecanoate weakly inhibits acetylcholinesterase (AChE) .
    Methyl tridecanoate-d25
  • HY-13325
    Aβ aggregation modulator-1

    		Drug Derivative Amyloid-β Neurological Disease
    Aβ aggregation modulator-1 is a stimulator of amyloid-β (Aβ) fibrillogenesis. Aβ aggregation modulator-1 binds hydrophobic residues in Aβ peptides and stabilizes β-sheet-rich protofibrils and fibrils. Aβ aggregation modulator-1 accelerates Aβ polymerization and reduces concentrations of small, toxic Aβ oligomers in heterogeneous aggregation reactions. Aβ aggregation modulator-1 suppresses long-term potentiation (LTP) inhibition by Aβ 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-162832
    Amyloid-β-IN-1

    		Amyloid-β Neurological Disease
    Amyloid-β-IN-1 (compound 13) is a synthetic peptide containing the hydrophobic C-terminal region "VVIA-NH2" and its reverse sequence "AIVV-NH2" of Aβ42, which is an Aβ inhibitor. Amyloid-β-IN-1 can inhibit Aβ aggregation and has neuroprotective effects .
    Amyloid-β-IN-1
  • HY-P10876
    mcK6A1

    		Amyloid-β Neurological Disease
    mcK6A1 is an inhibitor for the aggregation of amyloid-β (Aβ), that selectively binds to the 16KLVFFA21 segment of Aβ42, forms an extended β-folded structure, and inhibits the formation of Aβ42 oligomers. mcK6A1 can be used in research of Alzheimer's disease and other amyloid-related diseases .
    mcK6A1

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