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Results for "

cerebral injury

" in MedChemExpress (MCE) Product Catalog:

101

Inhibitors & Agonists

8

Peptides

2

Inhibitory Antibodies

39

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-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-N2397
    9''-Methyl salvianolate B

    MSB

    		 DNA/RNA Synthesis PPAR NF-κB Autophagy Cardiovascular Disease Infection Inflammation/Immunology
    9''-Methyl salvianolate B (MSB) is a blood-brain barrier-permeable inhibitor with high affinity for g5Rp, with a Kd value of 117 nM against African swine fever virus (ASFV) g5Rp. 9''-Methyl salvianolate B also acts as a ZBP1 inhibitor. It exhibits strong binding affinity to key proteins in the PPARγ/NF-κB pathway. 9''-Methyl salvianolate B blocks the interaction between ASFV g5Rp and host proteins eIF5A or RPS15. It restores hypusination modification of eIF5A, promotes autophagy (Autophagy), and inhibits ASFV replication. 9''-Methyl salvianolate B effectively disrupts ZBP1-mediated PANoptosome assembly. It effectively alleviates myocardial ischemia/reperfusion injury. 9''-Methyl salvianolate B can be used in studies related to African swine fever .
    9''-Methyl salvianolate B
  • HY-125773
    β-cyano-L-Alanine

    Beta-cyano-l-alanine

    		 Endogenous Metabolite Neurological Disease
    β-cyano-L-Alanine (Beta-cyano-l-alanine), a nitrile of widespread occurrence in higher plants, is enzymatically produced by cyanoalanine synthase from cyanide and cysteine as substrates . β-cyano-L-Alanine abolishes the protective effect of ethanol on cerebral ischemia/reperfusion (I/R) injury .
    β-cyano-L-Alanine
  • 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-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-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-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-B0531
    Triflusal

    		COX Phosphodiesterase (PDE) NF-κB NO Synthase Prostaglandin Receptor Infection Neurological Disease Inflammation/Immunology Cancer
    Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease .
    Triflusal
  • HY-N0353
    Curdione
    2 Publications Verification

    (+)-Curdione

    		 Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Cancer
    Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC50 = 1.1 μM) and cyclooxygenase 2 expression .
    Curdione
  • HY-162596
    NRL-1049

    BA-1049 free base

    		 ROCK Neurological Disease
    NRL-1049 (BA-1049 (free base)) is an orally available and selective ROCK2 inhibitor with IC50 values of 0.59 µM for ROCK2 and 26 µM for ROCK1, respectively. NRL-1049 modulates ROCK signaling, preserves blood-brain barrier integrity, reduces edema, seizures and hemorrhage, and alleviates cerebral cavernous malformation lesion burden. NRL-1049 can be used for the study of acute brain injury, ischemic stroke, and cerebral cavernous malformations .
    NRL-1049
  • HY-N0507
    Rosavin

    		TNF Receptor Interleukin Related Neurological Disease Inflammation/Immunology
    Rosavin, an orally bioactive phenylpropanoid from Rhodiola rosea L. (RRL), is an adaptogen that enhances the body’s response to environmental stress. Rosavin significantly influences bone tissue metabolism by inhibiting osteoclastogenesis and promoting osteoblast differentiation, also impacts various diseases, demonstrating antidepressant, adaptogenic, and anxiolytic effects in mouse models. Additionally, Rosavin improves survival, reducing intestinal damage in irradiated rats and Ischemia-reperfusion(I/R)-induced cerebral injury in vivo by regulating inflammation and oxidative stress, making it a promising candidate for research in radiation-induced intestinal injury, I/R-induced cerebral injury and osteoporosis .
    Rosavin
  • HY-N6784
    Oligomycin B

    		ATP Synthase Bacterial Apoptosis Antibiotic Infection Neurological Disease
    Oligomycin B is an antibiotic that acts as a non-selective inhibitor of ATP Synthase. Oligomycin B increases mitochondrial membrane potential. Oligomycin B induces apoptosis and necrosis. Oligomycin B impairs the motility of Plasmopara viticola zoospores and induces their lysis. Oligomycin B inhibits Magnaporthe oryzae (wheat blast fungus) and suppresses the development of wheat blast. Oligomycin B reduces hyphal growth and spore germination of Botrytis cinerea, and protects Arabidopsis thaliana against Botrytis cinerea infection. Oligomycin B exacerbates cytotoxic brain edema in rats with cerebral cortical contusion, increases intracranial pressure and brain water content, and aggravates mitochondrial damage in these rats. Oligomycin B is used in studies related to grape downy mildew, traumatic brain injury, wheat blast, and gray mold .
    Oligomycin B
  • 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-N0541
    Pseudoginsenoside F11
    2 Publications Verification

    Ginsenoside A1

    		 Amyloid-β JNK MDM-2/p53 Caspase SOD Glutathione Peroxidase NO Synthase Cardiovascular Disease Neurological Disease
    Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of Aβ1-40, downregulates the expression of JNK2, p53 and activated Caspase 3, and restores the activities of SOD and Glutathione peroxidase. Pseudoginsenoside F11 inhibits the excessive activation of μ-Calpain and restores the level of neuronal Nitric oxide synthase. Pseudoginsenoside F11 reduces infarct volume, alleviates cerebral edema, decreases neuronal loss, improves neurological deficits and enhances long-term functional outcomes in transient cerebral ischemia models. Pseudoginsenoside F11 antagonizes Methamphetamine-induced behavioral deficits, dopamine level reduction and neurotoxicity without altering the baseline behaviors of normal mice. Pseudoginsenoside F11 can be used in studies related to Alzheimer's disease, transient cerebral ischemic injury and Methamphetamine-induced neurotoxicity .
    Pseudoginsenoside F11
  • HY-N0546
    Ligustroflavone
    2 Publications Verification

    Nuezhenoside

    		 CaSR RIP kinase Mixed Lineage Kinase TGF-beta/Smad Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
    Ligustroflavone is an orally active flavonoid compound. Ligustroflavone can be extracted from Ligustrum lucidum. Ligustroflavone antagonizes the calcium-sensing receptor (CaSR), inhibits the RIPK1/RIPK3/MLKL pathway, and downregulates TGF-β/Smad signaling. Ligustroflavone regulates calcium metabolism, protects bone tissue, reduces cerebral ischemic injury, and inhibits liver fibrosis. Ligustroflavone can be used in the study of diabetic osteoporosis, ischemic stroke, and liver fibrosis .
    Ligustroflavone
  • HY-B0023
    Azelnidipine
    3 Publications Verification

    CS 905

    		 Calcium Channel MEK Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Azelnidipine (CS 905) is a dihydropyridine calcium channel blocker that is effective orally. Azelnidipine inhibits the intracellular calcium ion flow and lower blood pressure by selectively blocking L-type calcium channel on the membrane of vascular smooth muscle. Azelnidipine inhibits esophageal squamous cell carcinoma proliferation by targeting MEK1/2. Azelnidipine also has anti-inflammatory, antioxidant and neuroprotective effects .
    Azelnidipine
  • HY-N5063
    Plantainoside D
    2 Publications Verification

    		 Angiotensin-converting Enzyme (ACE) IKK Calcium Channel PKC Reactive Oxygen Species (ROS) NF-κB Apoptosis Sirtuin NOD-like Receptor (NLR) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Plantainoside D, a phenylethanoid glycosides, is a IKK-β inhibitor with diverse biological activities. Plantainoside D shows inhibitory activity of angiotensin-converting enzyme (ACE) with an IC50 of 2.17 mM. Plantainoside D significantly reduces the release of glutamate from nerve terminals in the cerebral cortex of rats by inhibiting the voltage-dependent calcium channel (VDCCs) and protein kinase C (PKC) signaling cascade. Plantainoside D significantly alleviates cell apoptosis by inhibiting the generation of ROS and the activation of NF-κB. Plantainoside D significantly improves acute lung injury (ALI) induced by sepsis by regulating the Sirt3/NLRP3 signaling pathway. Plantainoside D can be used for the study of neuroprotection, antioxidant, anti-inflammation, antihypertension .
    Plantainoside D
  • HY-W016409
    Ethyl 3,4-dihydroxybenzoate
    1 Publications Verification

    Protocatechuic acid ethyl ester

    		 HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) NO Synthase Autophagy Apoptosis Metabolic Disease Cancer
    Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-dihydroxybenzoate
  • HY-P6442
    Chemerin15

    		Chemerin Receptor Syk ERK Src p38 MAPK P-selectin Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Chemerin15 is an anti-inflammatory peptide derived from Chemerin. Chemerin15 binds to ChemR23. Chemerin15 inhibits TNFα-induced activation of Syk, ERK and Src kinases. Chemerin15 increases the expression of p-p38 mRNA and protein. Chemerin15 mediates phagocytosis, resolution of inflammation, CD62L shedding and downregulation of PSGL-1 expression in macrophages and microglia. Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury via ChemR23. Chemerin15 enhances microglial phagocytosis, thereby alleviating cerebral ischemia-reperfusion injury .
    Chemerin15
  • 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-43521
    Ibrutinib-MPEA

    		Target Protein Ligand-Linker Conjugates Btk STAT Inflammation/Immunology Cancer
    Ibrutinib-MPEA is an orally active, blood-brain barrier permeable inhibitor of BTK and STAT5. As a derivative of Ibrutinib (HY-10997) conjugated with a PROTAC linker, Ibrutinib-MPEA allows the synthesis of a series of PROTAC molecules. Ibrutinib-MPEA significantly reduces the proliferation of neoplastic mast cells and primary mastocytoma cells by inducing apoptosis and inhibiting IgE-dependent histamine release. Ibrutinib-MPEA is applicable to the research of canine mast cell tumors, cerebral ischemia/reperfusion injury in diabetic mice, and neuroinflammation-related diseases .
    Ibrutinib-MPEA
  • HY-N0385
    Gomisin J
    3 Publications Verification

    		 NO Synthase AMPK CaMK NF-κB Keap1-Nrf2 Cardiovascular Disease Inflammation/Immunology
    Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc .
    Gomisin J
  • HY-W404916
    Probenecid sodium
    Maximum Cited Publications
    43 Publications Verification

    		 Influenza Virus Interleukin Related Cardiovascular Disease Infection Neurological Disease Inflammation/Immunology
    Probenecid sodium is an orally active, blood-brain barrier-permeable Pannexin 1 channel inhibitor. Probenecid sodium exhibits anti-inflammatory, antiviral, and neuroprotective activities. Probenecid sodium can be used in research related to multiple sclerosis, focal cerebral ischemic injury, influenza virus infection, and nephropathy .
    Probenecid sodium
  • HY-N0392
    Polygalasaponin F

    		Toll-like Receptor (TLR) PI3K Akt NF-κB MDM-2/p53 Caspase MEK Bcl-2 Family p38 MAPK Mitophagy Reactive Oxygen Species (ROS) Apoptosis Calcium Channel Cardiovascular Disease Infection Neurological Disease
    Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease .
    Polygalasaponin F
  • HY-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-W008344
    2-Chloroadenosine

    		Nucleoside Antimetabolite/Analog Apoptosis Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    2-Chloroadenosine is an adenosine analog, a transporter permeabilizer of nucleoside transporters, and a competitive uridine influx inhibitor (apparent Ki=33 μM). 2-Chloroadenosine binds to nitrobenzylthioinosine with high affinity (apparent Ki=0.18 mM). 2-Chloroadenosine promotes Apoptosis and increases cerebral blood flow. 2-Chloroadenosine has anticonvulsant properties. 2-Chloroadenosine is used to study infection, inflammatory diseases, cancer, blood-related diseases, lung injury, epilepsy, and kidney disease .
    2-Chloroadenosine
  • 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
    3 Publications Verification

    		 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-P6437A
    Drp1 peptide inhibitor P110 TFA

    		Dynamin Cardiovascular Disease Neurological Disease
    Drp1 peptide inhibitor P110 (Compound P110) TFA is a selective Drp1 peptide inhibitor with neuroprotective properties. Drp1 peptide inhibitor P110 TFA can inhibit the activation of Drp1, prevent MPTP (HY-15608)-induced Drp1 mitochondrial translocation, and alleviate MPTP-induced dopaminergic neuron loss, dopaminergic nerve terminal damage, and behavioral deficits, and can be used in the study of Alzheimer's disease. Additionally, Drp1 peptide inhibitor P110 TFA can reduce mitochondrial damage and organ injury in animal models of Huntington's disease, cerebral ischemic injury, and myocardial infarction .
    Drp1 peptide inhibitor P110 TFA
  • HY-N0670
    Tenacissoside H
    1 Publications Verification

    Tenacissimoside C

    		 PI3K Akt NF-κB Apoptosis Neurological Disease Inflammation/Immunology Cancer
    Tenacissoside H (Tenacissimoside C) is a compound found in Caulis Marsdeniae Tenacissimae. Tenacissoside H shows anti-inflammation, anti-tumor and neuroprotective effects. Tenacissoside H inhibits PI3K/Akt and NF-κB signaling pathway. Tenacissoside H inhibits cancer cells proliferation, S phase arrest, and inhibits tumor growyh in mice. Tenacissoside H promotes neurological recovery of ischemia-reperfusion injury in mice by inhibiting inflammation and apoptosis. Tenacissoside H can be used for the research of cancer, inflammation and neurological diseases, such as esophageal cancer and cerebral ischemia .
    Tenacissoside H
  • HY-101481
    Flurbiprofen axetil

    		COX Apoptosis MEK ERK PPAR AMPK NF-κB Interleukin Related TNF Receptor STAT Wnt Neurological Disease Inflammation/Immunology Cancer
    Flurbiprofen axetil is a non-selective COX inhibitor and a nonsteroidal anti-inflammatory agent with anti-inflammatory and analgesic effects. Flurbiprofen axetil inhibits basal-like breast cancer metastasis by inhibiting the MEK/ERK signaling pathway. Flurbiprofen axetil can promote neuroprotection after focal cerebral ischemia in rats by partially activating PPAR-γ. Flurbiprofen axetil alleviates cerebral ischemia/reperfusion injury by reducing inflammation in a transient global cerebral ischemia/reperfusion rat model. Flurbiprofen axetil can alleviate inflammatory responses and cognitive function in a mild cognitive impairment (MCI) SD rat model through the AMPKα/NF-κB signaling pathway .
    Flurbiprofen axetil
  • HY-120327
    KY-226
    2 Publications Verification

    		 Phosphatase Neurological Disease Metabolic Disease
    KY-226 is a potent, selective, orally active and allosteric protein tyrosine phosphatase 1B (PTP1B) inhibitor with an IC50 of 0.25 μM, and without PPARγ agonist activity. KY-226 exerts anti-diabetic and anti-obesity effects by enhancing insulin and leptin signaling, respectively. KY-226 also protects neurons from cerebral ischemic injury .
    KY-226
  • HY-N2282
    Zingiberen newsaponin

    Zingiberensis newsaponin

    		 Aldose Reductase JAK STAT Autophagy Apoptosis NF-κB SOD Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Zingiberen Newsaponin (Zingiberensis newsaponin) is an orally active type of steroid saponin compound. Zingiberen Newsaponin exerts anti-hepatocellular carcinoma (HCC) effects by inhibiting autophagy and the AKR1C1/JAK2/STAT3 pathway. Zingiberen Newsaponin activates oxidative stress (upregulates ROS and MDA) and mitochondrial pathways, promoting cancer cell apoptosis. Zingiberen Newsaponin alleviates cerebral ischemia-reperfusion (I/R) injury by decreasing the concentration of pro-inflammatory cytokines and inhibits NF-κB. Zingiberen Newsaponin can enhance the activity of SOD, eliminate free radicals and protect nerve cells. Zingiberen Newsaponin induces platelet aggregation .
    Zingiberen newsaponin
  • 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-P6437
    Drp1 peptide inhibitor P110

    		Dynamin Cardiovascular Disease Neurological Disease
    Drp1 peptide inhibitor P110 (Compound P110) is a selective Drp1 peptide inhibitor with neuroprotective properties. Drp1 peptide inhibitor P110 can inhibit the activation of Drp1, prevent MPTP-induced Drp1 mitochondrial translocation, and alleviate MPTP-induced dopaminergic neuron loss, dopaminergic nerve terminal damage, and behavioral deficits, and can be used in the study of Alzheimer's disease. Additionally, Drp1 peptide inhibitor P110 can reduce mitochondrial damage and organ injury in animal models of Huntington's disease, cerebral ischemic injury, and myocardial infarction .
    Drp1 peptide inhibitor P110
  • HY-101318
    β-Funaltrexamine hydrochloride
    2 Publications Verification

    β-FNA hydrochloride

    		 Opioid Receptor p38 MAPK STAT NF-κB NO Synthase Toll-like Receptor (TLR) Cardiovascular Disease Neurological Disease
    β-Funaltrexamine (β-FNA) hydrochloride is a blood-brain barrier-permeable, selective and irreversible μ-opioid receptor antagonist with immunomodulatory, anti-inflammatory and neuroprotective activities. β-Funaltrexamine hydrochloride inhibits p38 MAPK and TLR4 signaling by blocking μ-opioid receptors, and reduces the transcriptional activities of NF-κB, AP-1, CREB and Stat. Furthermore, β-Funaltrexamine hydrochloride inhibits iNOS activation and pro-inflammatory microglial polarization, converting microglia to an anti-inflammatory phenotype, thereby downregulating neuroinflammation and ameliorating neuronal degeneration. β-Funaltrexamine hydrochloride is widely applicable to research related to stroke, cerebral ischemia/reperfusion injury and neurodegenerative diseases .
    β-Funaltrexamine hydrochloride
  • HY-N0935
    Ligustrazine hydrochloride
    Maximum Cited Publications
    11 Publications Verification

    Chuanxiongzine hydrochloride; Tetramethylpyrazine hydrochloride

    		 Reactive Oxygen Species (ROS) Akt NO Synthase Aminotransferases (Transaminases) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Ligustrazine hydrochloride is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine hydrochloride reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine hydrochloride possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis .
    Ligustrazine hydrochloride
  • HY-107802
    Breviscapine
    2 Publications Verification

    Breviscapinun

    		 NF-κB Interleukin Related TGF-beta/Smad Calcium Channel Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Breviscapine (Breviscapinun) is a flavonoid compound with antioxidant, anti-inflammatory, anti-fibrotic, and neuroprotective activities. Breviscapine ameliorates cerebral ischemia/reperfusion injury and vascular dementia, and inhibits the formation of postoperative abdominal adhesions. The mechanism of action of Breviscapine involves the regulation of oxidative stress, inflammatory cytokines, signaling pathways such as TGF-β/Smad, and cellular calcium overload. Breviscapine is used for research on diseases including cardiovascular and cerebrovascular diseases .
    Breviscapine
  • HY-N2045
    Musk ketone
    1 Publications Verification

    		 Environmental Pollutants Apoptosis Akt Cytochrome P450 PI3K Neurological Disease
    Musk ketone is a widely used artificial fragrance. Musk ketone is also a cytochrome P450 enzyme inducer. Musk ketone shows mutagenic and comutagenic effects in Hep G2 cells and induces neural stem cell proliferation and differentiation in cerebral ischemia via activation of the PI3K/Akt signaling pathway. In the brain, musk ketone is neuroprotective against stroke injury through inhibition of cell apoptosis .
    Musk ketone
  • HY-103435
    Vialinin A
    2 Publications Verification

    Terrestrin A

    		 Deubiquitinase TNF Receptor E1/E2/E3 Enzyme Keap1-Nrf2 Inflammation/Immunology Cancer
    Vialinin A (Terrestrin A) is a p-terphenyl compound that can be derived from a Chinese edible mushroom. Vialinin A is an inhibitor of ubiquitin-specific peptidase 4 (USP4) and has anti-inflammatory and antioxidant properties. Vialinin A can alleviate cerebral ischaemia-reperfusion injury-induced neurological deficits and neuronal apoptosis. Vialinin A promotes activation of Keap1-Nrf2-ARE signaling pathway and increases the protein degradation of Keap1. Vialinin A possesses various pharmacological activities in cancer, Kawasaki disease, asthma, and pathological scarring. Vialinin A is a potent inhibitor of TNF-α, USP4, USP5, and sentrin/SUMO-specific protease 1 (SENP1). Vialinin A can be studied in reseach for autoimmune diseases, cancer and ischaemic stroke .
    Vialinin A
  • HY-N0853A
    Alisol A 24-acetate
    1 Publications Verification

    Alisol A 24-monoacetate; Alisol A monoacetate

    		 AMPK Carnitine Palmitoyltransferase (CPT) Acyltransferase Fatty Acid Synthase (FASN) Acetyl-CoA Carboxylase Bcl-2 Family PPAR Nuclear Factor of activated T Cells (NFAT) PI3K Akt PKA ERK Apoptosis Autophagy Cardiovascular Disease Infection Neurological Disease Metabolic Disease Endocrinology
    Alisol A 24-acetate (Alisol A monoacetate) is an orally active derivative of protostane-type tetracyclic triterpenoid. Alisol A 24-acetate upregulates the expression of adiponectin, AMPKα, CPT1, and ACOX1; downregulates the expression of SREBP-1c, ACC, FAS, Bcl-2, Bcl-xl, PPAR-γ, perilipin A, and NFATc1; inhibits the activity of PI3K/Akt/mTOR and HMGR; and activates the PKA and ERK signaling pathways. Alisol A 24-acetate regulates cell apoptosis (apoptosis), autophagy (Autophagy, hepatic lipid accumulation, inflammatory response, neuroprotection, MRSA membrane integrity, and osteoclast differentiation. Alisol A 24-acetate can be used in research related to non-alcoholic fatty liver disease, nephrotoxicity, obesity, global cerebral ischemia-reperfusion injury, bacterial infection, and osteoporosis .
    Alisol A 24-acetate
  • HY-143333
    Nrf2 activator-3
    1 Publications Verification

    		 Keap1-Nrf2 Neurological Disease Inflammation/Immunology
    Nrf2 activator-3 is a potent Nrf2 activator. Nrf2 activator-3 is used for cerebral ischemic injury research .
    Nrf2 activator-3
  • 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-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-138646
    Poly(deoxyadenylic-thymidylic) acid sodium
    4 Publications Verification

    Poly(dA:dT) sodium

    		 Cyclic GMP-AMP Synthase STING Inflammation/Immunology
    Poly(deoxyadenylic-thymidylic) acid (Poly(dA:dT)) sodium is a double-stranded DNA stimulant. Poly(deoxyadenylic-thymidylic) acid sodium is recognized by the intracellular DNA sensor DDX41 and activates the innate immune pathway via the adaptor protein STING, inducing the production of cytokines such as type I interferons. Poly(deoxyadenylic-thymidylic) acid sodium also serves as an in vitro transcription template for free RNA polymerase .
    Poly(deoxyadenylic-thymidylic) acid sodium
  • HY-P11315
    MG1 peptide

    		Biochemical Assay Reagents Cardiovascular Disease Neurological Disease
    MG1 peptide is an M1 microglia-targeting peptide with blood-brain barrier permeability. MG1 peptide can be used in studies related to ischemic stroke and cerebral ischemia-reperfusion injury .
    MG1 peptide
  • 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-170790
    HZS60

    		TRP Channel Neurological Disease
    HZS60 is a NMDAR/TRPM4 inhibitor with brain permeability that can improve cerebral ischemia. HZS60 has significant neuroprotective effects on primary neuronal ischemic damage caused by NMDA and oxygen-glucose deprivation/reoxygenation. HZS60 exhibits good pharmacokinetic characteristics and can inhibit cerebral ischemia-reperfusion injury. HZS60 can be used as a potential inhibitor of ischemic stroke .
    HZS60
  • 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

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