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Results for "

brain infarct

" in MedChemExpress (MCE) Product Catalog:

29

Inhibitors & Agonists

2

Peptides

1

Inhibitory Antibodies

8

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-108841
    Raleukin
    50+ Cited Publications

    Kineret; Anakinra

    		 Interleukin Related Inflammation/Immunology Cancer
    Raleukin (AMG-719) is a recombinant, nonglycosylated human interleukin-1 receptor (IL-1R) antagonist. Raleukin significantly reduces neutrophil accumulation in blood vessels and brain infarct volume as well as improves motor coordination performance in ischemic stroke mice model. Anakinra can be used to study chronic inflammatory disorders like rheumatoid arthritis and cardiovascular recurrence post-myocardial infarction .
    Raleukin
  • HY-50722
    NNC 55-0396
    5 Publications Verification

    NNC 55-0396 dihydrochloride

    		 Calcium Channel Cytochrome P450 Cardiovascular Disease Neurological Disease Cancer
    NNC 55-0396 (NNC 55-0396 dihydrochloride) is a blood-brain-barrier-permeable T-type Ca 2+ channel inhibitor and pan-P450 inhibitor. NNC 55-0396 selectively inhibits T-type Ca 2+ channels, suppresses HIF-1α expression and stability and inhibits Kv currents. NNC 55-0396 reduces brain infarct and attenuates neurological dysfunction. NNC 55-0396 inhibits the activity of multiple P450 enzymes. NNC 55-0396 (free base) can be used for the research of brain injury, hypertension, and glioblastoma .
    NNC 55-0396
  • HY-17355A
    Dexpramipexole dihydrochloride
    2 Publications Verification

    (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride

    		 ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole dihydrochloride
  • HY-B1065
    Aceglutamide

    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-N0745
    Senkyunolide I

    		Caspase ERK Keap1-Nrf2 Heme Oxygenase (HO) Apoptosis Neurological Disease Inflammation/Immunology
    Senkyunolide I is an orally active, blood-brain barrier-permeable metabolite of Z-ligustilide (HY-N0401A) . Senkyunolide I is isolated from Ligusticum chuanxiong. Senkyunolide I upregulates p-Erk1/2 and Nrf2/HO-1, and inhibits Caspase 3. Senkyunolide I alleviates Apoptosis. Senkyunolide I increases the pain threshold in mice and reduces acetic acid-induced writhing responses in mice. Senkyunolide I improves neurological deficits, reduces infarct volume and alleviates cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Senkyunolide I protects renal function and structural integrity in a mouse model of renal ischemia-reperfusion injury. Senkyunolide I is applicable to research related to focal cerebral ischemia-reperfusion injury, migraine, and renal ischemia-reperfusion injury .
    Senkyunolide I
  • HY-N12060
    Ginkgo biloba extract

    		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-P5883
    TAT-M2NX

    tatM2NX

    		 TRP Channel Cardiovascular Disease Neurological Disease
    TAT-M2NX (tatM2NX) is a selective inhibitor targeting human TRPM2 channels and exerts inhibitory effects on ischemic stroke. TAT-M2NX reduces H2O2-induced calcium influx via TRPM2 channels. After traumatic brain injury in mice, TAT-M2NX preserves hippocampal long-term potentiation, improves memory function, and reduces infarct volume after middle cerebral artery occlusion, but it shows no effect on female mice. TAT-M2NX can be used in studies related to traumatic brain injury and ischemic stroke .
    TAT-M2NX
  • HY-13769A
    TPT-260 Dihydrochloride
    2 Publications Verification

    NSC55712; TPU-260 Dihydrochloride

    		 Drug Derivative Amyloid-β Beta-secretase Cardiovascular Disease Neurological Disease Inflammation/Immunology
    TPT-260 Dihydrochloride (NSC55712), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (Kd = ~5 µM). TPT-260 Dihydrochloride increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 Dihydrochloride inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 Dihydrochloride improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 Dihydrochloride exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 Dihydrochloride can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease .
    TPT-260 Dihydrochloride
  • HY-N0430
    Coptisine

    Coptisin

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine
  • HY-N0430A
    Coptisine Sulfate
    5 Publications Verification

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine Sulfate
  • HY-N2125
    Parishin C

    		5-HT Receptor iGluR Caspase Interleukin Related TNF Receptor SOD NF-κB Neurological Disease Inflammation/Immunology
    Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
    Parishin C
  • HY-17355B
    Dexpramipexole
    2 Publications Verification

    (R)-Pramipexole; R-(+)-Pramipexole; KNS-760704

    		 PINK1/Parkin Glutathione Peroxidase Sodium Channel ATP Synthase NOD-like Receptor (NLR) Mitophagy Ferroptosis Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole
  • HY-66010
    Cinepazide Maleate

    MD-67350

    		 Calcium Channel Cardiovascular Disease
    Cinepazide Maleate (MD-67350) is a piperazine derivative and acts as a weak calcium channel blocker. Cinepazide Maleate is a potent vasodilator and can be used for the research of cerebrovascular diseases, including ischemic stroke, brain?infarct et. al .
    Cinepazide Maleate
  • HY-126049
    (S)-Oxiracetam

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

    		 Apoptosis Neurological Disease
    (S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
    (S)-Oxiracetam
  • HY-17355BS
    Dexpramipexole-d3 dihydrochloride

    (R)-Pramipexole-d3 dihydrochloride; R-(+)-Pramipexole-d3 dihydrochloride; KNS-760704-d3 dihydrochloride

    		 Isotope-Labeled Compounds ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole-d3 dihydrochloride
  • HY-151547
    MRS4719

    		P2X Receptor Neurological Disease
    MRS4719 is a potent P2X4 receptor antagonist with an IC50 value of 0.503 μM for human P2X4 receptor. MRS4719 can reduce infarct volume and reduce brain atrophy, showing neuroprotective and neuro-rehabilitative activities in ischemic stroke model. MRS4719 also reduces ATP-induced [Ca 2+]i influx in primary human monocyte-derived macrophages. MRS4719 can be used to research ischemic stroke .
    MRS4719
  • HY-13769
    TPT-260

    TPU260

    		 Drug Derivative Beta-secretase Amyloid-β Cardiovascular Disease Neurological Disease Inflammation/Immunology
    TPT-260 (TPU260), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (Kd = ~5 µM). TPT-260 increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease .
    TPT-260
  • HY-175675
    P2Y1 antagonist 4

    		P2Y Receptor Keap1-Nrf2 Cardiovascular Disease Neurological Disease
    P2Y1 antagonist 4 is a selective P2Y1 receptor antagonist with excellent blood-brain barrier (BBB) penetration. P2Y1 antagonist 4 inhibits P2Y1 receptor-mediated cytosolic Ca 2+ increase (IC50 = 1.95 μM) and platelet aggregation (IC50 = 3.24 μM) induced by ADP in rabbit washed platelets. P2Y1 antagonist 4 significantly upregulates the level of nuclear Nrf2 protein in H2O2-treated HT22 cells. P2Y1 antagonist 4 reduces myocardial infarct size in a mouse acute myocardial infarction (MI) model. P2Y1 antagonist 4 can be used for the study of ischemic stroke and myocardial infarction .
    P2Y1 antagonist 4
  • HY-66010A
    Cinepazide

    		Calcium Channel Cardiovascular Disease
    Cinepazide is a piperazine derivative and acts as a weak calcium channel blocker. Cinepazide is a potent vasodilator and can be used for the research of cerebrovascular diseases, including ischemic stroke, brain infarct et. al .
    Cinepazide
  • HY-151546
    MRS4596

    		P2X Receptor Neurological Disease
    MRS4596 is a potent and selective P2X4 receptor antagonist with an IC50 value of 1.38 μM for human P2X4 receptor. MRS4596 has neuroprotective and neuro-rehabilitative activities in ischemic stroke model. MRS4596 can be used in research of ischemic stroke .
    MRS4596
  • HY-N2125R
    Parishin C (Standard)

    		Reference Standards 5-HT Receptor iGluR Caspase Interleukin Related TNF Receptor SOD NF-κB Neurological Disease Inflammation/Immunology
    Parishin C (Standard) is the analytical standard of Parishin C (HY-N2125). This product is intended for research and analytical applications. Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
    Parishin C (Standard)
  • HY-151547S
    MRS4719-d3

    		Isotope-Labeled Compounds P2X Receptor Neurological Disease
    MRS4719-d3 is the deuterium labeled MRS4719 (HY-151547). MRS4719 is a potent P2X4 receptor antagonist with an IC50 value of 0.503 μM for human P2X4 receptor. MRS4719 can reduce infarct volume and reduce brain atrophy, showing neuroprotective and neuro-rehabilitative activities in ischemic stroke model. MRS4719 also reduces ATP-induced [Ca 2+]i influx in primary human monocyte-derived macrophages. MRS4719 can be used to research ischemic stroke .
    MRS4719-d3
  • 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-17355AR
    Dexpramipexole dihydrochloride (Standard)

    (R)-Pramipexole dihydrochloride (Standard); R-(+)-Pramipexole dihydrochloride (Standard); KNS-760704 dihydrochloride (Standard)

    		 Reference Standards ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole dihydrochloride (Standard)
  • HY-B1065R
    Aceglutamide (Standard)

    α-N-Acetyl-L-glutamine (Standard); N2-Acetylglutamine (Standard)

    		 Reference Standards Keap1-Nrf2 Akt ASK1 Apoptosis Neurological Disease
    Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) (Standard) is the analytical standard of Aceglutamide (HY-B1065). This product is intended for research and analytical applications. 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 (Standard)
  • HY-50722B
    NNC 55-0396 free base

    		Calcium Channel Cytochrome P450 Cardiovascular Disease Neurological Disease Cancer
    NNC 55-0396 free base is a blood-brain-barrier-permeable T-type Ca 2+ channel inhibitor and pan-P450 inhibitor. NNC 55-0396 free base selectively inhibits T-type Ca2+ channels, suppresses HIF-1α expression and stability and inhibits Kv currents. NNC 55-0396 free base reduces brain infarct and attenuates neurological dysfunction. NNC 55-0396 free base inhibits the activity of multiple P450 enzymes. NNC 55-0396 (free base) can be used for the research of brain injury, hypertension, and glioblastoma .
    NNC 55-0396 free base
  • HY-180267
    (R)-Chloro-butylphthalide-O-NBP

    		Drug Derivative Cardiovascular Disease Neurological Disease
    (R)-Chloro-butylphthalide-O-NBP, a chiral 3-n-butylphthalide derivative, is a neuroprotective agent. (R)-Chloro-butylphthalide-O-NBP shows potent blood-brain barrier (BBB) protective function. In vivo, (R)-Chloro-butylphthalide-O-NBP significantly reduces infarct volume and markedly preserves BBB integrity. (R)-Chloro-butylphthalide-O-NBP can be used for the research of ischemic stroke .
    (R)-Chloro-butylphthalide-O-NBP
  • HY-183654
    Vadadustat prodrug-1

    		HIF/HIF Prolyl-Hydroxylase Cardiovascular Disease Neurological Disease
    Vadadustat prodrug-1 is a near-infrared activated photocaged, blood-brain barrier-permeable neuroprotective prodrug of Vadadustat. Vadadustat prodrug-1 masks the acidic pharmacophore of Vadadustat, and releases active Vadadustat upon irradiation at 650 nm to inhibit PHD2. Vadadustat prodrug-1 reduces cell damage, infarct volume and cerebral edema, and promotes neurological function recovery. Vadadustat prodrug-1 can be used for the research of ischemic stroke .
    Vadadustat prodrug-1
  • HY-175824
    PSD-95/nNOS PPI-IN-1

    		iGluR NO Synthase Apoptosis Reactive Oxygen Species (ROS) Neurological Disease
    PSD-95/nNOS PPI-IN-1 is a inhibitor targeting the PSD-95/nNOS interaction with potential blood-brain barrier penetration. PSD-95/nNOS PPI-IN-1 binds to the PSD-95 PDZ2 domain with high affinity (Ki = 19.45 μM). PSD-95/nNOS PPI-IN-1 inhibits glutamate-induced excitotoxicity by reducing intracellular ROS levels and inhibiting apoptosis. PSD-95/nNOS PPI-IN-1 significantly reduces cerebral infarct volume in rat tMCAO models. PSD-95/nNOS PPI-IN-1 can be used for the study of acute ischemic stroke .
    PSD-95/nNOS PPI-IN-1

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