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Results for "

cerebral level

" in MedChemExpress (MCE) Product Catalog:

49

Inhibitors & Agonists

1

Peptides

17

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0045
    Ginsenoside Rg1
    Maximum Cited Publications
    15 Publications Verification

    Panaxoside A; Panaxoside Rg1

    		 Amyloid-β NF-κB Apoptosis Neurological Disease Inflammation/Immunology Cancer
    Ginsenoside Rg1 is one of the major active components of Panax ginseng. Ginsenoside Rg1 ameliorates the impaired cognitive function, displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.
    Ginsenoside Rg1
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    		 Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-122218
    JHU-083
    5+ Cited Publications

    		 Glutaminase Neurological Disease
    JHU-083, a proagent of 6-diazo-5-oxo-L-norleucine (DON; HY-108357), is an orally active and selective glutaminase antagonist. JHU-083 blocks glutaminase activity in brain CD11b + cells and experimental cerebral malaria (ECM) resulting in a net decrease of glutamate levels in the animals .
    JHU-083
  • HY-113126
    3-Hydroxyisobutyric acid

    		Endogenous Metabolite ATP Synthase Neurological Disease Metabolic Disease
    3-Hydroxyisobutyric acid is an intermediate in the metabolic pathways of L-valine and thymine, and can be found in urine. 3-Hydroxyisobutyric acid is a secreted mediator of endothelial cell fatty acid transport and insulin resistance. 3-Hydroxyisobutyric acid can also inhibit key enzymes of energy metabolism in the cerebral cortex of young rats. The levels of 3-Hydroxyisobutyric acid are closely related to various diseases such as 3-hydroxyisobutyric aciduria, diabetes, and ketoacidosis .
    3-Hydroxyisobutyric acid
  • HY-14668
    Lomitapide mesylate
    5+ Cited Publications

    AEGR-733 mesylate; BMS-201038 mesylate

    		 Microsomal Triglyceride Transfer Protein (MTP) mTOR LDLR Autophagy Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    Lomitapide (AEGR-733; BMS-201038) mesylate is an orally active microsomal triglyceride transfer protein (MTP) inhibitor and a selective mTORC1 inhibitor with lipid-lowering activity and BBB permeability. Lomitapide mesylate significantly reduces plasma LDL levels by blocking the assembly and secretion of very-low-density lipoprotein (VLDL). Lomitapide mesylate inhibits mTORC1 in an ATP-dependent manner, thereby inducing AMPK-independent autophagic cell death and suppressing cancer cell growth and apoptosis. Lomitapide mesylate also enhances tumor infiltration of CD8 + T cells. In addition, Lomitapide mesylate inhibits HDAC, improves endothelial function, effectively alleviates vascular inflammation and oxidative stress, and exerts neuroprotective effects in a cerebral ischemia/reperfusion injury model. Lomitapide mesylate can be used in research on related diseases such as colorectal cancer, breast cancer, melanoma, ischemic stroke, and familial hypercholesterolemia .
    Lomitapide mesylate
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-B2167R
    Docosahexaenoic acid (Standard)

    DHA (Standard); Cervonic acid (Standard)

    		 Reference Standards Endogenous Metabolite Neurological Disease Cancer
    Docosahexaenoic acid (Standard) is the analytical standard of Docosahexaenoic acid. This product is intended for research and analytical applications. Docosahexaenoic Acid (DHA) is an omega-3 fatty acid abundantly present brain and retina. It can be obtained directly from fish oil and maternal milk. In Vitro: Docosahexaenoic acid (DHA) is essential for the growth and functional development of the brain in infants. DHA is also required for maintenance of normal brain function in adults. The inclusion of plentiful DHA in the diet improves learning ability and memory . DHA is an essential requirement in every step of brain development like neural cell proliferation, migration, differentiation, synaptogenesis. The multiple double bonds and unique structure allow DHA to impart special membrane characteristics for effective cell signaling. Many development disorders like dyslexia, autism spectrum disorder, attention deficit hyperactivity disorder, schizophrenia etc. are causally related to decreased level of DHA . DHA is a potent RXR ligand inducing robust RXR activation already at low micro molar concentrations. The EC50 for RXRα activation by DHA is about 5-10 μM fatty acid . In Vivo: Docosahexaenoic acid administration over 10 weeks significantly reduces the number of reference memory errors, without affecting the number of working memory errors, and significantly increases the docosahexaenoic acid content and the docosahexaenoic acid/arachidonic acid ratio in both the hippocampus and the cerebral cortex . DHA treatment exerts neuroprotective actions on an experimental mouse model of PD. There is a decrease tendency in brain lipid oxidation of MPTP mice but it does not significantly .
    Docosahexaenoic acid (Standard)
  • HY-120380
    FeTMPyP

    		MOFs PARP Neurological Disease
    FeTMPyP is an orally active poly (ADP-ribose) polymerase (PARP) inhibitor. FeTMPyP inhibits cell death, nitrotyrosine formation, and depolarization of mitochondrial transmembrane potential. FeTMPyP reduces homocysteine-induced nitrosative stress and partially restores TFEB protein and mRNA levels. FeTMPyP improves functional and behavioral deficits caused by chronic constriction injury in rats. FeTMPyP alleviates acute cerebral infarction in a rat model of middle cerebral artery occlusion with mild hyperglycemia. FeTMPyP can be used in studies related to neuropathic pain, renal aging, ischemic penumbra, and hyperglycemic stroke .
    FeTMPyP
  • HY-N0695
    Schisantherin B
    1 Publications Verification

    Gomisin-B; Wuweizi ester-B; Schisantherin-B

    		 PI3K Akt mTOR GSK-3 Tau Protein TNF Receptor Interleukin Related Apoptosis Neurological Disease Inflammation/Immunology
    Schisantherin B (Gomisin-B) is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression .
    Schisantherin B
  • HY-128879A
    VP3.15 dihydrobromide

    		Phosphodiesterase (PDE) GSK-3 Tau Protein Cardiovascular Disease Neurological Disease Inflammation/Immunology
    VP3.15 dihydrobromide is a highly potent, orally bioavailable, and CNS-penetrant PDE7-GSK3 dual inhibitor, with IC50 values of 1.59 μM and 0.88 μM against PDE7 and GSK3, respectively . VP3.15 dihydrobromide elevates intracellular cAMP levels, suppresses immune responses, enhances remyelination, limits excessive tau phosphorylation, and alleviates neuroinflammation and neuronal loss. VP3.15 dihydrobromide promotes oligodendrocyte precursor cell differentiation, improves in vivo remyelination, inhibits autoimmune encephalomyelitis, and mitigates germinal matrix-intraventricular hemorrhage-related brain injury, cerebral atrophy, ventricular enlargement, and cognitive impairment. VP3.15 dihydrobromide can be used in research related to multiple sclerosis and germinal matrix-intraventricular hemorrhage .
    VP3.15 dihydrobromide
  • 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-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-11095
    NPS 2390

    		mGluR CaSR PI3K Akt mTOR Autophagy Apoptosis Bcl-2 Family Caspase Cardiovascular Disease Neurological Disease
    NPS 2390 is an allosteric antagonist of calcium-sensing receptor (CaSR) and mGluR1/5. NPS 2390 inhibits the PI3K/Akt/mTOR signaling pathway, reduces hypoxia-induced intracellular calcium elevation, decreases the expression of autophagy (autophagy) proteins, regulates the expression of phenotypic marker proteins, and inhibits the proliferation of pulmonary artery smooth muscle cells. NPS 2390 attenuates the endogenous apoptosis (apoptosis) pathway, increases the expression level of Bcl-2, downregulates the expression levels of Bax, cytochrome c and caspase-3, alleviates cerebral edema and improves neurological function in rat models. NPS 2390 can be used in studies related to hypoxic pulmonary hypertension, traumatic brain injury, stroke and pain .
    NPS 2390
  • HY-B0158R
    Cytidine (Standard)

    Cytosine β-D-riboside (Standard); Cytosine-1-β-D-ribofuranoside (Standard)

    		 Reference Standards Nucleoside Antimetabolite/Analog Endogenous Metabolite Neurological Disease
    Cytidine (Standard) is the analytical standard of Cytidine. This product is intended for research and analytical applications. Cytidine is a pyrimidine nucleoside and acts as a component of RNA. Cytidine is a precursor of uridine. Cytidine controls neuronal-glial glutamate cycling, affecting cerebral phospholipid metabolism, catecholamine synthesis, and mitochondrial function . In Vivo:Cytidine decreases glutamate/glutamine levels and induces earlier improvement of depressive symptoms .
    Cytidine (Standard)
  • HY-132280
    Tirilazad

    U 74006F free base

    		 Reactive Oxygen Species (ROS) SARS-CoV Virus Protease Neurological Disease Inflammation/Immunology
    Tirilazad (U 74006F free base) is a neuroprotective agent. Tirilazad can also bind tightly to the main protease of the COVID-19 virus and exert anti-SARS-CoV-2 activity. Tirilazad scavenges hydroxyl and lipid peroxyl free radicals and maintains the levels of endogenous antioxidants. Tirilazad reduces cerebral infarct volume and improves neurobehavioral scores in animal models of focal ischemia. Tirilazad can be used in research related to ischemic stroke and subarachnoid hemorrhage .
    Tirilazad
  • HY-179055
    PROTAC DAPK1 Degrader-1

    		PROTACs DAPK Neurological Disease
    PROTAC DAPK1 Degrader-1 (Compound CP1) is a DAPK1 PROTAC degrader with a DC50 of 119.6 nM. PROTAC DAPK1 Degrader-1 significantly increased the MDM2 protein level. PROTAC DAPK1 Degrader-1 significantly reduced the levels of cleaved caspase-3 and cleaved PARP in a cell apoptosis model induced by the neurotoxin ceramide, indicating that it effectively inhibits neuronal apoptosis by degrading DAPK1. PROTAC DAPK1 Degrader-1 can be used to study neurological diseases such as cerebral ischemia and traumatic brain injury (pink: DAPK1 ligand (HY-179071); blue: CRBN ligand (HY-10984); black: linker (HY-40171)) .
    PROTAC DAPK1 Degrader-1
  • HY-W392413
    Glutathione monoethyl ester

    		Drug Derivative Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Glutathione monoethyl ester is a glutathione derivative that can be transported into cells and hydrolyzed into glutathione. Glutathione monoethyl ester downregulates the gene expression of TEN1 and CTC1 while upregulating TERT expression. Glutathione monoethyl ester enhances telomerase activity, promotes proliferation and differentiation in aged bone marrow stromal cells, while elevating glutathione levels and reducing oxidative stress, protein aggregation and cell death in motor neuronal cells. Glutathione monoethyl ester confers broad multi-organ protection against cerebral ischemia, renal injury, liver damage, and pancreatitis. Glutathione monoethyl ester can be used for the research of amyotrophic lateral sclerosis, stroke, acute renal failure, liver injury, and acute pancreatitis .
    Glutathione monoethyl ester
  • HY-N2439
    Methyl isoeugenol

    		Environmental Pollutants Pyroptosis SOD Quinone Reductase Keap1-Nrf2 NF-κB Cardiovascular Disease
    Methyl isoeugenol is an orally active, blood-brain barrier-permeable isoeugenol-type eugenol analog. Methyl isoeugenol promotes the nuclear translocation of Nrf2, upregulates the expressions of HO-1, NQO1 and SOD, and reduces the expression level of MDA. Methyl isoeugenol decreases the nuclear translocation of NF-κB. Methyl isoeugenol inhibits NLRP3 inflammasome-mediated pyroptosis. Methyl isoeugenol reduces cerebral infarction volume and regulates the M1/M2 phenotypic balance of microglia. Methyl isoeugenol can be used for the research of cerebral ischemia-reperfusion injury .
    Methyl isoeugenol
  • HY-N0320
    Salvianolic acid D

    		Bcl-2 Family Caspase Toll-like Receptor (TLR) MyD88 NF-κB Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Salvianolic acid D is a depside. Salvianolic acid D can be isolated from Salvia miltiorrhiza (Danshen). Salvianolic acid D promotes the expression of Bcl-2, and inhibits the expressions of Bax, Cleaved caspase-3 and -9. Salvianolic acid D reduces the expression levels of TLR4, MyD88 and TRAF6 proteins both in vitro and in vivo, and significantly inhibits the nuclear translocation of NF-κB. Salvianolic acid D inhibits the cytoplasmic translocation of HMGB1. Salvianolic acid D suppresses inflammatory responses and alleviates cerebral ischemia-reperfusion injury. Salvianolic acid D serves as a potential antiplatelet active component .
    Salvianolic acid D
  • HY-113402R
    Gamma-glutamylcysteine (Standard)

    γ-Glu-Cys (Standard)

    		 Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-102043
    PDM-631

    		Phosphodiesterase (PDE) Neurological Disease
    PDM-631 is a selective and orally active PDE2A inhibitor with blood-brain barrier penetration. PDM-631 exhibits potent inhibitory activity against human and rat recombinant PDE2A with IC50 values of 1.5 nM and 4.2 nM, respectively. PDM-631 increases cGMP levels in the rat cerebral cortex. PDM-631 can be used for the study of schizophrenia and neurodegenerative disorders .
    PDM-631
  • HY-118570
    5-Oxoprolyltryptophan

    		Biochemical Assay Reagents Neurological Disease
    5-Oxoprolyltryptophan is a model substrate for investigating the increase of serotonin at the cerebral level .
    5-Oxoprolyltryptophan
  • HY-N12249
    7-Deoxy-trans-dihydronarciclasine

    		Amyloid-β TMV Infection Neurological Disease Inflammation/Immunology
    7-Deoxy-trans-dihydronarciclasine, an alkaloid, is a tobacco mosaic virus (TMV) inhibitor (IC50: 1.80 μM). 7-Deoxy-trans-dihydronarciclasine is an anti-neuroinflammatory agent. 7-Deoxy-trans-dihydronarciclasine decreases the Aβ and APP levels in the cerebral cortex of Tg2576 mice .
    7-Deoxy-trans-dihydronarciclasine
  • HY-N0045R
    Ginsenoside Rg1 (Standard)

    Panaxoside A (Standard); Panaxoside Rg1 (Standard)

    		 Reference Standards Amyloid-β NF-κB Apoptosis Neurological Disease Inflammation/Immunology Cancer
    Ginsenoside Rg1 (Standard) is the analytical standard of Ginsenoside Rg1. This product is intended for research and analytical applications. Ginsenoside Rg1 is one of the major active components of Panax ginseng. Ginsenoside Rg1 ameliorates the impaired cognitive function, displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.
    Ginsenoside Rg1 (Standard)
  • HY-W087952R
    (R)-(-)-2-Butanol (Standard)

    		Drug Intermediate Reference Standards Endocrinology
    Ginsenoside Rg1 (Standard) is the analytical standard of Ginsenoside Rg1. This product is intended for research and analytical applications. Ginsenoside Rg1 is one of the major active components of Panax ginseng. Ginsenoside Rg1 ameliorates the impaired cognitive function, displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.
    (R)-(-)-2-Butanol (Standard)
  • HY-146351
    HDAC-IN-38

    		HDAC Neurological Disease
    HDAC-IN-38 (compound 13) is a potent HDAC inhibitor. HDAC-IN-38 shows similar micro-molar inhibitory activity toward HDAC1, 2, 3, 5, 6, and 8. HDAC-IN-38 increases cerebral blood flow (CBF), attenuates cognitive impairment, and improves hippocampal atrophy. HDAC-IN-38 also increases the level of histone acetylation (H3K14 or H4K5) .
    HDAC-IN-38
  • HY-120985
    Araguspongin B

    		Calcium Channel Neurological Disease
    Xestospongins and araguspongins are marine natural products first isolated from Pacific basin sponges, and noted to have vasodilatory properties.1 Inositol phosphates (IP) are important signal transduction messengers acting via IP3 receptors to promote the mobilization of Ca2+ from intracellular stores.2 Araguspongin B antagonizes the calcium-releasing action of inositol 1,4,5-trisphosphate at the receptor level in cerebral microsomes, with an IC50 of 0.6 μM. It is nearly as potent as xestospongin C as an antagonist of the IP3 receptor.
    Araguspongin B
  • HY-175521
    HIF-1α-IN-8

    		HIF/HIF Prolyl-Hydroxylase IKK NF-κB Apoptosis Reactive Oxygen Species (ROS) Inflammation/Immunology
    HIF-1α-IN-8 is an orally active HIF-1α inhibitor, with an IC50 of 2.02 μM. HIF-1α-IN-8 significantly suppresses the expression of inflammation factors of IL-6 and NO, reduces hypoxia-induced ROS production and apoptosis in C8-D1A cells. HIF-1α-IN-8 inhibits HIF-1α/IKKα/NF-κB signaling pathway and reduces the expression of blood-brain barrier permeability-related proteins. HIF-1α-IN-8 reduces brain water content and oxidative stress level in mice with high altitude cerebral edema (HACE) model. HIF-1α-IN-8 can be used for the study of high altitude cerebral edema (HACE) .
    HIF-1α-IN-8
  • HY-113402AR
    Gamma-glutamylcysteine TFA (Standard)

    γ-Glu-Cys TFA (Standard)

    		 Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-116062
    JNJ-7925476 hydrochloride

    		Monoamine Transporter Dopamine Transporter Adrenergic Receptor Others
    JNJ-7925476 (hydrochloride) is a triple monoamine uptake inhibitor with the ability to regulate neurotransmitter levels and antidepressant activity. JNJ-7925476 (hydrochloride) can be rapidly absorbed into the plasma in rats, with a higher concentration in the brain than in plasma. It can induce an increase in the levels of extracellular serotonin, dopamine, and norepinephrine in the rat cerebral cortex, and exhibits antidepressant activity in the mouse tail suspension test.
    JNJ-7925476 hydrochloride
  • HY-111066
    JNJ-37822681

    		Dopamine Receptor Others
    JNJ-37822681 is a fast dissociating D2 antagonist with activity in inhibiting schizophrenia. JNJ-37822681 has high specificity for D2 receptors and is effective in animal models, inducing increased levels of extracellular serotonin, dopamine, and norepinephrine in the rat cerebral cortex, and exhibiting antidepressant activity in the mouse tail suspension test, while having a good brain distribution and lower prolactin release.
    JNJ-37822681
  • HY-174127
    P2Y1 antagonist 3

    		P2Y Receptor Neurological Disease
    P2Y1 antagonist 3 (compound 36b) is a blood-brain barrier (BBB)-penetrant P2Y1 antagonist with an IC50 of 0.50 μM. P2Y1 antagonist 3 exhibits protective effects in a rat middle cerebral artery occlusion (MCAO) model and demonstrates neuroprotective activity against oxidative stress by upregulating nuclear Nrf2 protein levels .
    P2Y1 antagonist 3
  • HY-113126A
    3-Hydroxyisobutyric acid sodium

    		Endogenous Metabolite ATP Synthase Neurological Disease Metabolic Disease
    3-Hydroxyisobutyric acid sodium is an intermediate in the metabolic pathways of L-valine and thymine, and can be found in urine. 3-Hydroxyisobutyric acid sodium is a secreted mediator of endothelial cell fatty acid transport and insulin resistance. 3-Hydroxyisobutyric acid sodium can also inhibit key enzymes of energy metabolism in the cerebral cortex of young rats. The levels of 3-Hydroxyisobutyric acid sodium are closely related to various diseases such as 3-hydroxyisobutyric aciduria, diabetes, and ketoacidosis .
    3-Hydroxyisobutyric acid sodium
  • HY-W116433
    SK609

    		Dopamine Receptor Neurological Disease
    SK609 is a selective dopamine D3 receptor agonist with activity that improves dopamine and norepinephrine levels in the cerebral cortex. SK609 has been successfully used to suppress dyskinesias in Parkinson's disease models and alleviated muscle twitches induced by L-dopa. SK609 improved performance in sustained attention tasks by significantly reducing misses and false alarms. SK609 may provide an inhibitory option for suppressing movement and cognitive impairment in patients with Parkinson's disease .
    SK609
  • HY-168096
    iNOs-IN-5

    		NO Synthase Apoptosis Cardiovascular Disease Neurological Disease
    iNOs-IN-5 (Compound BN-4) is an inhibitor for iNOS with an IC50 of 0.1707 μM, and reduces NO levels in LPS (HT-D1056)-induced RAW264.7 cells. iNOs-IN-5 reduces the hypoxic injury stimulated ROS and lactate dehydrogenase expression, and exhibits anti-necrosis and anti-apoptosis efficacy. iNOs-IN-5 exhibits anti-cerebral ischemia and neuroprotective activities in SD rat models. iNOs-IN-5 is blood-brain barrier penetrable .
    iNOs-IN-5
  • HY-132280R
    Tirilazad (Standard)

    U 74006F free base (Standard)

    		 Reference Standards Reactive Oxygen Species (ROS) SARS-CoV Virus Protease Neurological Disease Inflammation/Immunology
    Tirilazad (U 74006F free base) Standard is the analytical standard of Tirilazad (HY-132280). This product is intended for research and analytical applications. Tirilazad (U 74006F free base) is a neuroprotective agent. Tirilazad can also bind tightly to the main protease of the COVID-19 virus and exert anti-SARS-CoV-2 activity. Tirilazad scavenges hydroxyl and lipid peroxyl free radicals and maintains the levels of endogenous antioxidants. Tirilazad reduces cerebral infarct volume and improves neurobehavioral scores in animal models of focal ischemia. Tirilazad can be used in research related to ischemic stroke and subarachnoid hemorrhage .
    Tirilazad (Standard)
  • HY-174126
    P2Y1 antagonist 2

    		P2Y Receptor Cardiovascular Disease
    P2Y1 antagonist 2 (Compound 19) is a P2Y1 receptor antagonist (IC50: 0.49 μM). P2Y1 antagonist 2 has significant antiplatelet aggregation activity and exerts its effects by inhibiting P2Y1 receptor. P2Y1 antagonist 2 can upregulate nuclear Nrf2 protein levels, exhibit neuroprotective effects, and resist oxidative stress damage. P2Y1 antagonist 2 can effectively reduce cerebral infarction area and improve neurobehavioral function, and can be used in the study of ischemic stroke .
    P2Y1 antagonist 2
  • 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-N0695R
    Schisantherin B (Standard)

    Gomisin-B (Standard); Wuweizi ester-B (Standard); Schisantherin-B (Standard)

    		 Reference Standards PI3K Akt mTOR GSK-3 Tau Protein TNF Receptor Interleukin Related Apoptosis Neurological Disease Inflammation/Immunology
    Schisantherin B (Gomisin-B) (Standard) is the analytical standard of Schisantherin B. This product is intended for research and analytical applications. Schisantherin B is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression.
    Schisantherin B (Standard)
  • HY-116062A
    JNJ-7925476

    		Histone Methyltransferase Neurological Disease
    JNJ-7925476 is a triple reuptake inhibitor that selectively and potently inhibits the activity of the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT). JNJ-7925476 is rapidly absorbed into the blood and its concentration in the brain is 7-fold higher than that in plasma. The occupancy ED(50) values of JNJ-7925476 for SERT, NET, and DAT in the rat brain are 0.18, 0.09, and 2.4 mg/kg, respectively. JNJ-7925476 rapidly induces a significant increase in the levels of extracellular serotonin, dopamine, and norepinephrine in the rat cerebral cortex in a dose-dependent manner. JNJ-7925476 exhibits potent antidepressant-like activity in the mouse tail suspension test. These results suggest that JNJ-7925476 has in vivo efficacy in biochemical and behavioral models of depression .
    JNJ-7925476
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine ammonium
  • 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-182295
    Negundoside

    		Reactive Oxygen Species (ROS) Apoptosis MMP Bacterial Parasite Cardiovascular Disease Infection Neurological Disease
    Negundoside is an iridoid glycoside compound. Negundoside exhibits hepatoprotective effects, reduces ROS, lipid peroxidation and intracellular calcium ion levels, and prevents the decrease of mitochondrial membrane potential (MMP) and apoptosis (apoptosis). Negundoside has neuroprotective effects, improves behavioral deficits, alleviates oxidative damage, and ameliorates cerebral infarction. Negundoside also possesses antibacterial and antiparasitic activities .
    Negundoside
  • HY-181738
    GPR17 agonist 2

    		Transmembrane Glycoprotein Cardiovascular Disease Neurological Disease
    GPR17 agonist 2 (compound 10) is a human GPR17 agonist and selective P2Y receptor non-activator.GPR17 agonist 2 modulates intracellular cAMP levels through functional activation of its target receptor.GPR17 agonist 2 can be used for the research of multiple sclerosis, cerebral ischemia, traumatic brain injury, spinal cord injury .
    GPR17 agonist 2
  • HY-105854A
    Pipoxolan

    		Ras MEK ERK PI3K Akt MMP Keap1-Nrf2 Heme Oxygenase (HO) Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Pipoxolan is an orally active smooth muscle relaxant, anti-inflammatory agent and anticancer agent. Pipoxolan modulates PI3K/AKT signaling pathways, and reduces the levels of Ras/MEK/p-ERK, MMP-2 and MMP-9. Pipoxolan inhibits pro-inflammatory transcription factor pathways, activates Nrf2/HO-1, and suppresses the production of pro-inflammatory mediators. Pipoxolan induces ROS generation, endogenous mitochondrial Apoptosis, and G0/G1 cell cycle arrest. Pipoxolan reduces cerebral infarction size and inhibits intimal hyperplasia. Pipoxolan can be used in research related to cerebral ischemia, intimal hyperplasia, oral squamous cell carcinoma, leukemia and lung cancer .
    Pipoxolan
  • HY-W975902
    MDL-27531

    		Glycine Receptor (GlyR) Neurological Disease
    MDL-27531 acts functionally like a glycine agonist. MDL-27531 selectively reduces hindlimb contractions. MDL-27531 selectively reverses strychnine-induced seizures in mice. MDL-27531 inhibits pentylenetetrazol-induced seizures with an ED50 of 55 mg/kg. MDL-27531 promotes the binding of benzodiazepine antagonist Ro 15-1788 to cerebral cortex of mice without changing GABA levels. MDL-27531 can be studied in research on reflex control dysfunction .
    MDL-27531
  • HY-160713
    Betamethasone succinate

    NSSL-BMS

    		 TNF Receptor Interleukin Related Infection Inflammation/Immunology
    Betamethasone succinate (NSSL-BMS) is a nano-formulation that can cross the blood-brain barrier. Betamethasone succinate is prepared by encapsulating the Betamethasone (HY-13570) semi-succinate in PEG-liposomes. Betamethasone succinate utilizes the enhanced permeation and retention effects of liposomes to target and deliver the potent glucocorticoid to the inflammatory sites. Betamethasone succinate inhibits the secretion of pro-inflammatory cytokines (such as TNF-α and IL-6) while maintaining the level of anti-inflammatory cytokine TGF-β. Betamethasone succinate can be used in the research of arthritis and cerebral malaria .
    Betamethasone succinate
  • HY-181879
    PROTAC mHTT Degrader-1

    		PROTACs Huntingtin Neurological Disease
    PROTAC mHTT Degrader-1 is a blood-brain barrier-penetrant mutant huntingtin (mHTT) PROTAC degrader. PROTAC mHTT Degrader-1 specifically recognizes pathogenic mHTT aggregates and recruits Cereblon (CRBN), thereby inducing ubiquitination and proteasomal degradation of mHTT. PROTAC mHTT Degrader-1 alleviates mHTT-induced cytotoxicity and neuroinflammation. In the R6/2 Huntington's disease mouse model, PROTAC mHTT Degrader-1 reduces cerebral protein aggregation levels and improves body weight, motor coordination and survival rate of animals. PROTAC mHTT Degrader-1 can be used for research on PROTAC therapies for Huntington's disease and other neurodegenerative diseases .
    PROTAC mHTT Degrader-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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