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neurotoxic Aβ

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P1363
    β-Amyloid (1-42), human TFA
    20+ Cited Publications

    Amyloid β-peptide (1-42) (human) TFA

    Amyloid-β Neurological Disease
    β-Amyloid (1-42) (Amyloid β-peptide (1-42), human TFA, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human TFA remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human TFA, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human TFA
  • HY-P1363A
    β-Amyloid (1-42), human
    20+ Cited Publications

    Amyloid β-peptide (1-42) (human)

    Amyloid-β Neurological Disease
    β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human
  • HY-P1363B

    Amyloid-β Neurological Disease
    β-Amyloid (1-42), human, HFIP-treated, a 42-amino acid peptide that has been treated with HFIP from β-Amyloid (1-42), human (HY-P1363A), is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human, HFIP-treated remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, HFIP-treated, after being dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4°C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37°C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human, HFIP-treated
  • HY-P0128
    β-Amyloid (25-35)
    40+ Cited Publications

    Amyloid beta-peptide (25-35); 25-35; β-Amyloid peptide (25-35)

    Amyloid-β Neurological Disease
    β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells .
    β-Amyloid (25-35)
  • HY-B0034
    Donepezil Hydrochloride
    20+ Cited Publications

    E2020

    Cholinesterase (ChE) Neurological Disease Cancer
    Donepezil Hydrochloride (E2020) is a reversible, selective AChE inhibitor with an IC50 of 6.7 nM for AChE activity. Donepezil shows high selectivity for AChE over BuChE . Donepezil exhibits neuroprotective effect on Aβ42 neurotoxicity .
    Donepezil Hydrochloride
  • HY-P1061
    Colivelin
    Maximum Cited Publications
    92 Publications Verification

    STAT Amyloid-β Neurological Disease
    Colivelin is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro . Colivelin exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease . Colivelin has the potential for the treatment of alzheimer's disease and ischemic brain injury
    Colivelin
  • HY-P0128A
    β-Amyloid (25-35), HFIP-treated
    40+ Cited Publications

    Amyloid beta-peptide (25-35), HFIP-treated; 25-35, HFIP-treated; β-Amyloid peptide (25-35), HFIP-treated

    Amyloid-β Neurological Disease
    β-Amyloid (25-35) (Amyloid beta-peptide (25-35)), HFIP-treated is a β-Amyloid (25-35) (HY-P0128) treated with HFIP. β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells .
    β-Amyloid (25-35), HFIP-treated
  • HY-P1061A
    Colivelin TFA
    Maximum Cited Publications
    92 Publications Verification

    STAT Amyloid-β Apoptosis Neurological Disease
    Colivelin TFA is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro . Colivelin TFA exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease . Colivelin TFA has the potential for the treatment of alzheimer's disease and ischemic brain injury .
    Colivelin TFA
  • HY-113283

    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-16009

    (+)-Phenserine; ANVS401

    α-synuclein Neurological Disease Inflammation/Immunology
    Buntanetap ((+)-Phenserine) is a selective acetylcholinesterase inhibitor. Buntanetap is a multiple neurotoxic protein translation inhibitor with oral activity, including amyloid precursor protein (APP), α-synuclein (αSYN) and huntingtin protein (HTT). Buntanetap reduces the production of β-amyloid precursor protein by blocking its mRNA translation. Buntanetap has anti-inflammatory effects and can be used in the study of Alzheimer's disease and Parkinson's disease .
    Buntanetap
  • HY-N7046

    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

    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-N12060

    Bcl-2 Family Caspase Apoptosis Autophagy Reactive Oxygen Species (ROS) Akt JNK ERK Cardiovascular Disease Neurological Disease
    Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
    Ginkgo biloba extract
  • HY-13505
    AM281
    1 Publications Verification

    Cannabinoid Receptor Neurological Disease
    AM281 is a selective CB1 receptor antagonist with an IC50 of 9.91 nM. AM281 inhibits CB2 receptor with an IC50 of 13000 nM .
    AM281
  • HY-B0770
    Artemotil
    1 Publications Verification

    β-Arteether; (+)-Arteether; Arteether

    CXCR Parasite Infection Cancer
    Artemotil (β-Arteether) has antimalarial activity for the treatment of chloroquine-resistant Plasmodium falciparum malaria with an IC50 of 1.61 nM. Artemotil also has central nervous system (CNS) neurotoxicity and anorectic toxicity in rats, dogs and monkeys .
    Artemotil
  • HY-N0541
    Pseudoginsenoside F11
    2 Publications Verification

    Ginsenoside A1

    Amyloid-β JNK MDM-2/p53 Caspase SOD Glutathione Peroxidase NO Synthase Cardiovascular Disease Neurological Disease
    Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of Aβ1-40, downregulates the expression of JNK2, p53 and activated Caspase 3, and restores the activities of SOD and Glutathione peroxidase. Pseudoginsenoside F11 inhibits the excessive activation of μ-Calpain and restores the level of neuronal Nitric oxide synthase. Pseudoginsenoside F11 reduces infarct volume, alleviates cerebral edema, decreases neuronal loss, improves neurological deficits and enhances long-term functional outcomes in transient cerebral ischemia models. Pseudoginsenoside F11 antagonizes Methamphetamine-induced behavioral deficits, dopamine level reduction and neurotoxicity without altering the baseline behaviors of normal mice. Pseudoginsenoside F11 can be used in studies related to Alzheimer's disease, transient cerebral ischemic injury and Methamphetamine-induced neurotoxicity .
    Pseudoginsenoside F11
  • HY-N0061
    Ethyl ferulate
    3 Publications Verification

    Reactive Oxygen Species (ROS) Neurological Disease
    Ethyl ferulate, a naturally lipophilic derivative of ferulic acid originally derived from Rhizoma Chuanxiong, induces heme oxygenase-1 (HO-1) and protects rat neurons against oxidative stress . Ethyl ferulate also protects neurons against amyloid β peptide (1-42)-induced oxidative stress and neurotoxicity .
    Ethyl ferulate
  • HY-W014589
    2,4-Di-tert-butylphenol
    2 Publications Verification

    2,4-DTBP

    Endogenous Metabolite Fungal Apoptosis RAR/RXR Amyloid-β Infection Neurological Disease Inflammation/Immunology Cancer
    2,4-Di-tert-butylphenol (2,4-DTBP) is an orally active RXRα activator and a human estrogen receptor ligand with anti-inflammatory and antioxidant activities, which can induce apoptosis in tumor cells. 2,4-Di-tert-butylphenol can activate the RXRα subtype in LXRα/RXRα, PPARγ/RXRα, and hormone receptor β/RXRα. 2,4-Di-tert-butylphenol also has antiviral and antifungal activities and has the potential to inhibit Aβ-induced neurotoxicity. 2,4-Di-tert-butylphenol can be used as an intermediate in the preparation of antioxidants and UV stabilizers, and is also used in the manufacture of drugs and fragrances .
    2,4-Di-tert-butylphenol
  • HY-W010041

    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-N7675

    NF-κB TGF-beta/Smad Syk Cardiovascular Disease Neurological Disease Metabolic Disease
    Flavanomarein is a substance with cytoprotective, anti-inflammatory and antioxidant activities, with a Ka of 3.064e-5 M against human Syk. Flavanomarein enhances the phosphorylation level of AKT, regulates the expression of PKC-δ, P85α, PKC-β1, Sirt1, Bcl-2 and ICAD, and inhibits the nuclear translocation of NF-κB p65. Flavanomarein regulates EMT marker proteins, promotes the proliferation of HK-2 cells, and protects neuronal cells from 6-OHDA-induced neurotoxic damage. Flavanomarein can be used in studies related to Parkinson's disease and diabetic nephropathy.
    Flavanomarein
  • HY-101448
    TMI-1
    1 Publications Verification

    WAY-171318

    MMP Apoptosis Interleukin Related TNF Receptor Caspase Infection Neurological Disease Inflammation/Immunology Cancer
    TMI-1 (WAY-171318) inhibits TNF converting enzyme (TACE) (IC50 of 8.4 nM), ADAM-TS-4, ADAM-17 and various MMPs with oral activity. TMI-1 significantly suppresses the secretion of TNF-α , alleviating collagen-induced arthritis in mice. TMI-1 inhibits cancer cell proliferation, induces apoptosis through a caspase-dependent pathway. TMI-1 also reverses TRPV1 upregulation and lowers the levels of inflammatory factors (TNF-αIL-1βIL-6) in nerve cells, protecting against paclitaxel-induced neurotoxicity. TMI-1 leads to changes in pro-atherogenic lipoprotein profiles, but does not affect the progression of early lesions .
    TMI-1
  • HY-W041608

    NF-κB Toll-like Receptor (TLR) Bacterial Infection Inflammation/Immunology
    Methylchloroisothiazolinone is a widely used fungicide and also an aquatic pollutant with pro-inflammatory activity and neurotoxicity. Methylchloroisothiazolinone induces the production of pro-inflammatory cytokines (such as IL-1β, TNF-α, IL-6) by activating the NF-κB signaling pathway and upregulating TLR4 expression, thereby triggering allergic contact dermatitis. Methylchloroisothiazolinone reduces cholinesterase activity and exacerbates oxidative stress by impairing catalase activity and disrupting redox balance. Methylchloroisothiazolinone poses significant harm to Mediterranean mussels, reducing the viability of hemocytes and digestive gland cells, inhibiting immune phagocytic function, and disrupting osmoregulatory capacity. Methylchloroisothiazolinone is used in studies on allergic contact dermatitis and related immunotoxicity mechanisms .
    Methylchloroisothiazolinone
  • HY-149845

    PROTACs GSK-3 Neurological Disease
    PROTAC GSK-3β Degrader-1 (compound 1) is a degrader targets GSK-3β degradation with an IC50 value of 833 nM. PROTAC GSK-3β Degrader-1 contains SB-216763 (a GSK-3β inhibitor), a PEG linker and a CRBN (E3 ligase liand). PROTAC GSK-3β Degrader-1 reduces the neurotoxicity induced by Aβ25-35 peptide and CuSO4. PROTAC GSK-3β Degrader-1 can be used to research in Alzheimer's disease .
    PROTAC GSK-3β Degrader-1
  • HY-105066
    Davunetide
    1 Publications Verification

    Microtubule/Tubulin Amyloid-β Neurological Disease
    Davunetide is an eight amino acid snippet derived from activity-dependent neuroprotective protein (ADNP), a neurotrophic factor that exists in the mammalian CNS. Davunetide possesses neuroprotective, neurotrophic and cognitive protective roperties. Davunetide, a microtubule-stabilizing peptide, interacts with and stabilises neuron-specific βIII-tubulin in vitro. Davunetide penetrates the blood-brain barrier and is non-toxic. Davunetide inhibits Aβ aggregation and Aβ-induced neurotoxicity .
    Davunetide
  • HY-115498

    Apoptosis NO Synthase Interleukin Related COX Neurological Disease Inflammation/Immunology
    ARN14494 is a potent and selective serine palmitoyltransferase (SPT) inhibitor, with an IC50 of 27.3 nM. ARN14494 affects the CNS in terms of anti-inflammation and neuroprotection. ARN14494 protects neurons from β-amyloid 1-42-induced neurotoxicity through a variety of mechanisms, including anti-oxidation, anti-apoptosis, and anti-inflammation. ARN14494 can be used for Alzheimer’s disease research .
    ARN14494
  • HY-N13742

    Dihydrohonokiol

    GABA Receptor Neurological Disease
    Dihydrohonokiol B (Dihydrohonokiol) is an anxiolytic agent. Dihydrohonokiol B can reduce the neurotoxicity induced by amyloid β protein by stimulating the GABAC receptor. Dihydrohonokiol B can be used in the research of neurodegenerative diseases such as Alzheimer's disease .
    Dihydrohonokiol B
  • HY-W585874

    EAAT Apoptosis Neurological Disease Metabolic Disease
    Nε-(Carboxyethyl) lysine is an advanced glycation end product (AGE). Nε-(Carboxyethyl) lysine induces cross-linking between proteins, thereby affecting protein structure and function and causing protein denaturation. Nε-(Carboxyethyl) lysine binds to the RAGE receptor, affects cell signal transduction, and regulates processes such as inflammatory responses, cell proliferation, and apoptosis. Nε-(Carboxyethyl) lysine affects glutamate transporters, reduces glutamate uptake and S100β protein secretion, influences neurotransmission in the nervous system, and exhibits diabetes-related neurotoxicity .
    Nε-(Carboxyethyl)lysine
  • HY-W014589R

    2,4-DTBP (Standard)

    Reference Standards Endogenous Metabolite Fungal Apoptosis RAR/RXR Amyloid-β Infection Neurological Disease Inflammation/Immunology Cancer
    2,4-Di-tert-butylphenol (Standard) is the analytical standard of 2,4-Di-tert-butylphenol (HY-W014589). This product is intended for research and analytical applications. 2,4-Di-tert-butylphenol (2,4-DTBP) is an orally active RXRα activator and a human estrogen receptor ligand with anti-inflammatory and antioxidant activities, which can induce apoptosis in tumor cells. 2,4-Di-tert-butylphenol can activate the RXRα subtype in LXRα/RXRα, PPARγ/RXRα, and hormone receptor β/RXRα. 2,4-Di-tert-butylphenol also has antiviral and antifungal activities, and has the potential to inhibit Aβ-induced neurotoxicity. 2,4-Di-tert-butylphenol can be used as an intermediate in the preparation of antioxidants and UV stabilizers, and is also used in the manufacture of pharmaceuticals and fragrances .
    2,4-Di-tert-butylphenol (Standard)
  • HY-W749327

    2,4-DTBP-d21

    Isotope-Labeled Compounds RAR/RXR Amyloid-β Fungal Apoptosis Endogenous Metabolite Infection Neurological Disease Inflammation/Immunology Cancer
    2,4-Di-tert-butylphenol-d21 (2,4-DTBP-d21) is the deuterium labeled 2,4-Di-tert-butylphenol (HY-W014589). 2,4-Di-tert-butylphenol (2,4-DTBP) is an orally active RXRα activator and a human estrogen receptor ligand with anti-inflammatory and antioxidant activities, which can induce apoptosis in tumor cells. 2,4-Di-tert-butylphenol can activate the RXRα subtype in LXRα/RXRα, PPARγ/RXRα, and hormone receptor β/RXRα. 2,4-Di-tert-butylphenol also has antiviral and antifungal activities and has the potential to inhibit Aβ-induced neurotoxicity. 2,4-Di-tert-butylphenol can be used as an intermediate in the preparation of antioxidants and UV stabilizers, and is also used in the manufacture of drugs and fragrances .
    2,4-Di-tert-butylphenol-d21
  • HY-155534

    17β-HSD Others
    17β-HSD10-IN-1 (compound 9) is an orally active inhibitor of 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) with blood-brain permeability. 17β-HSD10-IN-1 doesn't result additional effects for mitochondrial off-targets and cytotoxic or neurotoxic effects .
    17β-HSD10-IN-1
  • HY-P5807A

    β-Mammal toxin Cn2 TFA

    Sodium Channel Neurological Disease
    Cn2 toxin TFA (β-Mammal toxin Cn2 TFA) is a single-chain β-scorpion neurotoxic peptide that is the main toxin in scorpion venom. Cn2 toxin (TFA) specifically targets mammalian voltage-gated sodium channels (VGSC) Nav1.6 .
    Cn2 toxin TFA
  • HY-B0034S

    E2020-d5

    Cholinesterase (ChE) Neurological Disease
    Donepezil-d5 (hydrochloride) is deuterium labeled Donepezil (Hydrochloride). Donepezil Hydrochloride (E2020) is a reversible, selective AChE inhibitor with an IC50 of 6.7 nM for AChE activity. Donepezil shows high selectivity for AChE over BuChE . Donepezil exhibits neuroprotective effect on Aβ42 neurotoxicity .
    Donepezil-d5 hydrochloride
  • HY-P1517

    Amyloid-β Neurological Disease
    β-Amyloid (31-35) is the shortest sequence of native Amyloid-β peptide that retains neurotoxic activity.
    β-Amyloid (31-35)
  • HY-153416

    Amyloid-β Neurological Disease
    QR-0217 is a potent Aβ1-40 aggregation inhibitor with an IC50 value of 7.5 µM. QR-0217 inhibits α-synuclein aggregation. QR-0217 reduces memory impairments caused by Aβ neurotoxicity .
    QR-0217
  • HY-N3562

    Reactive Oxygen Species (ROS) Neurological Disease
    Cedrin is a natural flavonoid that can be found in Cedrus deodara. Cedrin protects PC12 cells against neurotoxicity induced by Aβ1-42. Cedrin can reduce reactive oxygen species overproduction, increase the activity of superoxide dismutase and decrease malondialdehyde content .
    Cedrin
  • HY-171349

    γ-secretase Amyloid-β Neurological Disease
    Amyloid-β-IN-3 (EX.113) is a selective γ-secretase inhibitor. Amyloid-β-IN-3 inhibits Aβ42 secretion in H4 cells with an EC50 value of 148 nM. Amyloid-β-IN-3 regulates the γ-secretase catalytic activity to decrease Aβ42 production, thereby alleviating neurotoxicity caused by Aβ deposition. Amyloid-β-IN-3 is promising for research of Alzheimer's disease (AD) .
    Amyloid-β-IN-3
  • HY-177906

    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-B0034S1

    E2020-d4

    Cholinesterase (ChE) Neurological Disease
    Donepezil-d4 (hydrochloride) is the deuterium labeled Donepezil hydrochloride. Donepezil Hydrochloride (E2020) is a reversible, selective AChE inhibitor with an IC50 of 6.7 nM for AChE activity. Donepezil shows high selectivity for AChE over BuChE . Donepezil exhibits neuroprotective effect on Aβ42 neurotoxicity .
    Donepezil-d4 hydrochloride
  • HY-16009B

    (+)-Phenserine L-Tartrate; ANVS401 L-Tartrate

    Amyloid-β Neurological Disease
    Buntanetap L-Tartrate (Phenserine L-Tartrate) is a selective AChE inhibitor (IC50 = 22.2 nM). Buntanetap is a multiple neurotoxic protein translation inhibitor with oral activity, including amyloid precursor protein (APP), α-synuclein (αSYN) and huntingtin protein (HTT). Buntanetap reduces the production of β-amyloid precursor protein by blocking its mRNA translation. Buntanetap has anti-inflammatory effects and can be used in the study of Alzheimer's disease and Parkinson's disease .
    Buntanetap L-Tartrate
  • HY-177854

    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-174305

    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-149542

    Tau Protein Apoptosis GSK-3 Neurological Disease
    GSK-3β inhibitor 15 (Compound 54) is a GSK-3β inhibitor (IC50: 3.4 nM). GSK-3β inhibitor 15 inhibits Aβ1-42-induced GSK-3β and tau protein phosphorylation. GSK-3β inhibitor 15 inhibits LPS-induced iNOS expression. GSK-3β inhibitor 15 has neuroprotective effects on Aβ1-42-induced neurotoxicity. GSK-3β inhibitor 15 can be used for research of Alzheimer’s disease (AD) .
    GSK-3β inhibitor 15
  • HY-P1363S1

    Isotope-Labeled Compounds Amyloid-β Neurological Disease
    β-Amyloid (1-42), human, Ala( 13C3, 15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human, Ala(13C3,15N) TFA
  • HY-146678

    HDAC Amyloid-β Cholinesterase (ChE) Neurological Disease
    HDAC6-IN-5 (compound 11b) is a potent and BBB-penetrated HDAC6 inhibitor, with an IC50 of 0.025 μM. HDAC6-IN-5 exhibits strong inhibitory activity against Aβ1-42 self-aggregation and AChE, with IC50 values of 3.0 and 0.72 μM. HDAC6-IN-5 can enhance neurite outgrowth without significant neurotoxicity .
    HDAC6-IN-5
  • HY-146679

    HDAC Amyloid-β Cholinesterase (ChE) Neurological Disease
    HDAC6-IN-6 (compound 6a) is a potent and BBB-penetrated HDAC6 inhibitor, with an IC50 of 0.025 μM. HDAC6-IN-6 exhibits strong inhibitory activity against Aβ1-42 self-aggregation and AChE, with IC50 values of 3.0 and 0.72 μM. HDAC6-IN-6 can enhance neurite outgrowth without significant neurotoxicity .
    HDAC6-IN-6
  • HY-14533

    K162

    Amyloid-β Neurological Disease
    K 01-162 (K162) inhibits the fibril formation of Aβ peptides and eliminates their neurotoxicity. K 01-162 binds with Aβ42 peptide with an EC50 value of 80 nM. K 01-162 binds directly to AβO with a KD value of 19 μM. K 01-162 is capable of penetrating the brain and can be used for the research of Alzheimer’s disease .
    K 01-162
  • HY-116377

    Steroid Sulfatase Neurological Disease
    DU-14 is a potent steroid sulfatase inhibitor with an IC50 of 55.8 nM. DU-14 inhibits the MCF-7 cell proliferation (IC50 = 38.7 nM). DU-14 has neuroprotective effects against neurotoxic Aβ, suggesting that up-regulation of endogenous DHEAS by DU-14 could be beneficial to the alleviation of Aβ-induced impairments in spatial memory and synaptic plasticity .
    DU-14
  • HY-13505R

    Cannabinoid Receptor Neurological Disease
    AM281 (Standard) is the analytical standard of AM281. This product is intended for research and analytical applications. AM281 is a selective CB1 receptor antagonist with an IC50 of 9.91 nM. AM281 inhibits CB2 receptor with an IC50 of 13000 nM .
    AM281 (Standard)
  • HY-P10035

    Amyloid-β Neurological Disease
    β Amyloid(28-35) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid oligomers are neurotoxic, and β Amyloid(28-35) human can interact with neuronal membranes, regulate secondary structure and neurotoxicity, and cause Alzheimer's disease. β Amyloid(28-35) human has anisotropic effects on the acidic phospholipid DPH, resulting in enhanced internal fluidity of lipid membrane bilayers .
    β Amyloid(28-35) human
  • HY-N8103

    Amyloid-β Neurological Disease
    Heishuixiecaoline A is a germacrane-type sesquiterpenoid. Heishuixiecaoline A shows protective effect on the neurotoxicity of PC12 cells induced by Aβ25-35 .
    Heishuixiecaoline A

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