Search Result
Results for "
amyloid aggregation
" in MedChemExpress (MCE) Product Catalog:
1
Isotope-Labeled Compounds
Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
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- HY-153417
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Amyloid-β
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Neurological Disease
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Anti-amyloid agent-1 is a potent anti-amyloid compound and inhibits amyloid aggregation. Anti-amyloid agent-1, compound ex1140 from patent WO2012119035A1, provides a useful method for amyloidosis treatment research .
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- HY-153430
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Amyloid-β
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Neurological Disease
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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 .
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- HY-144775
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Cholinesterase (ChE)
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Neurological Disease
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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 .
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- HY-146347
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Monoamine Oxidase
Amyloid-β
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Neurological Disease
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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 .
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- HY-P10037
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Amyloid-β
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Neurological Disease
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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) .
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- HY-147820
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- HY-153431
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- HY-P3845
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Amyloid-β
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Neurological Disease
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(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 .
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- HY-P3846
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Amyloid-β
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Neurological Disease
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(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 .
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- HY-W004287
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- HY-W010041
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Amyloid-β
Endogenous Metabolite
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Neurological Disease
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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 .
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- HY-P1051
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amyloid β-Protein (12-28)
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P5968
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β(25-35)KA
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Amyloid-β
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Neurological Disease
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[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 .
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- HY-P1051A
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amyloid β-Protein (12-28) (TFA); amyloid Beta-Peptide (12-28) (human) TFA; β-amyloid protein fragment(12-28) TFA
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Amyloid-β
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Neurological Disease
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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 .
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- HY-163441
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Cholinesterase (ChE)
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Neurological Disease
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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 .
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- HY-W004287S
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- HY-124876
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SC-D
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α-synuclein
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Neurological Disease
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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 .
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- HY-P1378
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P1378A
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Amyloid-β
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Neurological Disease
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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 .
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- HY-146140
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Amyloid-β
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Neurological Disease
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Aβ-IN-4 (compound 12) is a potent amyloid β (Aβ) inhibitor. Aβ-IN-4 inhibits Aβ42 aggregation. However, Aβ-IN-4 can not alleviate the neurotoxicity of Aβ42 in SH-SY5Y cells. Aβ-IN-4 can not change the aggregation state of Aβ42 into a nontoxic one .
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- HY-146139
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Amyloid-β
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Neurological Disease
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Aβ-IN-3 (compound 1) is a potent amyloid β (Aβ) inhibitor. Aβ-IN-3 inhibits Aβ42 aggregation. However, Aβ-IN-3 can not alleviate the neurotoxicity of Aβ42 in SH-SY5Y cells. Aβ-IN-3 can not change the aggregation state of Aβ42 into a nontoxic one .
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- HY-N2898
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Cholinesterase (ChE)
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Neurological Disease
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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 .
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- HY-157296
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Cholinesterase (ChE)
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Neurological Disease
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AChE-IN-47 (compound g17) is a AChE inhibitor with the IC50 of 0.24 μM. AChE-IN-47 inhibits amyloid β peptides self-aggregation. AChE-IN-47 displays neuroprotective effects and effectively suppresses the intracellular accumulation of reactive oxygen species .
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- HY-163320
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Cholinesterase (ChE)
Amyloid-β
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Neurological Disease
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AChE/Aβ-IN-5 (compound AV-2) is a bifunctional inhibitor that targets AChE and auto-induced Aβ (Amyloid-β) aggregation. AChE/Aβ-IN-5 can significantly improve scopolamine- and Aβ-induced cognitive impairment in mice .
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- HY-N12321
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Others
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Metabolic Disease
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2',3'-Dihydroxy-4',6'-dimethoxychalcone (compound 1) can inhibit Amyloid β-protein (Aβ42) fibrillization and aggregation. 2',3'-Dihydroxy-4',6'-dimethoxychalcone has oral activity and can be detected in the brain .
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- HY-157441
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Cholinesterase (ChE)
Amyloid-β
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Neurological Disease
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AChE/Aβ-IN-4 is a dual inhibitor of acetylcholinesterase (AChE) and β-amyloid (Aβ) aggregation, with the IC50 values of 1.72 ± 0.18 μM and 1.42 ± 0.3 μM, respectively. AChE/Aβ-IN-4 plays an impotant role in neurological disorders, such as Alzheimer’s disease .
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- HY-117259
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ALZ-801
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P5370
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Amyloid-β
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Others
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Scrambled β-amyloid (1-40) is a biological active peptide. (Aβ (1-40) together with Aβ (1-42) are two major C-terminal variants of the Aβ protein constituting the majority of Aβs. These undergo post-secretory aggregation and deposition in the Alzheimer’s disease brain. This peptide is the scrambled sequence of Abeta 1-40 HY-P0265)
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- HY-N0373
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Amyloid-β
Apoptosis
NOD-like Receptor (NLR)
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Neurological Disease
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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 .
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- HY-136813
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Beta-secretase
Amyloid-β
Cholinesterase (ChE)
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Neurological Disease
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Multitarget AD inhibitor-1 is a selective and reversible butyrylcholinesterase (BuChE) inhibitor with IC50s of 7.22 μM and 1.55 μM for hBuChE and eqBuChE (BuChE from equine serum), respectively. Multitarget AD inhibitor-1 inhibits β-secretase (IC50hBACE-1=41.60 μM), amyloid β aggregation (IC50Aβ=3.09 μM), tau aggregation. Multitarget AD inhibitor-1, a diphenylpropylamine derivative, has the potential for multifunctional disease-modifying anti-Alzheimer’s research .
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- HY-146142
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Cholinesterase (ChE)
Amyloid-β
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Neurological Disease
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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 .
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- HY-157440
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Amyloid-β
Reactive Oxygen Species
Cholinesterase (ChE)
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Neurological Disease
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AChE/Aβ-IN-3 (compound AM5) is a dual inhibitor of AChE and Amyloid-β aggregation with IC50<.sub> values of 1.29 and 4.93 μM, respectively. AChE/Aβ-IN-3 has antioxidant properties that scavenge ROS and restore their normal levels. AChE/Aβ-IN-3 can be used in the study of neurological diseases, such as Alzheimer's disease .
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- HY-101855
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Anle138b
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Amyloid-β
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Neurological Disease
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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 .
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- HY-146399
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Cholinesterase (ChE)
ROS Kinase
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Neurological Disease
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AChE/BChE-IN-9 (Compound 7a) is a potent, orally active AChE and BChE inhibitor with IC50 values of 5.74 μM and 14.05 μM against hAChE and eqBChE, respectively. AChE/BChE-IN-9 is also an efficacious antioxidant with an IC50 of 57.35 μM. AChE/BChE-IN-9 is able to chelate iron and modulates aggregation of amyloid β1-42. AChE-IN-16 can cross the BBB .
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- HY-152110
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Cholinesterase (ChE)
Monoamine Oxidase
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Neurological Disease
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Dual AChE-MAO B-IN-5, indanone derivative, is a potent dual AChE/MAO-B inhibitior with IC50 values of 0.0224, 0.0412, and 0.1116 μM for AChE, MAO-B and MAO-A, respectively. Dual AChE-MAO B-IN-5 has antioxidant activity and prevents β-amyloid plaque aggregation. Dual AChE-MAO B-IN-5 can be used for Alzheimer’s disease (AD) research .
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- HY-P1047
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[Pro18, Asp21] β-amyloid (17-21)
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Amyloid-β
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Neurological Disease
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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 .
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- HY-149211
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Cholinesterase (ChE)
Beta-secretase
Amyloid-β
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Neurological Disease
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AChE/BChE-IN-12 (compound 10b), a 3,5-dimethoxy analogue, is a potent AChE, BChE, and β-secretase-1 (BACE-1) inhibitor, with IC50 values of 2.57, 3.26, and 10.65 μM, respectively. AChE/BChE-IN-12 crosses the blood-brain barrier via passive diffusion and inhibits the self-aggregation of amyloid-β monomers. AChE/BChE-IN-12 can be used for Alzheimer’s disease (AD) research .
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- HY-152114
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Monoamine Oxidase
Cholinesterase (ChE)
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Neurological Disease
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AChE/BChE/MAO-B-IN-4, an indan-1-one derivative, is a potent MAO-B inhibitor with an IC50 of 0.0393 μM for human MAO-B. AChE/BChE/MAO-B-IN-4 is a potent AChE and BChE enzyme inhibitor, with IC50s of 0.0458 μM and 0.075 μM for human AChE and BChE enzyme, respectively. AChE/BChE/MAO-B-IN-4 shows significant antioxidant activity and prevent β-amyloid plaque aggregation. AChE/BChE/MAO-B-IN-4 has the potential for Alzheimer's disease (AD) research .
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- HY-112636
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Amyloid-β
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Others
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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 .
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- HY-146314
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Monoamine Oxidase
Amyloid-β
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Neurological Disease
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MAO-B-IN-9 (compound 16) is a potent, selective, BBB-penetrated, irreversible and time-dependent MAO-B (monoamine oxidase B) inhibitor, with an IC50 of 0.18 μM. MAO-B-IN-9 prevents Aβ1-42-induced neuronal cell death. MAO-B-IN-9 shows neuroprotective effects, which may be the result of its Aβ1-42 anti-aggregation effects . MAO-B-IN-9 is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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Cat. No. |
Product Name |
Target |
Research Area |
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- HY-P4886
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Peptides
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Neurological Disease
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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) .
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- HY-P10037
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Amyloid-β
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Neurological Disease
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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) .
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- HY-P3845
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Amyloid-β
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Neurological Disease
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(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 .
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- HY-P3846
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Amyloid-β
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Neurological Disease
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(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 .
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- HY-P1051
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amyloid β-Protein (12-28)
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P5968
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β(25-35)KA
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Amyloid-β
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Neurological Disease
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[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 .
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- HY-P1051A
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amyloid β-Protein (12-28) (TFA); amyloid Beta-Peptide (12-28) (human) TFA; β-amyloid protein fragment(12-28) TFA
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P1378
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P1378A
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Amyloid-β
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Neurological Disease
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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 .
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- HY-P5340
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Peptides
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Others
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Amyloid-Forming peptide GNNQQNY is a biological active peptide. (This is a heptapeptide from the N-terminal prion-determining domain of the yeast protein Sup35 that forms amyloid fibrils. The availability of its detailed atomic oligomeric structure makes it a good model for studying the early stage of aggregation. The GNNQQNY dimer forms three stable sheet structures. in-register parallel, off-register parallel, and anti-parallel. The in-register parallel dimer, which is close to the amyloid beta-sheet structure, has few interpeptide hydrogen bonds, making hydrophobic interactions more important and increasing the conformational entropy compared to the anti-parallel sheet.)
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- HY-P5370
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Amyloid-β
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Others
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Scrambled β-amyloid (1-40) is a biological active peptide. (Aβ (1-40) together with Aβ (1-42) are two major C-terminal variants of the Aβ protein constituting the majority of Aβs. These undergo post-secretory aggregation and deposition in the Alzheimer’s disease brain. This peptide is the scrambled sequence of Abeta 1-40 HY-P0265)
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- HY-P1047
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[Pro18, Asp21] β-amyloid (17-21)
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Amyloid-β
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Neurological Disease
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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 .
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Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
Cat. No. |
Product Name |
Chemical Structure |
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- HY-W004287S
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Methyl tridecanoate-d25 is the deuterium labeled Methyl tridecanoate. Methyl tridecanoate moderately inhibits β-amyloid aggregation. Methyl tridecanoate weakly inhibits acetylcholinesterase (AChE)[1].
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Cat. No. |
Product Name |
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Classification |
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- HY-146314
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Alkynes
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MAO-B-IN-9 (compound 16) is a potent, selective, BBB-penetrated, irreversible and time-dependent MAO-B (monoamine oxidase B) inhibitor, with an IC50 of 0.18 μM. MAO-B-IN-9 prevents Aβ1-42-induced neuronal cell death. MAO-B-IN-9 shows neuroprotective effects, which may be the result of its Aβ1-42 anti-aggregation effects . MAO-B-IN-9 is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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