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primary rat cortical neuron

" in MedChemExpress (MCE) Product Catalog:

18

Inhibitors & Agonists

1

Biochemical Assay Reagents

2

Peptides

4

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-100834
    5,7-Dichlorokynurenic acid
    1 Publications Verification

    5,7-DCKA

    		 iGluR Neurological Disease
    5,7-Dichlorokynurenic acid (5,7-DCKA) is a selective and competitive antagonist of the glycine site on NMDA receptor with a KB of 65 nM. 5,7-Dichlorokynurenic acid reduces NMDA-induced neuron injury. 5,7-Dichlorokynurenic acid increases social interaction time, increases open arm exploration time, disinhibits suppressed conflict responding in rodent models. 5,7-Dichlorokynurenic acid exhibits anxiolytic-like activity in rodent models and supports exploration of glycine’s role in NMDA receptor-mediated synaptic transmission .
    5,7-Dichlorokynurenic acid
  • 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-121362
    Evernic Acid

    		Bacterial Endogenous Metabolite TrxR Infection Neurological Disease Inflammation/Immunology Cancer
    Evernic Acid is an orally active thioredoxin reductase 1 (TrxR1) inhibitor and antiproliferative agent. Evernic Acid inhibits the proliferation and migration of human breast cancer cells. Evernic Acid blocks the NF-κB pathway by inhibiting p65 nuclear translocation and IκBα phosphorylation, thereby suppressing downstream inflammatory mediators. Evernic Acid acts as an antioxidant, anti-inflammatory agent and neuroprotective agent, protects neurons from cell death, mitochondrial dysfunction and oxidative stress damage, reduces astrocyte activation, and ameliorates dopaminergic neuron loss and neuroinflammation. Evernic Acid inhibits enoyl reductases FabI and FabZ of Plasmodium falciparum. Evernic Acid downregulates the expression of lasB and rhlA genes in Pseudomonas aeruginosa, inhibits quorum sensing and biofilm formation, and exerts antibacterial activity against Gram-positive bacteria, Gram-negative bacteria and fungi. Evernic Acid is applicable to research related to breast cancer, Parkinson's disease, bacterial infections and fungal infections .
    Evernic Acid
  • 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-N0392
    Polygalasaponin F

    		Toll-like Receptor (TLR) PI3K Akt NF-κB MDM-2/p53 Caspase MEK Bcl-2 Family p38 MAPK Mitophagy Reactive Oxygen Species (ROS) Apoptosis Calcium Channel Cardiovascular Disease Infection Neurological Disease
    Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease .
    Polygalasaponin F
  • 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-Y1269D
    Ammonium chloride, for molecular biology

    Salmiac, for molecular biology

    		 TGF-beta/Smad Apoptosis Chloride Channel Neurological Disease Cancer
    Ammonium chloride (Salmiac), for molecular biology is an inhibitor of Slc26a4 and SMAD2. Ammonium chloride, for molecular biology reduces the protein expression level of Slc26a4 in lung tissue, and attenuates ozone-induced increases in proinflammatory cytokines, inflammatory cells, pulmonary resistance, goblet cell hyperplasia, peribronchial inflammation and thiocyanate levels in mouse tissues and bronchoalveolar lavage fluid. Ammonium chloride, for molecular biology decreases the level of phosphorylated SMAD2, inhibits autophagy by reducing autophagy-related proteins, and enhances Cisplatin (HY-17394)-induced cancer cell apoptosis and DNA double-strand breaks. Ammonium chloride, for molecular biology also inhibits the TCA cycle, reduces ATP production, increases glucose utilization, regulates the levels of lactic acid, glutamic acid and ATP, and induces morphological degeneration of neuroblastoma cells. Ammonium chloride, for molecular biology can be used in studies related to ozone-induced airway injury, hepatocellular carcinoma, human cervical cancer, hepatic encephalopathy, Reye syndrome, epilepsy and neurodegenerative diseases .
    Ammonium chloride, for molecular biology
  • HY-P10360
    Tat-βsyn-degron

    		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-151962
    JNK3 inhibitor-5

    		JNK Apoptosis GSK-3 p38 MAPK Neurological Disease
    JNK3 inhibitor-5 (Compound 22b) is a potent and selective JNK3 inhibitor with an IC50 of 0.379 nM. JNK3 inhibitor-5 effectively protects the neuronal cells against amyloid beta-induced apoptosis. JNK3 inhibitor-5 has a high cell permeability and is predicted as BBB permeable .
    JNK3 inhibitor-5
  • HY-N8693
    Withanoside IV

    		COX Amyloid-β Sirtuin Reactive Oxygen Species (ROS) Apoptosis SARS-CoV Infection Neurological Disease
    Withanoside IV is an orally active, blood-brain barrier-permeable withanolide derivative. Withanoside IV specifically binds to the Sudlow I site of HSA, induces secondary structural changes in HSA, and forms stable HSA complexes. Withanoside IV inhibits the enzymatic activity of COX-2. Withanoside IV induces axonal regeneration, peripheral nervous system myelination and increased axonal density in spinal cord tissue, reduces reactive gliosis-related changes, and improves hindlimb motor function. Withanoside IV binds to amyloid-β 1-42 to inhibit its aggregation, induces neurite outgrowth and synapse reconstruction, repairs damaged axons and dendrites, enhances mitochondrial biogenesis, exerts neuroprotective effects via the BDNF and SIRT1 signaling pathways, reduces ROS production and neuronal apoptosis, and ameliorates memory deficits. Withanoside IV inhibits the activity of the SARS-CoV-2 main protease. Withanoside IV can be used in research related to spinal cord injury, Alzheimer's disease, and coronavirus disease 2019 (COVID-19) .
    Withanoside IV
  • HY-178153
    BPAM363

    		iGluR Neurological Disease
    BPAM363 is an orally active, selective positive allosteric modulator (PAM) of AMPARs with blood-brain barrier penetration. BPAM363 selectively potentiates AMPAR activity in human and rat models, with an EC2x value of 0.96 μM in rat embryonic cortex primary neurons. BPAM363 upregulates BDNF protein expression in rat primary cortical neuronal cultures. BPAM363 enhances AMPA-mediated excitatory postsynaptic responses in rat and mice. BPAM363 can be used for the study of cognitive disorders .
    BPAM363
  • HY-100458
    SCR-4026

    		NO Synthase Neurological Disease
    SCR-4026 is a neuroprotective agent with blood-brain barrier penetration ability. SCR-4026 exerts neuroprotective effects by disrupting the interaction between neuronal nNOS and PSD9, with an IC50 of 6.3 μM. SCR-4026 alleviates N-methyl-D-aspartate (NMDA)-induced excitotoxic damage in primary cortical neurons, and also protects neurons in the oxygen-glucose deprivation (OGD) model. SCR-4026 can reduce the cerebral infarct volume in the rat middle cerebral artery occlusion (MCAO) reperfusion model. SCR-4026 can be used for the study of stroke .
    SCR-4026
  • HY-100834A
    5,7-Dichlorokynurenic acid sodium

    5,7-DCKA sodium

    		 iGluR Neurological Disease
    5,7-Dichlorokynurenic acid (5,7-DCKA) sodium is a selective and competitive antagonist of the glycine site on NMDA receptor with a KB of 65 nM. 5,7-Dichlorokynurenic acid sodium reduces NMDA-induced neuron injury. 5,7-Dichlorokynurenic acid sodium increases social interaction time, increases open arm exploration time, disinhibits suppressed conflict responding in rodent models. 5,7-Dichlorokynurenic acid sodium exhibits anxiolytic-like activity in rodent models and supports exploration of glycine’s role in NMDA receptor-mediated synaptic transmission .
    5,7-Dichlorokynurenic acid sodium
  • HY-180345
    ND-7001

    		Prostaglandin Receptor Neurological Disease
    ND-7001 is an inhibitor of PDE2 with an IC50 of 0.05 μM. ND-7001 exhibits good selectivity agianst PDE3 and PDE4. ND-7001 increases cGMP levels in primary neuronal cultures of rat cerebral cortical neurons. ND-7001 displays anxiolytic effects .
    ND-7001
  • HY-126939
    MN-05

    		Reactive Oxygen Species (ROS) Calcium Channel iGluR Neurological Disease
    MN-05 is a dual neuroprotective and vasodilatory NMDA receptor inhibitor.MN-05 blocks calcium influx, reduces free radical production, and maintains mitochondrial membrane potential in cortical neurons exposed to glutamate.MN-05 dilates aortic rings against phenylephrine-induced contraction.MN-05 protects neurons against glutamate-induced injury in vitro.MN-05 can be used for the research of neurodegenerative diseases .
    MN-05
  • HY-182600
    KLK6-IN-1

    		Kallikrein Plasminogen/Plasmin Neurological Disease Inflammation/Immunology
    KLK6-IN-1 is a reversible small‑molecule inhibitor of KLK6, KLK1, and plasmin. KLK6-IN-1 shows IC50 values of 1.57 μM (KLK6), 5.1 μM (KLK1), 7.4 μM (plasmin), and Ki values of 0.8 μM (KLK6), 2.4 μM (KLK1), 1.3 μM (plasmin). KLK6-IN-1 is highly selective for KLK6 and its proteolytic network. KLK6-IN-1 induces oligodendrocyte differentiation by promoting oligodendrocyte precursor cell maturation. KLK6-IN-1 can be used for the research of multiple sclerosis .
    KLK6-IN-1
  • HY-121675A
    2-Bromo-LSD D-Tartrate

    BOL-148 D-Tartrate; Bromolysergide D-Tartrate

    		 5-HT Receptor G protein-coupled Bile Acid Receptor 1 Neurological Disease
    2-Bromo-LSD D-Tartrate (BOL-148 D-Tartrate) is a blood-brain barrier-permeable 5-HT2A partial agonist and competitive partial antagonist. 2-Bromo-LSD D-Tartrate acts as both a potent partial agonist (with an EC50 of 0.81 nM for Gq dissociation) and a potent partial antagonist (with a KB of 0.18 nM for Gq dissociation) at the 5-HT2A receptor. 2-Bromo-LSD D-Tartrate exhibits partial agonist activity at multiple aminergic GPCRs, including 5-HT2A. 2-Bromo-LSD D-Tartrate lacks 5-HT2B agonist activity. 2-Bromo-LSD D-Tartrate induces dendritogenesis and spinogenesis. 2-Bromo-LSD D-Tartrate reverses the behavioral effects of chronic stress and increases active coping behaviors in mice .
    2-Bromo-LSD D-Tartrate
  • HY-186073
    HDAC1 activator-1

    		HDAC Neurological Disease
    HDAC1 activator-1 is a specific HDAC1 activator with orally activity, exerting no significant effects on other HDAC family members. HDAC1 activator-1 exhibits neuroprotective activity, ameliorates cognitive and motor function deficits by reducing neuronal loss and gliosis. HDAC1 activator-1 specifically activates HDAC1 in SH-SY5Y cells and exerts regulatory effects on aberrant cell cycle and DNA damage. HDAC1 activator-1 can be used for the research of TDP-43 proteinopat1-related neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS) and cerebral ischemia-related neurological injury .
    HDAC1 activator-1

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