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Pathways Recommended: Neuronal Signaling
Results for "

neuronal death

" in MedChemExpress (MCE) Product Catalog:

92

Inhibitors & Agonists

1

Fluorescent Dyes

1

Biochemical Assay Reagents

25

Peptides

1

Inhibitory Antibodies

15

Natural
Products

5

Isotope-Labeled Compounds

1

Click Chemistry

2

Oligonucleotides

1

GMP Molecules

Targets Recommended:
Cat. No. 상품명 Target 연구분야 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
    β-Amyloid (1-42), human, HFIP-treated
    20+ Cited Publications

    		 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-16900
    Rolipram
    15+ Cited Publications

    (R,S)-Rolipram; (±)-Rolipram; ZK 62711

    		 Bacterial HIV Phosphodiesterase (PDE) Epigenetic Reader Domain Amyloid-β Infection Neurological Disease Cancer
    Rolipram is a PDE4 inhibitor, with blood-brain barrier permeability, that reverses β-amyloid-induced learning and memory impairment in rats. Rolipram elevates intracellular cAMP and clevels and regulates the cAMP/CREB signaling pathway, thereby alleviating neuroinflammation and apoptotic responses. Rolipram promotes neuronal differentiation of human bone marrow mesenchymal stem cells and inhibits Methamphetamine- and morphine-induced hyperlocomotion in mice. Rolipram also reduces the viability of glioblastoma stem-like cells and enhances Bevacizumab (HY-P9906)-induced cell death. Rolipram inhibits the expression of proinflammatory cytokines and enhances central noradrenergic transmission. Rolipram is mainly used in studies related to various central nervous system diseases including Alzheimer's disease, major depressive disorder, glioblastoma multiforme, and multiple sclerosis .
    Rolipram
  • 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-N5134
    5'-Guanylic acid
    2 Publications Verification

    5'-GMP; 5'-guanosine monophosphate

    		 Endogenous Metabolite iGluR Neurological Disease Metabolic Disease
    5'-Guanylic acid is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid also causes neuronal cell death at high concentrations .
    5'-Guanylic acid
  • HY-W011474
    Geranylgeraniol

    		NF-κB Inflammation/Immunology
    Geranylgeraniol is an orally acitve vitamin K2 sub-type, an intermediate of the mevalonate pathway. Geranylgeraniol targets NF-kB signaling pathway and could alleviate LPS-induced microglial inflammation in animal model .
    Geranylgeraniol
  • HY-100355
    C18-Ceramide (d18:1/18:0)

    C18-Ceramide

    		 Endogenous Metabolite Neurological Disease Cancer
    C18-Ceramide (d18:1/18:0) is a bioactive molecule with multiple functions in cells, not a traditional agonist or inhibitor targeting a single site. It can act on multiple cellular targets, such as proteins related to endoplasmic reticulum stress (e.g., ATF-4, XBP-1, CHOP), proteins in the PI3K/AKT signaling pathway, and SNARE complex proteins. It exerts activities like inducing cell death, promoting autophagy, and regulating exocytosis through mechanisms such as activating endoplasmic reticulum stress, inhibiting the PI3K/AKT signaling pathway, and affecting lipid raft - related functions. It can be used in research on the mechanism of neuronal injury in the field of neuroscience and in the treatment research of cancers such as glioma in the field of oncology .
    C18-Ceramide (d18:1/18:0)
  • HY-17001A
    Flupirtine
    1 Publications Verification

    D 9998

    		 Potassium Channel iGluR GABA Receptor Neurological Disease Inflammation/Immunology
    Flupirtine (D 9998) is an orally active, blood-brain barrier-crossing non-opioid analgesic and neuroprotective agent. Flupirtine is a neuronal potassium channel opener (Kv7 activator), a NMDA receptor antagonist and a GABA receptor activator. Flupirtine stabilizes blood-brain-barrier integrity, reduces oxidative stress and brain leukocyte infiltration, enhances angioneurogenesis, suppresses calcium influx, stabilizes neuronal resting membrane potential, and counteracts focal cerebral ischemia. Flupirtine exhibits analgesic, muscle relaxant properties, protects neurons from excitotoxic, ischemic, or cytokine-mediated death. Flupirtine functions as a non-opioid analgesic without antipyretic or antiphlogistic properties, shows no relevant affinity to opiate receptor. Flupirtine can be used for the research of focal cerebral ischemia, pain, Alzheimer’s disease, or multiple sclerosis .
    Flupirtine
  • HY-30004
    1-Aminocyclopropane-1-carboxylic acid

    		Environmental Pollutants Endogenous Metabolite Cardiovascular Disease Metabolic Disease
    1-Aminocyclopropane-1-carboxylic acid is an endogenous metabolite. In the presence of low concentrations (1 μM) of glutamate, 1-Aminocyclopropane-1-carboxylic acid acts as a small molecule agonist of NMDA receptors with an EC50 of 0.7-0.9 μM. At high concentrations (10 μM) of glutamate, 1-Aminocyclopropane-1-carboxylic acid acts as a competitive antagonist of NMDA receptors with an EC50 of 81.6 nM. 1-Aminocyclopropane-1-carboxylic acid exerts neuroprotective activity by moderately activating NMDA receptors to prevent neuronal cell death in ischemic animal models. Additionally, 1-Aminocyclopropane-1-carboxylic acid is an antagonist of NMDA receptors, inducing blood pressure reduction and antioxidant effects in stroke-prone hypertensive rats. 1-Aminocyclopropane-1-carboxylic acid enhances object recognition memory and cognitive flexibility dependent on the prefrontal cortex, but does not affect impulsivity nor exhibit an antipsychotic-like profile. 1-Aminocyclopropane-1-carboxylic acid shows promise for research in the field of neurotoxicity. .
    1-Aminocyclopropane-1-carboxylic acid
  • HY-59291
    Levacetylleucine

    N-Acetyl-L-leucine

    		 Amino Acid Derivatives Neurological Disease Metabolic Disease Inflammation/Immunology
    Levacetylleucine (N-acetyl-L-leucine), an orally bioavailable and brain-penetrant compound, is an acetylated derivative of amino acid Leucine. Levacetylleucine is the active form of N-acetyl-leucine (NAL). Levacetylleucine attenuates neuronal death and neuroinflammation in the cortical tissue of mice. Levacetylleucine also potentially improves ameliorates lysosomal and metabolic dysfunction. Levacetylleucine improves compensation of postural symptoms after unilateral chemical labyrinthectomy (UL) in rats. Levacetylleucine is promising for research of neurological manifestations of Niemann-Pick disease type C, traumatic brain injury and neurodegeneration prevention .
    Levacetylleucine
  • 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-B0863
    Glyphosate
    1 Publications Verification

    		 Environmental Pollutants Necroptosis Apoptosis Autophagy Neurological Disease
    Glyphosate, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders .
    Glyphosate
  • HY-17001
    Flupirtine Maleate
    1 Publications Verification

    D 9998 Maleate

    		 Potassium Channel iGluR GABA Receptor Neurological Disease Inflammation/Immunology
    Flupirtine (D 9998) Maleate is an orally active, blood-brain barrier-crossing non-opioid analgesic and neuroprotective agent. Flupirtine Maleate is a neuronal potassium channel opener (Kv7 activator), a NMDA receptor antagonist and a GABA receptor activator. Flupirtine Maleate stabilizes blood-brain-barrier integrity, reduces oxidative stress and brain leukocyte infiltration, enhances angioneurogenesis, suppresses calcium influx, stabilizes neuronal resting membrane potential, and counteracts focal cerebral ischemia. Flupirtine Maleate exhibits analgesic, muscle relaxant properties, protects neurons from excitotoxic, ischemic, or cytokine-mediated death. Flupirtine Maleate functions as a non-opioid analgesic without antipyretic or antiphlogistic properties, shows no relevant affinity to opiate receptor. Flupirtine Maleate can be used for the research of focal cerebral ischemia, pain, Alzheimer’s disease, or multiple sclerosis .
    Flupirtine Maleate
  • HY-N7922
    Urolithin M5
    1 Publications Verification

    Decarboxyellagic acid

    		 Influenza Virus p38 MAPK EGFR Akt Reactive Oxygen Species (ROS) Apoptosis Infection Neurological Disease
    Urolithin M5 (Decarboxyellagic acid) is an orally active influenza virus neuraminidase inhibitor and neuroprotective agent, with IC50 values of 174.8 μM (HK68), 191.5 μM (pdm09), 243.2 μM (WSN) and 257.1 μM (PR8) against four influenza virus neuraminidases, respectively. Urolithin M5 inhibits viral neuraminidase activity, thereby blocking influenza virus replication (including oseltamivir (HY-13317)-resistant strains), protecting infected mammals from death and improving pulmonary edema. Urolithin M5 forms a hydrogen-bond stabilized complex with IGF1R, and binds to MAPK14, AKT1, NFKB1 and EGFR. Urolithin M5 reduces reactive oxygen species production, inhibits neuronal apoptosis, restores mitochondrial transmembrane potential, and promotes neurite outgrowth of damaged neuronal cells. Urolithin M5 can be used in research related to influenza virus infection and Alzheimer's disease .
    Urolithin M5
  • HY-16974
    Afoxolaner
    1 Publications Verification

    		 GABA Receptor Chloride Channel Parasite Infection
    Afoxolaner is an orally active isoxazoline insecticide/acaricide against Ixodes scapularis in dogs. Afoxolaner acts on the insect γ-aminobutyric acid receptor (GABA) and glutamate receptors, inhibiting GABA & glutamate-regulated uptake of chloride ions, resulting in excess neuronal stimulation and death of the arthropod .
    Afoxolaner
  • HY-P1333
    Dynorphin A
    1 Publications Verification

    		 Opioid Receptor Apoptosis Caspase Endogenous Metabolite Neurological Disease
    Dynorphin A is an endogenous opioid peptide involved in inhibitory neurotransmission in the central nervous system (CNS). Dynorphin A is a highy potent kappa opioid receptor (KOR) agonist, and is also an agonist for other opioid receptors, such as mu (MOR) and delta (DOR). Dynorphin A can induce neuronal death, and can be used in the research of neurological disease .
    Dynorphin A
  • HY-W010970
    5'-Guanylic acid disodium salt
    2 Publications Verification

    5'-GMP disodium salt; 5'-guanosine monophosphate disodium salt

    		 Endogenous Metabolite iGluR Neurological Disease Metabolic Disease
    5'-Guanylic acid disodium salt is the disodium salt form of 5'-Guanylic acid (HY-N5134). 5'-Guanylic acid disodium salt is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid disodium salt regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid disodium salt is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid disodium salt also causes neuronal cell death at high concentrations .
    5'-Guanylic acid disodium salt
  • HY-114332
    GNE-8505

    		MAP3K JNK Neurological Disease Metabolic Disease
    GNE-8505 is an orally active, blood-brain barrier-permeable selective dual leucine zipper kinase (DLK) inhibitor. GNE-8505 has an IC50 of 0.144 μM for pJNK, and EC50 of 0.457 μM for DRG. GNE-8505 inhibits the DLK/JNK pathway, reduces stress-induced c-Jun phosphorylation levels, decreases neuronal death and suppresses axonal degeneration. GNE-8505 reduces phosphorylated c-Jun levels in the retina, spinal cord and brain tissues of mice. GNE-8505 is applicable to research related to Alzheimer's disease and amyotrophic lateral sclerosis (ALS) .
    GNE-8505
  • HY-15322
    PRT062607
    4 Publications Verification

    P505-15; PRT-2607; BIIB-057

    		 Syk Apoptosis Caspase Inflammation/Immunology Cancer
    PRT062607 (P505-15; PRT-2607) is an orally active ATP-competitive Syk inhibitor with an IC50 value of 1 nM, and exhibits at least 80-fold selectivity over other kinases. PRT062607 blocks B cell antigen receptor-mediated activation, Fcε receptor 1-mediated basophil degranulation and microglial phagocytosis, and induces caspase-dependent apoptosis and microglial death. PRT062607 inhibits tumor growth and peripheral nerve injury-induced mechanical allodynia, and prevents neuronal loss. PRT062607 can be used in research related to rheumatoid arthritis, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, neurodegenerative diseases and neuropathic pain .
    PRT062607
  • HY-101449
    Adaptaquin
    2 Publications Verification

    		 HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Inflammation/Immunology
    Adaptaquin is a BBB-penetrable HIF-PHDs inhibitor. Adaptaquin has anti-inflammatory and neuroprotective effects. Adaptaquin can effectively inhibit lipid peroxidation, maintain mitochondrial function, and reduce neuronal death. Adaptaquin can be used in the research of nervous system diseases such as Parkinson's disease .
    Adaptaquin
  • HY-P10638
    TAT-CN21

    		CaMK Cardiovascular Disease Neurological Disease
    TAT-CN21 is a potent CaMKII inhibitor with an IC50 of 77.2 nM. TAT-CN21 inhibits both calcium/calmodulin-dependent and autonomously activated CaMKII, blocks glutamate-induced translocation of CaMK IIα, and reverses the enhanced phosphorylation of CaMKII at Thr286 following excitotoxic injury. TAT-CN21 shows application potential in studies related to ischemic stroke by reducing neuronal excitotoxicity and exacerbating pre-existing long-term neuronal death prior to injury. TAT-CN21 improves definitive behaviors in rats with residual nerve injury without altering indicators such as mechanical/thermal hyperalgesia or spatial memory. TAT-CN21 can also be used in studies related to neuropathic pain .
    TAT-CN21
  • HY-N1860
    3-O-Methylquercetin

    		Phosphodiesterase (PDE) NO Synthase Infection Neurological Disease Inflammation/Immunology
    3-O-Methylquercetin is an inhibitor of cAMP and CGMP-phosphodiesterase (PDE) with IC50 at 13.8 μM and 14.3 μM, respectively. 3-O-Methylquercetin is an inhibitor of β-secretase with an IC50 of 6.5 μM. 3-O-Methylquercetin has a neuroprotective effect against neuronal death caused by oxidative damage. 3-O-Methylquercetin has strong antiviral activity against poliovirus, coxsackie virus and human rhinovirus. 3-O-Methylquercetin has anti-inflammatory and trachea-relaxing effects and can be used in the study of inflammatory diseases and asthma .
    3-O-Methylquercetin
  • HY-103661
    BI-6C9
    3 Publications Verification

    		 Mitochondrial Metabolism Apoptosis Neurological Disease
    BI-6C9 is a highly specific BH3 interacting domain (Bid) inhibitor, which prevents mitochondrial outer membrane potential (MOMP) and mitochondrial fission, and protects the cells from mitochondrial apoptosis inducing factor (AIF) release and caspase-independent cell death in neurons .
    BI-6C9
  • HY-160229
    ssRNA40 sodium

    R-1075 sodium

    		 Toll-like Receptor (TLR) MyD88 Caspase Reactive Oxygen Species (ROS) Autophagy Pyroptosis HIV Infection Neurological Disease
    ssRNA40 sodium (R-1075 sodium) is a single-stranded RNA40 derived from HIV-1. ssRNA40 sodium activates the TLR7, TLR8, TLR2, RIG-I, MDA5, MyD88, Caspase-3, IRE1α, NLRP3 inflammasome and IRF7 signaling pathways. ssRNA40 sodium alters mRNA expression in neutrophils, induces pro-inflammatory cytokines, ROS, autophagy (autophagy), pyroptosis (pyroptosis), neuronal death, neurodegeneration, aggregate formation and NK cell activation. ssRNA40 sodium activates the expression of CD62L, CD11b, CD69, MX1, OAS1, ATG7, LC3B and XBP1 in immune cell and neuronal populations. ssRNA40 sodium causes cortical neuron loss and axonal damage in mice in a TLR7-dependent manner. ssRNA40 sodium can be used in research on HIV-1 infection, neurodegeneration, COVID-19 and HIV-associated neurological disorders .
    ssRNA40 sodium
  • HY-157959
    Orphenadrine

    (±)-Orphenadrine

    		 iGluR Cytochrome P450 Cholinesterase (ChE) Neurological Disease Cancer
    Orphenadrine ((±)-Orphenadrine) is a skeletal muscle relaxant and NMDA antagonist that also has antiparkinsonian, antihistamine, antitremor, antispasmodic, and analgesic effects. Orphenadrine inhibits the binding of [3H]MK-801 to the phencyclidine (PCP) binding site of the NMDA receptor. Orphenadrine is also an anticholinergic and CYP2B inducer. Orphenadrine may exert pro-tumor effects, causing CAR nuclear translocation, resulting in microsomal reactive oxygen species (ROS) production and oxidative stress. Orphenadrine also exerts neuronal protection, protecting rat cerebellar granule cells (CGC) from 3-NPA-induced death and has inhibitory potential against neurodegenerative diseases mediated by NMDA receptor overactivation .
    Orphenadrine
  • HY-19820A
    NSC45586 sodium
    1 Publications Verification

    		 Akt Ser/Thr Protease Apoptosis MMP Cardiovascular Disease Neurological Disease Inflammation/Immunology
    NSC45586 sodium is an inhibitor of PHLPP. NSC45586 sodium targets the PP2C phosphatase domains of PHLPP1 and PHLPP2, blocks the phosphatase activity of PHLPP, increases the expression level of FOXO1 in the nucleus, and reduces the protein expression of PHLPP1. NSC45586 sodium activates the AKT survival signaling pathway, enhances IGF-1-induced AKT activation, and inhibits the phosphorylation of AKT/ERK under basal conditions. NSC45586 sodium reduces staurosporine-induced neuronal death, preserves notochord cell morphology and KRT19 expression, inhibits cell apoptosis (apoptosis), improves the viability and proliferation of nucleus pulposus cells, upregulates the expression of ACAN/SOX9, and downregulates the expression of MMP13. NSC45586 sodium binds tightly to bovine serum albumin (bovine serum albumin), and exerts a more significant effect on nucleus pulposus in male individuals. NSC45586 sodium can be used in studies related to global cerebral ischemia and intervertebral disc degeneration .
    NSC45586 sodium
  • HY-N1970
    5,7-Dihydroxychromone
    2 Publications Verification

    		 Keap1-Nrf2 Caspase PARP Fungal Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    5,7-Dihydroxychromone is a flavonoid compound with antioxidant properties. 5,7-Dihydroxychromone induces Nrf2 nuclear translocation, increases Nrf2/ARE binding activity, and up-regulates Nrf2-dependent antioxidant genes HO-1, NQO1, GCLc. 5,7-Dihydroxychromone attenuates excessive ROS generation, inhibits activated caspase-3, caspase-9, cleaved PARP expression, and prevents neuronal apoptosis and cell death. 5,7-Dihydroxychromone increases LXRα and PPARγ mRNA expression, induces preadipocyte differentiation, and regulates blood glucose levels. 5,7-Dihydroxychromone inhibits radial growth of soil pathogenic fungi, radicle elongation of select seedlings, and transiently inhibits Bradyrhizobium sp. growth in high mannitol medium. 5,7-Dihydroxychromone can be used for the research of Parkinson’s disease, type 2 diabetes mellitus and pathogenic fungal infection .
    5,7-Dihydroxychromone
  • HY-P2275
    Peptide5

    		Gap Junction Protein Neurological Disease
    Peptide5, a connexin 43 mimetic peptide, reduce animals swelling, astrogliosis, and neuronal cell death after spinal cord injury
    Peptide5
  • HY-118355
    ALLM
    1 Publications Verification

    Calpain inhibitor II

    		 Proteasome Cathepsin Neurological Disease
    ALLM (Calpain inhibitor II) is a potent inhibitor of calpain and cathepsin proteases. ALLM inhibits neuronal cell death and improves chronic neurological function after spinal cord injury (SCI) .
    ALLM
  • HY-N5134R
    5'-Guanylic acid (Standard)

    5'-GMP (Standard); 5'-guanosine monophosphate (Standard)

    		 Reference Standards Endogenous Metabolite
    5'-Guanylic acid is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid also causes neuronal cell death at high concentrations .
    5'-Guanylic acid (Standard)
  • HY-121833
    Gambogic amide

    		Trk Receptor Akt ERK Neurological Disease Cancer
    Gambogic amide is a potent and selective agonist of TrkA and also induces its tyrosine phosphorylation and activation of downstream signaling, including Akt and MAPK. Gambogic amide specifically interacts with the cytoplasmic juxtamembrane domain of the TrkA receptor and triggers its dimerization, leading to activation. Gambogic amide has neuroprotective activity preventing glutamate-induced neuronal cell death. Gambogic amide has improved efficacy in a transient middle cerebral artery occlusion model of stroke and could be used to study neurodegenerative diseases and stroke .
    Gambogic amide
  • HY-153898
    rTRD01

    		Amyloid-β Neurological Disease
    rTRD01 is an orally active, specific TDP-43 binder that targets the RRM1 and RRM2 domains of TDP-43. rTRD01 partially disrupts the interaction between TDP-43 and c9orf72 repeat RNA, but does not affect the binding of TDP-43 to canonical binding sequences. rTRD01 exhibits significant neuroprotective effects in zebrafish models, improves motor function and protects against paraquat (a widely used herbicide)-induced neurodegeneration, with no teratogenicity at high concentrations. rTRD01 is not a general antioxidant and cannot counteract Rotenone (HY-B1756)-induced neuronal death. rTRD01 can be used to study amyotrophic lateral sclerosis and other TDP-43 proteinopathies .
    rTRD01
  • HY-P1247
    Calcineurin autoinhibitory peptide

    		Phosphatase Neurological Disease
    Calcineurin autoinhibitory peptide is a selective inhibitor of Ca 2+/calmodulin-dependent protein phosphatase (calcineurin), with an IC50 of ~10 μM. Calcineurin autoinhibitory peptide could protect neurons from excitatory neuronal death .
    Calcineurin autoinhibitory peptide
  • HY-W747676
    Glyphosate-13C

    		Isotope-Labeled Compounds Apoptosis Autophagy Necroptosis Neurological Disease
    Glyphosate- 13C is the 13C-labeled Glyphosate (HY-B0863). Glyphosate, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders .
    Glyphosate-13C
  • HY-P10019
    Pegsebrenatide

    NLY01

    		 GCGR Neurological Disease Inflammation/Immunology
    Pegsebrenatide (NLY01) is a blood-brain barrier-penetrant GLP-1R agonist. Pegsebrenatide alleviates retinal inflammation and neuronal death secondary to ocular hypertension . Pegsebrenatide significantly delays onset and reduces disease severity in experimental autoimmune encephalomyelitis . Pegsebrenatide inhibits the formation of A1 reactive astrocytes in nerve cells and reduces the loss of retinal ganglion cells and dopaminergic neurons. Pegsebrenatide exerts neuroprotective effects in a mouse model of Parkinson's disease by directly preventing microglia-mediated conversion of astrocytes to the A1 neurotoxic phenotype. Pegsebrenatide can be used for research on glaucoma, Parkinson's disease, and multiple sclerosis .
    Pegsebrenatide
  • HY-P2612
    WP9QY

    		TNF Receptor RANKL/RANK Apoptosis Inflammation/Immunology
    WP9QY is an inhibitor targeting TNFα and RANKL, which blocks the TNFα-TNFR1 interaction and inhibits TNFα-mediated apoptosis, cytotoxicity and bone destruction. WP9QY inhibits osteoclastogenesis and promotes osteoblast differentiation, induces chondrocyte proliferation and glycosaminoglycan production, and synergizes with TGF-β3 to promote chondrogenesis. WP9QY effectively repairs full-thickness articular cartilage defects in rabbits via intra-articular injection, and inhibits methylmercury-induced reduction of NeuN-positive cells in mouse brain slices. WP9QY can be applied to the research of diseases related to methylmercury-induced neuronal death, cartilage injury, osteoarthritis and bone loss .
    WP9QY
  • HY-179055
    PROTAC DAPK1 Degrader-1

    		PROTACs DAPK Neurological Disease
    PROTAC DAPK1 Degrader-1 (Compound CP1) is a DAPK1 PROTAC degrader with a DC50 of 119.6 nM. PROTAC DAPK1 Degrader-1 significantly increased the MDM2 protein level. PROTAC DAPK1 Degrader-1 significantly reduced the levels of cleaved caspase-3 and cleaved PARP in a cell apoptosis model induced by the neurotoxin ceramide, indicating that it effectively inhibits neuronal apoptosis by degrading DAPK1. PROTAC DAPK1 Degrader-1 can be used to study neurological diseases such as cerebral ischemia and traumatic brain injury (pink: DAPK1 ligand (HY-179071); blue: CRBN ligand (HY-10984); black: linker (HY-40171)) .
    PROTAC DAPK1 Degrader-1
  • HY-129101
    (-)-Eseroline fumarate

    Eseroline fumarate

    		 5-HT Receptor Neurological Disease
    (-)-Eseroline fumarate is a metabolic of Physostigmine (HY-N6608), an AChE inhibitor. (-)-Eseroline fumarate elicits a leakage of lactic acid dehydrogenase (LDH) from cancer cells. (-)-Eseroline fumarate also induces the release of adenine nucleotides and 5-hydroxytryptamine (5-HT) from neuronal cells, thus induce cell death. (-)-Eseroline fumarate inhibits the electrically evoked twitches of the mouse vas deferens and of the guinea-pig ileum .
    (-)-Eseroline fumarate
  • HY-W011474R
    Geranylgeraniol (Standard)

    		Reference Standards NF-κB Inflammation/Immunology
    Geranylgeraniol (Standard) is the analytical standard of Geranylgeraniol. This product is intended for research and analytical applications. Geranylgeraniol is an orally acitve vitamin K2 sub-type, an intermediate of the mevalonate pathway. Geranylgeraniol targets NF-kB signaling pathway and could alleviate LPS-induced microglial inflammation in animal model [4].
    Geranylgeraniol (Standard)
  • HY-W392413
    Glutathione monoethyl ester

    		Drug Derivative Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Glutathione monoethyl ester is a glutathione derivative that can be transported into cells and hydrolyzed into glutathione. Glutathione monoethyl ester downregulates the gene expression of TEN1 and CTC1 while upregulating TERT expression. Glutathione monoethyl ester enhances telomerase activity, promotes proliferation and differentiation in aged bone marrow stromal cells, while elevating glutathione levels and reducing oxidative stress, protein aggregation and cell death in motor neuronal cells. Glutathione monoethyl ester confers broad multi-organ protection against cerebral ischemia, renal injury, liver damage, and pancreatitis. Glutathione monoethyl ester can be used for the research of amyotrophic lateral sclerosis, stroke, acute renal failure, liver injury, and acute pancreatitis .
    Glutathione monoethyl ester
  • HY-W009300
    4-Hydroxyestrone
    1 Publications Verification

    4-OHE1

    		 Endogenous Metabolite Estrogen Receptor/ERR Sirtuin MDM-2/p53 PDI Ferroptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Cancer
    4-Hydroxyestrone (4-OHE1) is a brain-penetrant estrogen metabolite. 4-Hydroxyestrone shows neuroprotective effects involving increased cytoplasmic localization of p53 resulting from SIRT1-mediated p53 deacetylation. 4-Hydroxyestrone relies on PDI to mediate its protective effect against chemically induced ferroptosis in estrogen receptor-negative cancer cells. 4-Hydroxyestrone inhibits lipid peroxidation and lipid-ROS accumulation. 4-Hydroxyestrone blocks preovulatory luteinizing hormone surges in Rattus norvegicus. 4-Hydroxyestrone can be used for the researches of neurodegeneration, breast cancer and endocrine disease .
    4-Hydroxyestrone
  • HY-30004R
    1-Aminocyclopropane-1-carboxylic acid (Standard)

    		Reference Standards Endogenous Metabolite Cardiovascular Disease Metabolic Disease
    1-Aminocyclopropane-1-carboxylic acid (Standard) is the analytical standard of 1-Aminocyclopropane-1-carboxylic acid. This product is intended for research and analytical applications. 1-Aminocyclopropane-1-carboxylic acid is an endogenous metabolite. In the presence of low concentrations (1 μM) of glutamate, 1-Aminocyclopropane-1-carboxylic acid acts as a small molecule agonist of NMDA receptors with an EC50 of 0.7-0.9 μM. At high concentrations (10 μM) of glutamate, 1-Aminocyclopropane-1-carboxylic acid acts as a competitive antagonist of NMDA receptors with an EC50 of 81.6 nM. 1-Aminocyclopropane-1-carboxylic acid exerts neuroprotective activity by moderately activating NMDA receptors to prevent neuronal cell death in ischemic animal models. Additionally, 1-Aminocyclopropane-1-carboxylic acid is an antagonist of NMDA receptors, inducing blood pressure reduction and antioxidant effects in stroke-prone hypertensive rats. 1-Aminocyclopropane-1-carboxylic acid enhances object recognition memory and cognitive flexibility dependent on the prefrontal cortex, but does not affect impulsivity nor exhibit an antipsychotic-like profile. 1-Aminocyclopropane-1-carboxylic acid shows promise for research in the field of neurotoxicity. .
    1-Aminocyclopropane-1-carboxylic acid (Standard)
  • HY-P4704A
    α-Synuclein (61-95) (human) TFA

    		α-synuclein Neurological Disease
    α-Synuclein (61-95) (human) TFA is the hydrophobic core region of α-synuclein, and induces neuronal cell death. α-Synuclein (61-95) (human) TFA can be used for research of neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD) .
    α-Synuclein (61-95) (human) TFA
  • HY-W611371
    FP802

    		TRP Channel iGluR Neurological Disease
    FP802 is an orally active potent TwinF interface inhibitor that disrupts and detoxifies the NMDAR/TRPM4 death complex. FP802 exerts powerful neuroprotective effects in the 5xFAD mouse model of Alzheimer’s disease (AD) by preventing cognitive decline, preserving neuronal structural integrity, reducing amyloid-β plaque formation, and mitigating mitochondrial pathology . FP802 stops loss of motor neurons, reduces serum neurofilament light chain (NfL) levels, improves motor performance, and extends life in a mouse model of amyotrophic lateral sclerosis (ALS). FP802 can be used for AD and ALS research .
    FP802
  • HY-108248
    KU-32

    		HSP Cardiovascular Disease Neurological Disease Metabolic Disease
    KU-32 is a novel, novobiocin-based Hsp90 inhibitor that can protect against neuronal cell death.
    KU-32
  • HY-P2275B
    Peptide5 TFA

    		Gap Junction Protein NOD-like Receptor (NLR) Inflammation/Immunology
    Peptide5 TFA, a connexin 43 mimetic peptide, reduces animals swelling, astrogliosis, and neuronal cell death after spinal cord injury. Peptide5 TFA also inhibits NLRP3 inflammasome, and is an anti-inflammatory agent .
    Peptide5 TFA
  • HY-126049
    (S)-Oxiracetam

    (S)-(-)-Oxiracetam; (S)-ISF2522

    		 Apoptosis Neurological Disease
    (S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
    (S)-Oxiracetam
  • HY-16974R
    Afoxolaner (Standard)

    		Reference Standards GABA Receptor Chloride Channel Parasite Infection
    Afoxolaner (Standard) is the analytical standard of Afoxolaner. This product is intended for research and analytical applications. Afoxolaner is an orally active isoxazoline insecticide/acaricide against Ixodes scapularis in dogs. Afoxolaner acts on the insect γ-aminobutyric acid receptor (GABA) and glutamate receptors, inhibiting GABA & glutamate-regulated uptake of chloride ions, resulting in excess neuronal stimulation and death of the arthropod .
    Afoxolaner (Standard)
  • HY-110230
    Flupirtine-d4 hydrochloride

    D 9998-d4 hydrochloride

    		 Isotope-Labeled Compounds Potassium Channel iGluR GABA Receptor Neurological Disease Inflammation/Immunology
    Flupirtine-d4 (D 9998-d4) hydrochloride is the deuterium labeled Flupirtine hydrochloride (HY-W709349). Flupirtine hydrochloride is an orally active, blood-brain barrier-crossing non-opioid analgesic and neuroprotective agent. Flupirtine hydrochloride is a neuronal potassium channel opener (Kv7 activator), a NMDA receptor antagonist and a GABA receptor activator. Flupirtine hydrochloride stabilizes blood-brain-barrier integrity, reduces oxidative stress and brain leukocyte infiltration, enhances angioneurogenesis, suppresses calcium influx, stabilizes neuronal resting membrane potential, and counteracts focal cerebral ischemia. Flupirtine hydrochloride exhibits analgesic, muscle relaxant properties, protects neurons from excitotoxic, ischemic, or cytokine-mediated death. Flupirtine hydrochloride functions as a non-opioid analgesic without antipyretic or antiphlogistic properties, shows no relevant affinity to opiate receptor. Flupirtine hydrochloride can be used for the research of focal cerebral ischemia, pain, Alzheimer’s disease, or multiple sclerosis .
    Flupirtine-d4 hydrochloride

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