1. Search Result
Search Result
Results for "

neuronal damage

" in MedChemExpress (MCE) Product Catalog:

96

Inhibitors & Agonists

7

Peptides

2

Inhibitory Antibodies

38

Natural
Products

6

Isotope-Labeled Compounds

1

Oligonucleotides

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

    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
    Maximum Cited Publications
    24 Publications Verification

    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
    Maximum Cited Publications
    24 Publications Verification

    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-110281

    Endogenous Metabolite Cardiovascular Disease Neurological Disease
    Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke .
    Dehydroascorbic acid
  • HY-14541
    Olanzapine
    10+ Cited Publications

    LY170053

    5-HT Receptor Dopamine Receptor mAChR Adrenergic Receptor Autophagy Mitophagy Apoptosis Neurological Disease Cancer
    Olanzapine (LY170053) is a selective, orally active monoaminergic antagonist with high affinity binding to serotonin H1, 5HT2A/2C, 5HT3, 5HT6 (Ki=7, 4, 11, 57, and 5 nM, respectively), dopamine D1-4 (Ki=11 to 31 nM), muscarinic M1-5 (Ki=1.9-25 nM), and adrenergic α1 receptor (Ki=19 nM). Olanzapine is an atypical antipsychotic .
    Olanzapine
  • HY-153169
    6PPD-Q
    5+ Cited Publications

    6PPD-Quinone

    α-synuclein Environmental Pollutants Others
    6PPD-Q (6PPD-Quinone) is an environmental pollutant that can be detected in human urine and is widely present in the environment. 6PPD-Q targets and binds to CNR2, CNR1, AA2AR, LCAT, and TRPA1, with CNR2 exhibiting the highest binding affinity, potentially acting as a CNR2 receptor agonist to activate cannabinoid receptors. 6PPD-Q induces intestinal inflammation and barrier damage by disrupting mitochondrial function, reducing neuronal glycolysis metabolites and TCA cycle intermediates, and exacerbating α-synuclein (α-syn) aggregation. 6PPD-Q is applicable in research on environmental toxicology, neurodegenerative diseases, and inflammation-related disorders .
    6PPD-Q
  • HY-B1142
    Lipoamide
    5+ Cited Publications

    (±)-α-Lipoamide; DL-Lipoamide; DL-6,8-Thioctamide

    NO Synthase Others
    Lipoamide ((±)-α-Lipoamide) is a monocarboxylic acid derivative of a neutral amide, formed by the condensation of the carboxyl group of lipoic acid and ammonia. Lipoamide protects against oxidative stress-mediated neuronal cell damage and also acts as a coenzyme to transfer acetyl groups and hydrogen during pyruvate deacylation. Lipoamide also stimulates mitochondrial biogenesis in adipocytes through the endothelial NO synthase-cGMP-protein kinase G signaling pathway .
    Lipoamide
  • HY-124293
    AA147
    4 Publications Verification

    ATF6 Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    AA147 is a endoplasmic reticulum (ER) proteostasis regulator. AA147 promotes protection against oxidative damage in neuronal cells and prevents endothelial barrier dysfunction by activating ATF6 arm (selectively) of the unfolded protein response (UPR) and the NRF2 oxidative stress response. AA147 can rebalances XBP1s expression in vivo, and also induces survival motor neuron (SMN) expression and spinal motorneuron (MN) protection .
    AA147
  • HY-12688A
    Succinyl phosphonate trisodium salt
    Maximum Cited Publications
    13 Publications Verification

    Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β Neurological Disease Inflammation/Immunology
    Succinyl phosphonate trisodium salt is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate trisodium salt protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate trisodium salt corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate trisodium salt reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate trisodium salt improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate trisodium salt can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
    Succinyl phosphonate trisodium salt
  • 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-B1065

    α-N-Acetyl-L-glutamine; N2-Acetylglutamine

    Keap1-Nrf2 Akt ASK1 Apoptosis Neurological Disease
    Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research .
    Aceglutamide
  • HY-N6967

    (-)-α-Bisabolol

    Environmental Pollutants Apoptosis Neurological Disease Inflammation/Immunology
    Levomenol ((-)-α-Bisabolol), a monocyclic sesquiterpene alcohol, exerts antioxidant, anti-inflammatory, and anti-apoptotic activities. Levomenol also has neuroprotective effects and prevents neuronal damage and memory deficits through reduction of proinflammatory markers induced by permanent focal cerebral ischemia in mice. Levomenol attenuates nociceptive behaviour and central sensitisation in a rodent model of trigeminal neuropathic pain. Orally active .
    Levomenol
  • HY-P99797

    JR-141

    Transferrin Receptor Neurological Disease
    Pabinafusp alfa (JR-141) is a transferrin receptor-targeting antibody consisting of Iduronate 2-sulfatase (HY-P76399) and an anti-human transferrin receptor antibody. Pabinafusp alfa is blood-brain permeable and prevents heparan sulfate (HS) deposition in the central nervous system of mucopolysaccharidosis II (MPS II) mice. Pabinafusp alfa improves learning and prevents central nervous system neuronal damage in mice .
    Pabinafusp alfa
  • 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-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-113410

    Na+/K+ ATPase Mitochondrial Metabolism Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    3-Methylglutaric acid is a non-selective inhibitor of mitochondrial function and Na +, K +-ATPase, with an inhibition rate of 30% on rat cortical synaptosomal Na +, K +-ATPase. 3-Methylglutaric acid can induce reactive oxygen species (ROS) generation, thereby causing oxidative damage and inhibiting mitochondrial redox potential and ion pump function of cell membranes. 3-Methylglutaric acid can be used to study the neuropathological mechanisms of metabolic diseases and the role of oxidative stress-mediated neuronal damage in neurodegeneration .
    3-Methylglutaric acid
  • HY-107343

    Ethyl docosahexaenoate

    COX Neurological Disease Metabolic Disease
    Docosahexaenoic acid ethyl ester (Ethyl docosahexaenoate) is a 90% concentrated ethyl ester of docosahexaenoic acid manufactured from the microalgal oil. Docosahexaenoic acid ethyl ester enhances 6-hydroxydopamine-induced neuronal damage by induction of lipid peroxidation in mouse striatum. Docosahexaenoic acid (DHA) is a key component of the cell membrane, and its peroxidation is inducible due to the double-bond chemical structure. Docosahexaenoic acid has neuroprotective effects .
    Docosahexaenoic acid ethyl ester
  • HY-N1860

    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-W040045
    Callistephin chloride
    1 Publications Verification

    Pelargonidin-3-O-glucoside chloride

    Reactive Oxygen Species (ROS) COX NO Synthase p38 MAPK TNF Receptor Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Callistephin (Pelargonidin 3-O-glucoside) chloride is an anthocyanin. Callistephin chloride regulates the expression of inflammatory (reducing iNOS/TNF-α/COX-2) and apoptosis-related proteins by inhibiting p38 phosphorylation, and enhances the protective effect of Isoflurane (HY-A0134) on microglial cell damage. Callistephin chloride significantly reduces ROS levels, eliminates DPPH free radicals, protects retinal pigment epithelial cells, and inhibits lipid peroxidation. Callistephin chloride can alleviate glutamate excitotoxicity, reduce neuronal apoptosis, and protect cerebellar granule neurons. Callistephin chloride can inhibit the proliferation and metastasis of breast cancer cells by inducing apoptosis .
    Callistephin chloride
  • 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-N0762
    Isobavachin
    5 Publications Verification

    Cytochrome P450 UGT p38 MAPK NF-κB NO Synthase COX Fc Receptor (FcR) RANKL/RANK Keap1-Nrf2 Reactive Oxygen Species (ROS) Apoptosis Autophagy Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Isobavachin is an orally active, blood-brain barrier-penetrating prenylated flavonoid present in Psoralea corylifolia. Isobavachin inhibits human CYP2B6, CYP2C9, CYP2C19, UGT1A1, UGT1A9, and UGT2B7. Isobavachin suppresses MAPK activation, NF-κB nuclear translocation, overexpression of iNOS/COX-2, FcεRI-mediated signaling pathways, and RANKL-induced osteoclastogenesis. Isobavachin induces autophagy, cytotoxicity, neuronal differentiation, and NRF2 activation; it alleviates oxidative damage, inflammatory responses, apoptosis, iron accumulation, mitochondrial biogenesis, and mast cell degranulation. Isobavachin is applicable to research related to liver injury, inflammatory diseases, osteoporosis, liver cancer, prostate cancer, glioma, periodontitis-induced bone loss, and Alzheimer's disease .
    Isobavachin
  • HY-B0927

    (-)-β-Hydrastine; (1R,9S)-β-Hydrastine

    Tyrosine Hydroxylase Dopamine Receptor OAT Neurological Disease
    Hydrastine ((-)-β-Hydrastine; (1R,9S)-β-Hydrastine) is a selective competitive inhibitor of tyrosine hydroxylase (TH), inhibiting dopamine biosynthesis (IC50=20.7 μM, PC12 cells). Hydrastine also inhibits the organic cation transporter OCT1 (IC50=6.6 μM). Hydrastine may cause neuronal toxicity through mitochondrial dysfunction rather than oxidative stress damage, and can aggravate cell apoptosis when combined with L-DOPA. Hydrastine can be used to study Parkinson's disease-related dopaminergic neuronal damage .
    Hydrastine
  • HY-118700

    Guanidinobiotin

    NO Synthase Neurological Disease
    2-Iminobiotin (Guanidinobiotin) is a biotin (vitamin H or B7) analog. 2-Iminobiotin is a reversible nitric oxide synthases inhibitor with Kis of 21.8 and 37.5μM for murine iNOS and rat n-cNOS, respectively . 2-Iminobiotin superimposes on hypothermia protects human neuronal cells from hypoxia-induced cell damage .
    2-Iminobiotin
  • HY-W040128

    Antibiotic Autophagy JNK Bcl-2 Family Infection
    Kanamycins sulfate is a blood-brain barrier-permeable JNK1 and Bcl-2 modulator as well as an antibiotic, with broad-spectrum antibacterial, and biofilm-inhibiting activities, and it induces autophagy. Kanamycins sulfate promotes Bcl-2 phosphorylation to upregulate autophagy levels, triggering changes such as mitochondrial swelling and endoplasmic reticulum expansion. Consequently, it causes reversible neuronal damage in the dorsal cochlear nucleus without inducing significant neuronal apoptosis. In the presence of exogenous alanine or glucose, Kanamycins sulfate effectively kills drug-resistant bacteria, restores drug sensitivity of multidrug-resistant bacteria, and alleviates urinary tract and kidney infections in mice. Kanamycins sulfate can be applied to scientific research related to Mycobacterium tuberculosis, salmonellosis, brucellosis, shigellosis, urinary tract infections, and reversible neurotoxicity .
    Kanamycins sulfate
  • HY-160229

    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-113772

    NF-κB ERK JNK p38 MAPK Neurological Disease Inflammation/Immunology
    Inflachromene, a microglial inhibitor, binds to HMGB1 and HMGB2 and exerts anti-inflammatory effects. Inflachromene effectively downregulates proinflammatory functions of HMGB and reduces neuronal damage. Inflachromene can be used for the research of neuroinflammatory disorders .
    Inflachromene
  • HY-138668

    TRP Channel Neurological Disease
    JW-65 is a selective TRPC3 channel inhibitor with favorable blood-brain barrier penetration. JW-65 directly binds to human TRPC3 protein and modulates calcium signaling to reduce seizure susceptibility. JW-65 reduces seizure incidence, severity, and duration while prolonging seizure latency in multiple seizure models. JW-65 alleviates Aβ‑induced neuronal damage. JW-65 serves as a valuable tool for research on epilepsy, seizure disorders, and Alzheimer’s disease .
    JW-65
  • HY-N1414

    Trk Receptor NF-κB Amyloid-β Neurological Disease
    (E)-3',6-Disinapoylsucrose is an orally active, blood-brain barrier permeable neuroprotective agent that inhibits protein aggregation. (E)-3',6-Disinapoylsucrose exerts anxiolytic, anti-inflammatory and cognitive-enhancing effects. (E)-3',6-Disinapoylsucrose regulates the TrkB/BDNF signaling pathway, inhibits the expression of NF-κB p65, reduces pro-inflammatory cytokine levels, and alleviates neuronal damage. (E)-3',6-Disinapoylsucrose also enhances the functions of central 5-HT and noradrenergic systems, thereby improving spatial learning and memory abilities and reducing anxiety-like behaviors. (E)-3',6-Disinapoylsucrose can be used for the research of related diseases such as Alzheimer's disease, depression, memory impairment and anxiety disorder .
    (E)-3',6-Disinapoylsucrose
  • HY-N0909
    Notoginsenoside R2
    1 Publications Verification

    20(S)-Notoginsenoside R2; Ginsenoside Ng-R2

    Apoptosis MEK ERK Reactive Oxygen Species (ROS) Caspase COX β-catenin Src MDM-2/p53 JAK STAT Neurological Disease Metabolic Disease Inflammation/Immunology
    Notoginsenoside R2 (20(S)-Notoginsenoside R2; Ginsenoside Ng-R2) is an orally active notoginsenoside . Notoginsenoside R2 activates P90RSK and Nrf2 via the MEK1/2-ERK1/2 pathway to inhibit 6-OHDA-induced apoptotic damage in nerve cells. Notoginsenoside R2 upregulates SOX8/β-catenin by reducing miR-27a, thereby suppressing Aβ25-35-induced neuronal apoptosis and inflammatory responses . Notoginsenoside R2 alleviates lipid accumulation and mitochondrial dysfunction in diabetic nephropathy by inhibiting c-Src. Notoginsenoside R2 alleviates hepatic fibrosis by inducing hepatic stellate cell senescence and inhibiting the inflammatory microenvironment via JAK/STAT3 suppression . Notoginsenoside R2 can be used in research related to Parkinson's disease, Alzheimer's disease, diabetic nephropathy and hepatic fibrosis .
    Notoginsenoside R2
  • HY-N4098

    Apoptosis Neurological Disease
    Incensole acetate is a main constituent of Boswellia carterii resin, has neuroprotective effects against neuronal damage in traumatic and ischemic head injury. Incensole acetate reduces Aβ25–35-triggered apoptosis in hOBNSCs .
    Incensole Acetate
  • HY-133712

    Tunodafil

    Phosphodiesterase (PDE) Neurological Disease
    Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer's disease .
    Yonkenafil
  • HY-120553
    B-355252
    1 Publications Verification

    Apoptosis Neurological Disease
    B355252, a phenoxy thiophene sulfonamide small molecule, is a potent NGF receptor agonist. B355252 potentiates NGF-induced neurite outgrowth. B355252 protects ischemic neurons from neuronal loss by attenuating DNA damage, reducing ROS production and the LDH level, and preventing neuronal apoptosis. B355252 has anti-apoptotic effects in glutamate-induced excitotoxicity, as well as in a murine hippocampal cell line (HT22) model of Parkinson disease (PD) .
    B-355252
  • HY-125039
    N-Acetyl lysyltyrosylcysteine amide
    2 Publications Verification

    Glutathione Peroxidase Cardiovascular Disease Neurological Disease
    N-Acetyl lysyltyrosylcysteine amide is a potent, reversible, specific, and non-toxic tripeptide inhibitor of myeloperoxidase (MPO). N-Acetyl lysyltyrosylcysteine amide effectively inhibits MPO generation of toxic oxidants in vivo. N-Acetyl lysyltyrosylcysteine amide reduces neuronal damage and preserves brain tissue and neurological function in the stroked brain. N-Acetyl lysyltyrosylcysteine amide inhibits MPO-dependent hypochlorous acid (HOCl) generation, protein nitration, and LDL oxidation .
    N-Acetyl lysyltyrosylcysteine amide
  • HY-W012352

    Glutathione Peroxidase Ferroptosis Wnt β-catenin Apoptosis Cardiovascular Disease Neurological Disease
    2-Hydroxyanthraquinone is a product generated by the photochemical oxidation of Anthracene (ANT) (HY-Y0299). 2-Hydroxyanthraquinone induces ferroptosis in cardiomyocytes by depleting GSH and inhibiting GPX4, leading to cardiac developmental malformations. 2-Hydroxyanthraquinone causes damage to the cerebrovascular system and blood-brain barrier in zebrafish by downregulating the Wnt/β-catenin signaling pathway, as well as inducing inflammation and neuronal apoptosis. 2-Hydroxyanthraquinone can be used in studies related to cerebrovascular diseases and cardiotoxicity .
    2-Hydroxyanthraquinone
  • HY-136182A

    Na+/Ca2+ Exchanger Cardiovascular Disease Neurological Disease
    YM-244769 is a potent, selective and orally active Na +/Ca 2+ exchanger (NCX) inhibitor. YM-244769 preferentially inhibits NCX3 and suppresses the unidirectional outward NCX current (Ca 2+ entry mode), with IC50s of 18 nM and 50 nM, respectively. YM-244769 efficiently protects against hypoxia/reoxygenation-induced SH-SY5Y neuronal cell damage. YM-244769 can also increase urine volume and urinary excretion of electrolytes in mice .
    YM-244769
  • HY-N6669
    Methyl 3-O-methylgallate
    2 Publications Verification

    M3OMG

    Others Neurological Disease
    Methyl 3-O-methylgallate (M3OMG) possesses antioxidant effect and can protect neuronal cells from oxidative damage .
    Methyl 3-O-methylgallate
  • HY-120875

    RAR/RXR Neurological Disease
    HX600 is a synthetic agonist for RXR (Retinoid X Receptor) heterodimer complex. HX600 prevents ischemia-induced neuronal damage. HX600 has orally bioactivity .
    HX600
  • HY-108038

    nAChR Neurological Disease
    ABT-107 is a selective α7 neuronal nicotinic receptor agonist. ABT-107 protects against nigrostriatal damage in rats with unilateral 6-hydroxydopamine lesions .
    ABT-107
  • HY-118700A

    Guanidinobiotin hydrobromide

    NO Synthase Neurological Disease
    2-Iminobiotin hydrobromide (Guanidinobiotin hydrobromide) is a biotin (vitamin H or B7) analog. 2-Iminobiotin hydrobromide is a reversible nitric oxide synthases inhibitor with Kis of 21.8 and 37.5 μM for murine iNOS and rat n-cNOS, respectively . 2-Iminobiotin hydrobromide superimposes on hypothermia protects human neuronal cells from hypoxia-induced cell damage .
    2-Iminobiotin hydrobromide
  • HY-W654331

    2,3-Pyridinedicarboxylic Acid-13C3,15N

    Isotope-Labeled Compounds iGluR Endogenous Metabolite Inflammation/Immunology
    Quinolinic acid- 13C3, 15N (2,3-Pyridinedicarboxylic Acid- 13C3, 15N) is the 13C- and 15N-labeled Quinolinic acid (HY-100807). Quinolinic acid is an endogenous N-methyl-D-aspartate (NMDA) receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction .
    Quinolinic acid-13C3, 15N
  • HY-W392413

    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-12688

    Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β Neurological Disease Inflammation/Immunology
    Succinyl phosphonate is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .
    Succinyl phosphonate
  • 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-170790

    TRP Channel Neurological Disease
    HZS60 is a NMDAR/TRPM4 inhibitor with brain permeability that can improve cerebral ischemia. HZS60 has significant neuroprotective effects on primary neuronal ischemic damage caused by NMDA and oxygen-glucose deprivation/reoxygenation. HZS60 exhibits good pharmacokinetic characteristics and can inhibit cerebral ischemia-reperfusion injury. HZS60 can be used as a potential inhibitor of ischemic stroke .
    HZS60
  • HY-136182

    Na+/Ca2+ Exchanger Cardiovascular Disease Neurological Disease
    YM-244769 dihydrochloride is a potent, selective and orally active Na +/Ca 2+ exchanger (NCX) inhibitor. YM-244769 dihydrochloride preferentially inhibits NCX3 and suppresses the unidirectional outward NCX current (Ca 2+ entry mode), with IC50s of 18 nM and 50 nM, respectively. YM-244769 dihydrochloride efficiently protects against hypoxia/reoxygenation-induced SH-SY5Y neuronal cell damage. YM-244769 dihydrochloride can also increase urine volume and urinary excretion of electrolytes in mice .
    YM-244769 dihydrochloride
  • HY-155126

    Reactive Oxygen Species (ROS) Neurological Disease
    LZWL02003 is an anti-neuroinflammatory agent. LZWL02003 has protective effect on MPP +-induced neuronal damage, and reduces the expression of ROS. LZWL02003 improves cognition, memory, learning, and athletic ability in a Rotenone (HY-B1756)-induced PD rat model. LZWL02003 can be used for research of neurodegenerative disease .
    LZWL02003
  • HY-P3780

    Amyloid-β Neurological Disease
    Cys-Gly-Lys-Lys-Gly-Amyloid β-Protein (36-42) is the 36-42 fragment of Amyloid β-Protein. β-amyloid, a polypeptide made up of 36-43 amino acids, is the main component of amyloid plaques found in the brains of people with Alzheimer's disease. β-amyloid oligomers (Aβos) plays A key role in the progression of Alzheimer's disease (AD) by inducing neuronal damage and cognitive impairment .
    Cys-Gly-Lys-Lys-Gly-Amyloid β-Protein (36-42)
  • HY-P10360

    α-synuclein Neurological Disease
    Tat-βsyn-degron is an α-synuclein knockdown peptide that effectively degrades α-synuclein protein via the proteasome pathway. Tat-βsyn-degron effectively reduces α-synuclein protein levels in primary rat cortical neuron cultures. In a Parkinson's mouse toxicity model, Tat-βsyn-degron can alleviate parkinsonian toxin-induced neuronal damage and movement disorders .
    Tat-βsyn-degron
  • HY-107343R

    Ethyl docosahexaenoate (Standard)

    Endogenous Metabolite Reference Standards Neurological Disease Metabolic Disease
    Docosahexaenoic acid ethyl ester (Standard) is the analytical standard of Docosahexaenoic acid ethyl ester. This product is intended for research and analytical applications. Docosahexaenoic acid ethyl ester (Ethyl docosahexaenoate) is a 90% concentrated ethyl ester of docosahexaenoic acid manufactured from the microalgal oil. Docosahexaenoic acid ethyl ester enhances 6-hydroxydopamine-induced neuronal damage by induction of lipid peroxidation in mouse striatum. Docosahexaenoic acid (DHA) is a key component of the cell membrane, and its peroxidation is inducible due to the double-bond chemical structure. Docosahexaenoic acid has neuroprotective effects .
    Docosahexaenoic acid ethyl ester (Standard)
  • HY-146619

    Amyloid-β Serotonin Transporter Neurological Disease
    RAGE/SERT-IN-1 is a potent and orally active advanced glycation end products (RAGE) and serotonin transporter (SERT) inhibitor with IC50s of 8.26 μM and 31.09 nM, respectively. RAGE/SERT-IN-1 exhibits significant neuroprotective effect against Aβ25-35-induced neuronal damage and alleviates depressive behavior of mice. RAGE/SERT-IN-1 can be used for researching the comorbidity of Alzheimer's disease and depression .
    RAGE/SERT-IN-1

Inquiry Online

Your information is safe with us. * Required Fields.

Salutation

 

Country or Region *

Applicant Name *

 

Organization Name *

Department *

     

Email Address *

 

Product Name *

Cat. No.

 

Requested quantity *

Phone Number *

     

Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent: