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Results for "

neuron death

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adenosine Deaminase (2) Amyloid-β (2) Apoptosis (7) Autophagy (2) Bacterial (3) Calcium Channel (2) Caspase (4) Chloride Channel (1) Endogenous Metabolite (4) ERK (2) Ferroptosis (1) GABA Receptor (7) GCGR (1) Glutathione Peroxidase (2) HIV (1) iGluR (12) Insecticide (3) Isotope-Labeled Compounds (2) JNK (1) MAP3K (1) MDM-2/p53 (1) Mitochondrial Metabolism (2) MyD88 (1) Necroptosis (2) Neprilysin (1) Opioid Receptor (1) Parasite (1) Phosphatase (2) Potassium Channel (8) Pyroptosis (1) Reactive Oxygen Species (ROS) (2) Reference Standards (5) Toll-like Receptor (TLR) (1) Transferrin Receptor (1) TRP Channel (4) TrxR (1)
By Research Areas:	Cancer (5) Cardiovascular Disease (2) Infection (4) Inflammation/Immunology (12) Metabolic Disease (2) Neurological Disease (38)
Oligonucleotides:	CpG ODNs (1)

Inhibitors & Agonists

Screening Libraries

Peptides

Inhibitory Antibodies

Natural
Products

Isotope-Labeled Compounds

Oligonucleotides

Targets Recommended: DAPK Programmed Cell Death 4 (PDCD4) PD-1/PD-L1

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-P990110

Lecanemab (Mouse IGG2a) 1 Publications Verification Mab158	Amyloid-β	Neurological Disease
Lecanemab (Mouse IGG2a) (Mab158) is a monoclonal antibody that targets soluble β-amyloid and has the potential to reduce cognitive decline. The variable region of Lecanemab (Mouse IGG2a) is consistent with that of Lecanemab, while the constant region is of Mouse IGG2a sequence. Lecanemab (Mouse IGG2a) almost abolishes Aβ accumulation in astrocytes and rescues neurons from Aβ-induced cell death. Lecanemab (Mouse IGG2a) holds promise for research in the field of Alzheimer's disease .

HY-W013375

Thiorphan 3 Publications Verification	Neprilysin	Neurological Disease
Thiorphan is a selective neprilysin (NEP) inhibitor with an IC₅₀ of 6.9 nM. Thiorphan competitively binds to NEP and blocks its activity, preventing the degradation of neuropeptides such as substance P (SP) and neurokinin NKA. In the field of neonatal brain injury research, Thiorphan can increase the levels of SP and NKA, activate NK1 and NK2 receptors and downstream transduction pathways, and inhibit excessive activation of NMDA receptors. Thus, Thiorphan can protect neocortical neurons from excitotoxic cell death. Thiorphan may also inhibit NEP from enhancing bronchoconstriction and can be used in the study of respiratory diseases .

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 .

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 .

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 .

HY-N7368

Hibifolin	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) (K_i = 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) .

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) .

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 .

HY-123076

Pifithrin-α, p-Nitro, Cyclic 4 Publications Verification PFN-α	MDM-2/p53	Neurological Disease
Pifithrin-α, p-Nitro, Cyclic (PFN-α) is cell-permeable and active-form p53 inhibitor. Pifithrin-α, p-Nitro, Cyclic is one order magnitude more active than Pifithrin-α in protecting cortical neurons exposed to Etoposide (ED₅₀=30 nM). Pifithrin-α, p-Nitro, Cyclic behaves as a p53 posttranscriptional activity inhibitor. Pifithrin-α, p-Nitro, Cyclic do not prevent p53 phosphorylation on the S15 residue .

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 .

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 .

HY-139192

Brophenexin 3 Publications Verification NMDAR/TRPM4-IN-2	iGluR TRP Channel ERK	Neurological Disease
Brophenexin (compound 8) is a potent NMDAR/TRPM4 interaction interface inhibitor. Brophenexin shows neuroprotective activity. Brophenexin prevents NMDA-induced cell death and mitochondrial dysfunction in hippocampal neurons, with an IC₅₀ of 2.1 μM. Brophenexin protects mice from MCAO-induced brain damage and NMDA-induced retinal ganglion cell loss .

HY-P10409

SHLP2 Small humanin-like peptide 2	Apoptosis Reactive Oxygen Species (ROS)	Neurological Disease Metabolic Disease
SHLP2 (Small humanin-like peptide 2) is a small molecule peptide encoded by mitochondrial DNA, belonging to mitochondria derived peptide. SHLP2 has the activity of regulating apoptosis and inhibits cell death. SHLP2 binds to mitochondrial complex 1. SHLP2 improves mitochondrial metabolism by increasing respiration and biogenesis, reducing ROS, and decreasing mtDNA oxidation. SHLP2 also regulated energy homeostasis through the activation of hypothalamic neurons. SHLP2 can be used in the study of diseases related to mitochondrial dysfunction and anti-aging diseases, such as age-related macular degeneration and Parkinson’s disease .

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 .

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 .

HY-117924

AUTEN-67 Autophagy enhancer-67	Autophagy	Neurological Disease
AUTEN-67 (Autophagy enhancer-67) is an orally active autophagy enhancer and MTMR14 inhibitor. AUTEN-67 has anti-aging and neuroprotective effects. AUTEN-67 protects neurons from stress-induced cell death. AUTEN-67 also restores nesting behavior in a mice model of Alzheimer disease .

HY-139192A

Brophenexin free base 3 Publications Verification NMDAR/TRPM4-IN-2 free base	iGluR TRP Channel ERK	Neurological Disease
Brophenexin free base (compound 8) is a potent NMDAR/TRPM4 interaction interface inhibitor. Brophenexin free base shows neuroprotective activity. Brophenexin free base prevents NMDA-induced cell death and mitochondrial dysfunction in hippocampal neurons, with an IC₅₀ of 2.1 μM. Brophenexin free base protects mice from MCAO-induced brain damage and NMDA-induced retinal ganglion cell loss .

HY-P5142

ω-Hexatoxin-Hv1a ω-ACTX-Hv1; ω-Atracotoxin-HV1	Insecticide Calcium Channel Apoptosis Necroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a blocks L-type voltage-dependent Ca ²⁺ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .

HY-139008

RC363	Glutathione Peroxidase	Others
RC363 is a novel probucol analog with the activity to protect mouse hippocampal cells and primary cortical neurons from glutamate-induced oxidative cell death (ferroptosis) and increase glutathione peroxidase (GPx) 1 levels and activity.

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 .

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 .

HY-114550

LY339434	iGluR	Neurological Disease
LY339434 is a potent and selective agonist for the hydrochloride receptor GluR5. LY339434 affects the rapid death of neurons through n-methyl-D-aspartate (NMDA) receptors .

HY-139012

RC574	Ferroptosis Glutathione Peroxidase	Others
RC574 is a novel probucol analog with the activity to protect mouse hippocampal cells and primary cortical neurons from glutamate-induced oxidative cell death (ferroptosis) and increase glutathione peroxidase (GPx) 1 levels and activity.

HY-P3528

GPR	Caspase Apoptosis	Neurological Disease
GPR is a three amino acid peptide. GPR can rescue cultured rat hippocampal neurons from Aβ-induced neuronal death by inhibiting caspase-3/p53 dependent apoptosis. GPR can be used for the research of Alzheimer's disease (AD).

HY-P991380

TXB4	Transferrin Receptor	Neurological Disease
TXB4 is a brain-permeable human monoclonal antibody (mAb) targeting CD71. TXB4 prevents 6-OHDA-induced death of TH-positive neurons in the SNc in a 6-OHDA mouse model of Parkinson's disease (PD). TXB4 can be used in neurodegenerative diseases, acute brain and spinal cord injury, and depression research .

HY-177854

Aβ aggregation-IN-4	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) .

HY-W611371A

FP802 dihydrochloride	TRP Channel iGluR	Neurological Disease
FP802 dihydrochloride is an orally active potent TwinF interface inhibitor that disrupts and detoxifies the NMDAR/TRPM4 death complex. FP802 dihydrochloride 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 dihydrochloride 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 dihydrochloride can be used for AD and ALS research .

HY-100355R

C18-Ceramide (Standard)	Endogenous Metabolite Reference Standards	Neurological Disease Cancer
C18-Ceramide (Standard) is the analytical standard of C18-Ceramide. This product is intended for research and analytical applications. C18-Ceramide can promote exocytosis of glutamate from damaged neurons. C18-Ceramide promotes cell death in glioma cells. Ceramides is involved in diverse cellular functions, such as differentiation, cell cycle progression, cell-cell adhesion, senescence, and apoptosis .

HY-119513

Nizofenone	Others	Neurological Disease
Nizofenone is a neuroprotective agent which protects neurons from death following cerebral ischemia or anoxia. Nizofenone can be used in the research of acute neurological conditions, such as stroke .

HY-Z8942

Avermectin B2a	Insecticide Parasite Chloride Channel	Infection
Avermectin B2a is an insecticide targeting glutamate-gated chloride channels (GluCls). Avermectin B2a causes hyperpolarization of nematode/insect neurons and subsequent paralysis/death. Avermectin B2a is promising for research of agricultural pests .

HY-P1247A

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

HY-172455

TREK inhibitor-3	Potassium Channel	Neurological Disease
TREK inhibitor-3 (Cpd8l) is a selective and BBB-permeable TREK-1 inhibitor with an IC₅₀ of 0.81 μM. TREK inhibitor-3 has neuroprotective effects, which can significantly reduce the death of cortical neurons induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and improve brain injury in mice models of middle cerebral artery occlusion/reperfusion (MCAO/R). TREK inhibitor-3 can be used in the research of ischemic stroke .

HY-N7368R

Hibifolin (Standard)	Reference Standards Adenosine Deaminase Bacterial Caspase	Neurological Disease Inflammation/Immunology Cancer
Hibifolin (Standard) is the analytical standard of Hibifolin. This product is intended for research and analytical applications. Hibifolin is a flavonol glycoside that can be isolated from Helicteres isora. Hibifolin is an inhibitor of adenosine deaminase (ADA) (K_i = 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) .

HY-W709349

Flupirtine hydrochloride D 9998 hydrochloride	Potassium Channel iGluR GABA Receptor	Neurological Disease Inflammation/Immunology
Flupirtine (D 9998) 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 .

HY-17001R

Flupirtine Maleate (Standard) D 9998 Maleate (Standard)	Reference Standards Potassium Channel iGluR GABA Receptor	Neurological Disease Inflammation/Immunology
Flupirtine Maleate (Standard) is the analytical standard of Flupirtine Maleate (HY-17001). This product is intended for research and analytical applications. Flupirtine 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 .

HY-17001AR

Flupirtine (Standard) D 9998 (Standard)	Reference Standards Potassium Channel iGluR GABA Receptor	Neurological Disease Inflammation/Immunology
Flupirtine (Standard) (D 9998 (Standard)) is the analytical standard of Flupirtine (HY-17001A). This product is intended for research and analytical applications. Flupirtine 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 .

HY-186105A

(-)-P7C3-S243	Opioid Receptor Apoptosis	Neurological Disease
(-)-P7C3-S243 is an orally active, blood-brain barrier permeable neuroprotective agent. (-)-P7C3-S243 binds to μ-opioid Receptor and TSPO. (-)-P7C3-S243 inhibits the premature apoptosis death of newborn hippocampal neurons, protects mature nigral dopaminergic neurons, promotes neuronal survival and prevents cognitive impairment. (-)-P7C3-S243 ameliorates depression-like behaviors in rat models. (-)-P7C3-S243 is applicable to research related to Parkinson's disease and Alzheimer's disease .

HY-103661R

BI-6C9 (Standard)	Reference Standards Mitochondrial Metabolism Apoptosis	Neurological Disease
BI-6C9 (Standard) is the analytical standard of BI-6C9 (HY-103661). This product is intended for research and analytical applications. 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 .

HY-117578

KB 5666	Endogenous Metabolite	Neurological Disease
KB 5666 is a benzoxazine derivative with lipid peroxidation inhibitory activity. KB 5666 showed protective effects against post-ischemic neuronal death. KB 5666 effectively protected CA1 neurons when injected 5 minutes before or immediately after ischemia. KB 5666 also showed a dose-dependent protective effect when injected within 1 hour after ischemia. KB 5666 effectively prevented the significant decrease in microtubule-associated protein 2 immunoreactivity within the dendritic field of CA1 pyramidal cells. KB 5666 prevented the decrease in [3H]PDBu binding activity in different layers of the CA1 region after ischemia. The application of KB 5666 showed the ability to improve the cellular and functional consequences of ischemia .

HY-W709349S

Flupirtine-d6 hydrochloride D 9998-d6 hydrochloride	Isotope-Labeled Compounds Potassium Channel iGluR GABA Receptor	Neurological Disease
Flupirtine-d₆ (D 9998-d₆) 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 .

HY-P5142A

ω-Hexatoxin-Hv1a TFA ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA	Insecticide Apoptosis Calcium Channel Necroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) TFA is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a TFA blocks L-type voltage-dependent Ca ²⁺ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a TFA causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a TFA is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .

Cat. No.	Product Name

HY-L070

Neuroprotective Compound Library	1,748 compounds
Neurodegenerative diseases are characterised by progressive dysfunction and death of neurons, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis (MS). Neuroprotection is an approach to preserve neurons so that neurons cannot be hurt by different pathological factors in neurodegenerative diseases. Neuroprotectors are some agonists and antagonists targeting some key targets in neuroprotactive signal pathways, such as calcium and sodium channel blockers, GABA receptor agonists, NMDA receptor Antagonists, etc. Current neuroprotectors cannot reverse existing damage, but they may protect against further nerve damage and slow down any degeneration of the central nervous system (CNS) and still play important roles in the treatment of neurodegenerative diseases. MCE offers a unique collection of 1,748 compounds with potential neuroprotective activities. These compounds mainly act on some key targets in neuroprotetive signal pathways, such as calcium channel, sodium channel, adenosine A1 receptor, etc. MCE Neuroprotective Compopund Library is a useful tool in neuroprotective drug discovery.

Neuroprotective Compound Library

1,748 compounds

Neurodegenerative diseases are characterised by progressive dysfunction and death of neurons, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis (MS). Neuroprotection is an approach to preserve neurons so that neurons cannot be hurt by different pathological factors in neurodegenerative diseases. Neuroprotectors are some agonists and antagonists targeting some key targets in neuroprotactive signal pathways, such as calcium and sodium channel blockers, GABA receptor agonists, NMDA receptor Antagonists, etc. Current neuroprotectors cannot reverse existing damage, but they may protect against further nerve damage and slow down any degeneration of the central nervous system (CNS) and still play important roles in the treatment of neurodegenerative diseases.

MCE offers a unique collection of 1,748 compounds with potential neuroprotective activities. These compounds mainly act on some key targets in neuroprotetive signal pathways, such as calcium channel, sodium channel, adenosine A1 receptor, etc. MCE Neuroprotective Compopund Library is a useful tool in neuroprotective drug discovery.

HY-L086

Neurodegenerative Disease-related Compound Library	3,545 compounds
Neurodegenerative diseases are incurable and life-threatening conditions that result in progressive degeneration and/or death of nerve cells. Some common neurodegenerative diseases include Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Motor Neuron Disease (MND), Huntington’s Disease (HD), Spino-Cerebellar Ataxia (SCA), Spinal Muscular Atrophy (SMA), and Amyotrophic Lateral Sclerosis (ALS). Because the pathophysiology of neurodegenerative disorders is generally poorly understood, it is difficult to identify promising molecular targets and validate them. At the same time, about 85% of the drugs fail in clinical trials. Therefore, validating new targets and discovering new drugs to mitigate neurodegenerative disorders is need of the hour. MCE offers a unique collection of 3,545 compounds with anti-Neurodegenerative Diseases activities or targeting the unique targets of neurodegenerative diseases. MCE Neurodegenerative Disease-related Compound Library is a useful tool for exploring the mechanism of neurodegenerative diseases and discovering new drugs for neurodegenerative diseases.

Neurodegenerative Disease-related Compound Library

3,545 compounds

Neurodegenerative diseases are incurable and life-threatening conditions that result in progressive degeneration and/or death of nerve cells. Some common neurodegenerative diseases include Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Motor Neuron Disease (MND), Huntington’s Disease (HD), Spino-Cerebellar Ataxia (SCA), Spinal Muscular Atrophy (SMA), and Amyotrophic Lateral Sclerosis (ALS). Because the pathophysiology of neurodegenerative disorders is generally poorly understood, it is difficult to identify promising molecular targets and validate them. At the same time, about 85% of the drugs fail in clinical trials. Therefore, validating new targets and discovering new drugs to mitigate neurodegenerative disorders is need of the hour.

MCE offers a unique collection of 3,545 compounds with anti-Neurodegenerative Diseases activities or targeting the unique targets of neurodegenerative diseases. MCE Neurodegenerative Disease-related Compound Library is a useful tool for exploring the mechanism of neurodegenerative diseases and discovering new drugs for neurodegenerative diseases.

Cat. No.	Product Name	Target	Research Area

HY-P10409

SHLP2 Small humanin-like peptide 2	Apoptosis Reactive Oxygen Species (ROS)	Neurological Disease Metabolic Disease
SHLP2 (Small humanin-like peptide 2) is a small molecule peptide encoded by mitochondrial DNA, belonging to mitochondria derived peptide. SHLP2 has the activity of regulating apoptosis and inhibits cell death. SHLP2 binds to mitochondrial complex 1. SHLP2 improves mitochondrial metabolism by increasing respiration and biogenesis, reducing ROS, and decreasing mtDNA oxidation. SHLP2 also regulated energy homeostasis through the activation of hypothalamic neurons. SHLP2 can be used in the study of diseases related to mitochondrial dysfunction and anti-aging diseases, such as age-related macular degeneration and Parkinson’s disease .

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 .

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 .

HY-P5142

ω-Hexatoxin-Hv1a ω-ACTX-Hv1; ω-Atracotoxin-HV1	Insecticide Calcium Channel Apoptosis Necroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a blocks L-type voltage-dependent Ca ²⁺ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .

HY-P3528

GPR	Caspase Apoptosis	Neurological Disease
GPR is a three amino acid peptide. GPR can rescue cultured rat hippocampal neurons from Aβ-induced neuronal death by inhibiting caspase-3/p53 dependent apoptosis. GPR can be used for the research of Alzheimer's disease (AD).

HY-P1247A

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

HY-P5142A

ω-Hexatoxin-Hv1a TFA ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA	Insecticide Apoptosis Calcium Channel Necroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) TFA is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a TFA blocks L-type voltage-dependent Ca ²⁺ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a TFA causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a TFA is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .

Cat. No.	Product Name	Target	Research Area	Image

HY-P990110

Lecanemab (Mouse IGG2a) 1 Publications Verification Mab158	Amyloid-β	Neurological Disease
Lecanemab (Mouse IGG2a) (Mab158) is a monoclonal antibody that targets soluble β-amyloid and has the potential to reduce cognitive decline. The variable region of Lecanemab (Mouse IGG2a) is consistent with that of Lecanemab, while the constant region is of Mouse IGG2a sequence. Lecanemab (Mouse IGG2a) almost abolishes Aβ accumulation in astrocytes and rescues neurons from Aβ-induced cell death. Lecanemab (Mouse IGG2a) holds promise for research in the field of Alzheimer's disease .

HY-P991380

TXB4	Transferrin Receptor	Neurological Disease
TXB4 is a brain-permeable human monoclonal antibody (mAb) targeting CD71. TXB4 prevents 6-OHDA-induced death of TH-positive neurons in the SNc in a 6-OHDA mouse model of Parkinson's disease (PD). TXB4 can be used in neurodegenerative diseases, acute brain and spinal cord injury, and depression research .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-100355

C18-Ceramide (d18:1/18:0) C18-Ceramide	Structural Classification Alkaloids Neurological Disease Classification of Application Fields Other Alkaloids Endogenous metabolite Disease Research Fields Source Classification Cancer	Endogenous Metabolite
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 .

HY-N7368

Hibifolin	Flavonols Flavonoids other families Neurological Disease Classification of Application Fields Phenols Polyphenols Plants Inflammation/Immunology Disease Research Fields Source Classification	Adenosine Deaminase Bacterial Caspase
Hibifolin is a flavonol glycoside that can be isolated from Helicteres isora. Hibifolin is an inhibitor of adenosine deaminase (ADA) (K_i = 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) .

HY-121362

Evernic Acid	Structural Classification other families Classification of Application Fields Ketones, Aldehydes, Acids Plants Inflammation/Immunology Disease Research Fields Source Classification	Bacterial Endogenous Metabolite TrxR
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 .

HY-100355R

C18-Ceramide (Standard)	Alkaloids Other Alkaloids Endogenous metabolite Source Classification	Endogenous Metabolite Reference Standards
C18-Ceramide (Standard) is the analytical standard of C18-Ceramide. This product is intended for research and analytical applications. C18-Ceramide can promote exocytosis of glutamate from damaged neurons. C18-Ceramide promotes cell death in glioma cells. Ceramides is involved in diverse cellular functions, such as differentiation, cell cycle progression, cell-cell adhesion, senescence, and apoptosis .

HY-Z8942

Avermectin B2a	Structural Classification Microorganisms Antibiotics Source Classification	Insecticide Parasite Chloride Channel
Avermectin B2a is an insecticide targeting glutamate-gated chloride channels (GluCls). Avermectin B2a causes hyperpolarization of nematode/insect neurons and subsequent paralysis/death. Avermectin B2a is promising for research of agricultural pests .

HY-N7368R

Hibifolin (Standard)	Flavonols Structural Classification Flavonoids other families Phenols Polyphenols Plants Source Classification	Reference Standards Adenosine Deaminase Bacterial Caspase
Hibifolin (Standard) is the analytical standard of Hibifolin. This product is intended for research and analytical applications. Hibifolin is a flavonol glycoside that can be isolated from Helicteres isora. Hibifolin is an inhibitor of adenosine deaminase (ADA) (K_i = 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) .

Cat. No.	Product Name	Chemical Structure

HY-W709349S

Flupirtine-d6 hydrochloride

Flupirtine-d₆ (D 9998-d₆) 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 .

Cat. No.	Product Name		Classification

HY-160229

ssRNA40 sodium R-1075 sodium		CpG ODNs
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 .

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