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nervous system injury

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18

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N10546

    iGluR Trk Receptor ERK Apoptosis Autophagy Neurological Disease
    Ganglioside GM1 is a type of glycosphingolipid, mainly found on the cell membranes of the central nervous system of vertebrates. Ganglioside GM1 exerts neuroprotective effects by reducing excessive activation of NMDAR, activating TrkA and ERK1/2, and inhibiting oxidative stress and cell apoptosis and autophagy. Ganglioside GM1 can be used in the research of diseases such as traumatic brain injury, Parkinson's disease, Alzheimer's disease, and Huntington's disease .
    Ganglioside GM1
  • HY-D0186
    2'-Deoxyuridine
    3 Publications Verification

    Endogenous Metabolite Thymidylate Synthase Infection
    2’-deoxyuridine is a brain-penetrant pyrimidines nucleotide that is associated with nervous system diseases. 2'-Deoxyuridine could increase chromosome breakage and results in a decreased thymidylate synthetase activity. 2'-Deoxyuridine is a precursor in the synthesis of Edoxudine (HY-B1011) and also an analogue of 5-ethynyl-2'-deoxyuridine, EdU (HY-118411). 2’-deoxyuridine reduces microglial activation and improve oxidative stress damage by modulating glycolytic metabolism on the Aβ25-35-induced brain injury, which is promising for research of Alzheimer’s disease (AD) .
    2'-Deoxyuridine
  • HY-34431

    7H-Imidazo(4,5-d)pyrimidine

    Endogenous Metabolite PARP Neurological Disease Metabolic Disease Cancer
    Purine is an endogenous metabolite. Purine bases are the building blocks of the nucleic acids. Purine inhibits the activation of PARP. Purine protects against oxidant-induced cell injury. Purine can be used in the research of cancer and nervous system diseases .
    Purine
  • HY-19667A
    BMS-561392 formate
    2 Publications Verification

    DPC 333 formate

    TNF Receptor NF-κB Apoptosis p38 MAPK Neurological Disease Inflammation/Immunology
    BMS-561392 formate (DPC 333 formate) is a selective ADAM17(TACE) inhibitor. BMS-561392 formate inhibits TNF-α secretion by regulating signaling pathways such as p44 MAPK and NF-κB. BMS-561392 formate also affects the survival of central nervous system-related cells including oligodendrocytes and microglia. BMS-561392 formate promotes microglial apoptosis, enlarges the injury area and exacerbates astrogliosis in a mouse spinal cord injury model. BMS-561392 formate can be used in research related to spinal cord injury and inflammatory diseases .
    BMS-561392 formate
  • HY-N10424
    Brazilein
    2 Publications Verification

    Na+/K+ ATPase Apoptosis Interleukin Related NO Synthase Bacterial Parasite Cardiovascular Disease Infection Neurological Disease Inflammation/Immunology
    Brazilein is a compound with anti-inflammatory and neuroprotective activities, with an IC50 of 500 μM against guinea pig Na +,K +-ATPase. Brazilein reduces iNOS mRNA expression, thereby inhibiting nitric oxide production in immune cells. Brazilein suppresses inflammatory responses by reducing the mRNA expression of TNF-α and IL-6, but has no effect on IL-1β expression. Brazilein reduces the cerebral infarction volume and improves the neurological function scores of rats with cerebral ischemia-reperfusion injury. Brazilein induces apoptosis of splenic lymphocytes in mice. Brazilein inhibits humoral immune responses in mice, and causes thymus and spleen atrophy as well as body weight loss in mice. Brazilein also possesses antimalarial and antibacterial activities. Brazilein is also a red dye. Brazilein can be used in studies related to the infection, nervous system, cardiovascular system and inflammatory diseases .
    Brazilein
  • HY-N2000
    Bellidifolin
    1 Publications Verification

    STAT PI3K mTOR Akt Neurological Disease Inflammation/Immunology Cancer
    Bellidifolin is an orally active compound with antiproliferative, anti-inflammatory and antioxidant properties. Bellidifolin modulates key signaling pathways including STAT3, PI3K-Akt, mTOR and BRD4, and inhibits the viral protein R (Vpr). Bellidifolin induces cell cycle arrest and apoptosis, exerts significant antifibrotic effects, and protects the heart, liver and nervous system. Bellidifolin is applicable to the research of various diseases such as lung cancer, non-alcoholic fatty liver disease, myocardial hypertrophy and ischemic cranial nerve injury .
    Bellidifolin
  • HY-19667

    DPC 333

    TNF Receptor NF-κB Apoptosis p38 MAPK Neurological Disease Inflammation/Immunology
    BMS-561392 (BMS-561392) is a selective ADAM17(TACE) inhibitor. BMS-561392 inhibits TNF-α secretion by regulating signaling pathways such as p44 MAPK and NF-κB. BMS-561392 also affects the survival of central nervous system-related cells including oligodendrocytes and microglia. BMS-561392 promotes microglial apoptosis, enlarges the injury area and exacerbates astrogliosis in a mouse spinal cord injury model. BMS-561392 can be used in research related to spinal cord injury and inflammatory diseases .
    BMS-561392
  • HY-P5142

    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 .
    ω-Hexatoxin-Hv1a
  • HY-N10546A

    iGluR Trk Receptor ERK Apoptosis Autophagy Neurological Disease
    Ganglioside GM1 (bovine) ammonium is a type of glycosphingolipid, mainly found on the cell membranes of the central nervous system of vertebrates. Ganglioside GM1 (bovine) ammonium exerts neuroprotective effects by reducing excessive activation of NMDAR, activating TrkA and ERK1/2, and inhibiting oxidative stress and cell apoptosis and autophagy. Ganglioside GM1 (bovine) ammonium can be used in the research of diseases such as traumatic brain injury, Parkinson's disease, Alzheimer's disease, and Huntington's disease .
    Ganglioside GM1 (bovine) ammonium
  • HY-N4267

    Calcium Channel Platelet-activating Factor Receptor (PAFR) UGT Leukotriene Receptor TNF Receptor PGE synthase Interleukin Related Cardiovascular Disease Infection Inflammation/Immunology
    Yangambin is a PAF receptor antagonist and UGT1A1/UGT1A3 inhibitor, with an IC50 of 29.7 μM and a Ki of 17.1 μM against human UGT1A1, and an IC50 of 56.5 μM and a Ki of 66.8 μM against human UGT1A3. Yangambin blocks PAF-mediated responses, inhibits LTB4-mediated neutrophil infiltration, and suppresses inflammatory events and anaphylactic contraction. Yangambin acts as a central nervous system inhibitor to reduce spontaneous activity, and also exhibits analgesic, anticonvulsant, antileishmanial, vasodilatory and hypotensive effects. Yangambin blocks voltage-gated Ca 2+ channels, reduces the production of NO, TNF-α, IL-6 and PGE2 in cells, increases the production of IL-10, and exerts a protective effect against cardiovascular injury. Yangambin can be used in research related to allergies, cutaneous leishmaniasis, central nervous system diseases and cardiovascular diseases .
    Yangambin
  • HY-136903

    Calcium Channel Proteasome Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    SNJ-1945 is an orally active Calpain inhibitor that can cross the blood-brain barrier. SNJ-1945 protects rat hearts against cardiac arrest-reperfusion injury by inhibiting the hydrolysis of α-fodrin. SNJ-1945 inhibits VEGF-induced angiogenesis in retinal endothelial cells. SNJ-1945 also protects SH-SY5Y cells from damage induced by MPP+ (HY-W008719) and Rotenone (HY-B1756). SNJ-1945 exhibits anti-inflammatory and neuroprotective activities in a mouse model of multiple sclerosis. SNJ-1945 can be used for the research of cardiovascular, nervous system and inflammatory diseases .
    SNJ-1945
  • HY-169575

    PARP Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    PARP1-IN-36 (compound 11) is a 4-carboxamido-isoindolinone derivative and a selective PARP-1 inhibitor with a Kd < 0.01 μM. PARP1-IN-36 can be utilized in cancer, cardiovascular diseases, nervous system injury and inflammation research .
    PARP1-IN-36
  • HY-D0186R

    Reference Standards Endogenous Metabolite Thymidylate Synthase Infection
    2'-Deoxyuridine (Standard) is the analytical standard of 2'-Deoxyuridine. This product is intended for research and analytical applications. 2’-deoxyuridine is a brain-penetrant pyrimidines nucleotide that is associated with nervous system diseases. 2'-Deoxyuridine could increase chromosome breakage and results in a decreased thymidylate synthetase activity. 2'-Deoxyuridine is a precursor in the synthesis of Edoxudine (HY-B1011) and also an analogue of 5-ethynyl-2'-deoxyuridine, EdU (HY-118411). 2’-deoxyuridine reduces microglial activation and improve oxidative stress damage by modulating glycolytic metabolism on the Aβ25-35-induced brain injury, which is promising for research of Alzheimer’s disease (AD) . In Vitro:The interaction between the 2-deoxyuridine and the column increases the duration of retention of 2-deoxyuridine .
    Gradient elution with sodium acetate buffer-ACN eluent on two ZIC-HILIC homemade columns separates 2-deoxyuridine in under 9 min .
    In Vivo:2'-Deoxyuridine (34.42 ng/mL, gavage, 15 min) passes the blood-brain barrier (BBB) to enter the hippocampus of mice brain .
    2'-Deoxyuridine (20 mg/kg, gavage, daily for 4 weeks) improves cognition and memory loss and attenuates the damage to the hippocampus in Aβ25-35-induced mice model .
    2'-Deoxyuridine (Standard)
  • HY-174339

    Phosphodiesterase (PDE) Heme Oxygenase (HO) NF-κB Neurological Disease Inflammation/Immunology
    Neuroprotective agent 12 is an orally active and BBB-penetrable neuroprotective agent. Neuroprotective agent 12 has potent neuroprotective effects with robust anti-oxidation and anti-inflammation. Neuroprotective agent 12 significantly inhibits glutamate- and acrolein-induced cell death, reduces PDE4B expression but increases the HO-1, p-CREB and BDNF levels. Neuroprotective agent 12 exhibits potent neuroprotection in traumatic brain injury (TBI) mice model, promising for TBI and other central nervous system diseases .
    Neuroprotective agent 12
  • HY-W778990

    Isotope-Labeled Compounds Thymidylate Synthase Endogenous Metabolite Infection
    2-Deoxyuridine-1,2,3,4,5- 13C5 is the 13C-labeled 2'-Deoxyuridine (HY-D0186). 2’-deoxyuridine is a brain-penetrant pyrimidines nucleotide that is associated with nervous system diseases. 2'-Deoxyuridine could increase chromosome breakage and results in a decreased thymidylate synthetase activity. 2'-Deoxyuridine is a precursor in the synthesis of Edoxudine (HY-B1011) and also an analogue of 5-ethynyl-2'-deoxyuridine, EdU (HY-118411). 2’-deoxyuridine reduces microglial activation and improve oxidative stress damage by modulating glycolytic metabolism on the Aβ25-35-induced brain injury, which is promising for research of Alzheimer’s disease (AD) .
    2-Deoxyuridine-1,2,3,4,5-13C5
  • HY-N8693

    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-P992060

    CD20 NF-κB Inflammation/Immunology Cancer
    Anti-Mouse CD20 Antibody (18B12) is a B cell depleting agent that targets mouse CD20. Anti-Mouse CD20 Antibody (18B12) not only inhibits the growth of mesothelioma, lung cancer and thymoma, but also significantly enhances the efficacy of adenoviral tumor antigen vaccines and induces tumor regression by increasing the number of tumor-specific CD8 + T cells. Anti-Mouse CD20 Antibody (18B12) reduces B cell infiltration into the central nervous system of mice with experimental autoimmune encephalomyelitis, and delays motor dysfunction and neuronal death after spinal cord injury by alleviating inflammatory responses and tissue damage. Anti-Mouse CD20 Antibody (18B12) is widely applicable to research in fields related to mesothelioma, lung cancer, thymoma, experimental autoimmune encephalomyelitis and spinal cord injury .
    Anti-Mouse CD20 Antibody (18B12)
  • HY-P5142A

    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 .
    ω-Hexatoxin-Hv1a TFA

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