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Results for "

cerebral ischemia-reperfusion injury

" in MedChemExpress (MCE) Product Catalog:

48

Inhibitors & Agonists

3

Peptides

27

Natural
Products

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-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-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-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-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-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-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-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-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-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-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-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-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-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-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-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-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-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
  • HY-N0408R
    Picroside II (Standard)

    		Reference Standards NF-κB Reactive Oxygen Species (ROS) Apoptosis Influenza Virus Infection Neurological Disease Inflammation/Immunology Cancer
    Picroside II (Standard) is the analytical standard of Picroside II. This product is intended for research and analytical applications. Picroside II, an iridoid compound extracted from Picrorhiza, exhibits anti-inflammatory and anti-apoptotic activities. picroside II alleviates the inflammatory response in sepsis and enhances immune function by inhibiting the activation of NLRP3 inflammasome and NF-κB pathways . Picroside II is an antioxidant, exhibits a significant neuroprotective effect through reducing ROS production and protects the blood-brain barrier (BBB) after cerebral ischemia-reperfusion (CI/R) injury. Picroside II has antioxidant, anti-inflammatory, immune regulatory, anti-virus and other pharmacological activities .
    Picroside II (Standard)
  • 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-175548
    Nrf2 activator-21

    		Keap1-Nrf2 Apoptosis Caspase Neurological Disease
    Nrf2 activator-21 is a Nrf2 activator with dual antioxidant and neuroprotective properties. Nrf2 activator-21 binds to Keap1 Kelch domain and disrupts Keap1-Nrf2 interactions and activate antioxidant defense mechanisms. Nrf2 activator-21 reduces apoptosis and decreases caspase-3 activity in the hippocampal neurons. Nrf2 activator-21 targets cerebral ischemia/reperfusion injury (CIRI) via Nrf2 pathway activation. Nrf2 activator-21 improves neurological function, alleviates anxiety-like behavior, enhances memory in rats with 2-vessel occlusion (2VO)-induced CIRI. Nrf2 activator-21 can be used for the study of cerebral ischemia/reperfusion injury .
    Nrf2 activator-21
  • HY-172876
    FLY26

    		iGluR Reactive Oxygen Species (ROS) Trk Receptor Cardiovascular Disease
    FLY26 is a selective partial GluN2B antagonist with an IC50 value of 0.64 μM. FLY26 partially inhibits the GluN2B subunit of NMDA receptors, reduces calcium ion influx and reactive oxygen species (ROS) production and activates the BDNF/TrkB/CREB neuroprotective signaling pathway to alleviate neuronal excitotoxicity and mitochondrial dysfunction. FLY26 is promising for research of neurological deficits caused by cerebral ischemia-reperfusion injury .
    FLY26
  • HY-N0507R
    Rosavin (Standard)

    		Reference Standards TNF Receptor Interleukin Related Neurological Disease Inflammation/Immunology
    Rosavin (Standard) is the analytical standard of Rosavin. This product is intended for research and analytical applications. 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 (Standard)
  • HY-N2014R
    Verbenalin (Standard)

    		Reference Standards SARS-CoV Amyloid-β Ferroptosis Tau Protein Caspase Bcl-2 Family Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Verbenalin (Standard) is the analytical standard of Verbenalin. This product is intended for research and analytical applications. Verbenalin is an orally active terpenoid glycoside that can be extracted from the medicinal plant Verbena officinalis. Verbenalin has anti-inflammatory, antiviral, and neuroprotective effects. Verbenalin has a strong binding affinity to the nsp-12 protein of the SARS-CoV-2 virus. Verbenalin can be used in the research of inflammatory and nervous system diseases such as hepatitis and Alzheimer's disease .
    Verbenalin (Standard)
  • HY-14909R
    Bardoxolone (Standard)

    CDDO (Standard); RTA 401 (Standard)

    		 Keap1-Nrf2 Necroptosis SARS-CoV Virus Protease Reference Standards Infection Cardiovascular Disease Inflammation/Immunology
    Bardoxolone (Standard) is the analytical standard of Bardoxolone (HY-14909). This product is intended for research and analytical applications. Bardoxolone is an orally active activator of nuclear regulatory factor (NRf-2) and an inhibitor of SARS-CoV-2 3CL protease. Bardoxolone inhibits SARS-CoV-2 3CL protease with an EC50 value of 0.43 μM in vero cells. Bardoxolone also inhibits necroptosis in HT-29 cells with an EC50 value of 1.30 μM by blocking necrosome formation through inhibiting phosphorylation of RIPK1 and RIPK3. Bardoxolone can be used in research on COVID-19, TNF-induced systemic inflammatory response syndrome (SIRS), and cerebral ischemia-reperfusion injury .
    Bardoxolone (Standard)
  • HY-139117
    6,2′,4′-Trimethoxyflavone

    		Aryl Hydrocarbon Receptor Cardiovascular Disease
    6,2′,4′-Trimethoxyflavone is an AhR antagonist and has failed to show effective protective effects against cerebral ischemia/reperfusion injury in Sprague-Dawley rats .
    6,2′,4′-Trimethoxyflavone
  • 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-168065
    Keap1-Nrf2-IN-22

    		Keap1-Nrf2 Inflammation/Immunology
    Keap1-Nrf2-IN-22 (compound 19) is a Keap1-Nrf2 inhibitor， with a KD2 value of 42.2 nM for Keap1. Keap1-Nrf2-IN-22 can be used for the study of acute lung injury (ALI) and cerebral ischemia/reperfusion (I/R) injury .
    Keap1-Nrf2-IN-22
  • HY-101481R
    Flurbiprofen axetil (Standard)

    		Reference Standards COX Apoptosis MEK ERK PPAR AMPK NF-κB Interleukin Related TNF Receptor STAT Wnt Neurological Disease Inflammation/Immunology Cancer
    Flurbiprofen axetil (Standard) is the analytical standard of Flurbiprofen axetil. This product is intended for research and analytical applications. 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 (Standard)
  • HY-161992
    Nrf2 activator-11

    		Keap1-Nrf2 Apoptosis Neurological Disease Inflammation/Immunology
    Nrf2 activator-11 (compound M11) is a Nrf2 activator with blood-brain permeability. Nrf2 activator-11 has anti-oxidation, anti-inflammation, anti-ferroptosis and anti-apoptosis. Nrf2 activator-11 can be used to study cerebral  ischemia-reperfusion (CI/R) injury models .
    Nrf2 activator-11
  • HY-125773R
    β-cyano-L-Alanine (Standard)

    Beta-cyano-l-alanine (Standard)

    		 Endogenous Metabolite Reference Standards Neurological Disease
    β-cyano-L-Alanine (Standard) is the analytical standard of β-cyano-L-Alanine. This product is intended for research and analytical applications. 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 (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-N0392R
    Polygalasaponin F (Standard)

    		Reference Standards Toll-like Receptor (TLR) PI3K Akt NF-κB Inflammation/Immunology Cancer
    Polygalasaponin F (Standard) is the analytical standard of Polygalasaponin F. This product is intended for research and analytical applications. 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 (Standard)
  • HY-184089
    ATB1071

    		p62 Mitophagy Cardiovascular Disease Neurological Disease
    ATB1071 is a brain-penetrant and orally active p62/SQSTM1 activator. ATB1071 binds to the p62-ZZ domain, promotes PB1-dependent p62 self-polymerization, and activates p62-mediated mitophagy. ATB1071 can be used for the research of Leigh syndrome, cerebral ischemia-reperfusion injury[1].
    ATB1071
  • HY-182390
    Ferroptosis-IN-24

    		Ferroptosis Reactive Oxygen Species (ROS) Keap1-Nrf2 Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Ferroptosis-IN-24 is a non-classical ferroptosis inhibitor capable of crossing the blood-brain barrier, with nanomolar inhibitory activity against ferroptosis induced by RSL3 (HY-100218A) and Erastin (HY-15763). Ferroptosis-IN-24 alleviates oxidative stress, reduces lipid peroxidation accumulation, and restores redox homeostasis. Ferroptosis-IN-24 is applicable to research related to cerebral ischemia-reperfusion injury and acute liver injury .
    Ferroptosis-IN-24
  • HY-184115
    JHB-17

    		IKK Heme Oxygenase (HO) Keap1-Nrf2 Reactive Oxygen Species (ROS) Ferroptosis Cardiovascular Disease Neurological Disease
    JHB-17 is an IKKβ inhibitor with blood-brain barrier permeability, with an IC50 of 1.1 μM and a KD of 1.293 μM. JHB-17 is a non-ATP competitive inhibitor targeting the allosteric site of IKKβ, and it inhibits the phosphorylation of IKKβ. JHB-17 promotes the nuclear translocation of Nrf2, upregulates the expression of HO-1, SLC7A11 and glutathione, and reduces ROS to exert antioxidant effects. JHB-17 reduces cerebral infarction volume and improves neurobehavioral function. JHB-17 can be used in the research of cerebral ischemia-reperfusion injury .
    JHB-17
  • HY-N0353R
    Curdione (Standard)

    (+)-Curdione (Standard)

    		 Reference Standards Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO) Others
    Curdione (Standard) is the analytical standard of Curdione. This product is intended for research and analytical applications. 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 (Standard)
  • 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-160938
    β-Funaltrexamine

    β-FNA

    		 Opioid Receptor STAT NF-κB Toll-like Receptor (TLR) NO Synthase p38 MAPK Cardiovascular Disease Neurological Disease
    β-Funaltrexamine (β-FNA) is a blood-brain barrier-permeable, selective and irreversible μ-opioid receptor antagonist with immunomodulatory, anti-inflammatory and neuroprotective activities. β-Funaltrexamine 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 inhibits iNOS activation and pro-inflammatory microglial polarization, converting microglia to an anti-inflammatory phenotype, thereby downregulating neuroinflammation and ameliorating neuronal degeneration. β-Funaltrexamine is widely applicable to research related to stroke, cerebral ischemia/reperfusion injury and neurodegenerative diseases .
    β-Funaltrexamine
  • 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

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