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glutathione homeostasis

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-113324
    NADPH
    Maximum Cited Publications
    18 Publications Verification

    		 Endogenous Metabolite Cancer
    NADPH is a coenzyme of glutathione reductase (GR), thioredoxin reductase (TrxR) and NADPH oxidase (NOX), and participates in redox reactions as a hydrogen donor. NADPH has the characteristic of selectively participating in the regulation of cellular redox homeostasis. NADPH exerts antioxidant activity and resists reactive oxygen species (ROS) damage by providing reducing equivalents for the regeneration of glutathione (GSH) and thioredoxin (Trx); at the same time, it acts as a substrate of NOX to generate superoxide anions, mediating oxidative stress and immune response. NADPH participates in maintaining the intracellular reducing environment, biosynthesis and regulating gene expression (such as the Nrf2 pathway), and is mainly used in the study of oxidative stress-related diseases (such as cardiovascular diseases, neurodegenerative diseases, cancer) and immune regulation mechanisms .
    NADPH
  • 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-12542
    Dantrolene
    10+ Cited Publications

    F 368

    		 Calcium Channel Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dantrolene is an orally active, non-competitive glutathione reductase inhibitor with a Ki of 111.6 μM and an IC50 of 52.3 μM. Dantrolene is also a calcium channel protein inhibitor. Dantrolene inhibits the release of Ca 2+ from RyR1 and RyR3, which can be beneficial in a variety of pathologies caused by disruptions in calcium homeostasis (e.g., stroke, ischemia/reperfusion injury, and neurodegenerative diseases). Dantrolene offers relief of muscle spasms, malignant hyperthermia, and antitoxic, antipyretic, and anti-inflammatory properties .
    Dantrolene
  • HY-14657
    Dantrolene sodium
    10+ Cited Publications

    F 440

    		 Calcium Channel Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease
    Dantrolene sodium is an orally active, non-competitive glutathione reductase inhibitor with a Ki of 111.6 μM and an IC50 of 52.3 μM. Dantrolene sodium is also a calcium channel protein inhibitor. Dantrolene sodium inhibits the release of Ca 2+ from RyR1 and RyR3, which can be beneficial in a variety of pathologies caused by disruptions in calcium homeostasis (e.g., stroke, ischemia/reperfusion injury, and neurodegenerative diseases). Dantrolene sodium offers relief of muscle spasms, malignant hyperthermia, and antitoxic, antipyretic, and anti-inflammatory properties .
    Dantrolene sodium
  • HY-Y1147
    Diethyl maleate
    1 Publications Verification

    Maleic acid diethyl ester

    		 Biochemical Assay Reagents Others
    Diethyl maleate (DEM) is an orally available, effective glutathione (GSH) depletor that crosses the blood-brain barrier. Diethyl maleate covalently binds irreversibly to GSH via glutathione S-transferase with an in vitro IC50 of 0.1-0.5 mM. Diethyl maleate selectively depletes GSH in liver, lung, and brain tissues, exacerbating oxidative stress and enhancing hyperbaric oxygen toxicity. Diethyl maleate promotes precursor amino acid uptake and in turn promotes GSH synthesis by upregulating the activity of the cystine-glutamate transporter XO -. Diethyl maleate can be used to study redox homeostasis and GSH protection mechanisms in oxidative stress-related diseases such as hyperbaric oxygen injury and metabolic diseases[1][2][3].
    Diethyl maleate
  • 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-12542A
    Dantrolene sodium hemiheptahydrate
    10+ Cited Publications

    Dantrolene sodium hydrate

    		 Calcium Channel Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease
    Dantrolene sodium hemiheptahydrate is an orally active, non-competitive glutathione reductase inhibitor with a Ki of 111.6 μM and an IC50 of 52.3 μM. Dantrolene sodium hemiheptahydrate is also a calcium channel protein inhibitor. Dantrolene sodium hemiheptahydrate inhibits the release of Ca 2+ from RyR1 and RyR3, which can be beneficial in a variety of pathologies caused by disruptions in calcium homeostasis (e.g., stroke, ischemia/reperfusion injury, and neurodegenerative diseases). Dantrolene sodium hemiheptahydrate offers relief of muscle spasms, malignant hyperthermia, and antitoxic, antipyretic, and anti-inflammatory properties .
    Dantrolene sodium hemiheptahydrate
  • HY-P2989
    Pyruvate carboxylase

    		Endogenous Metabolite Metabolic Disease Cancer
    Pyruvate carboxylase is a key mitochondrial anaplerotic enzyme that catalyzes the conversion of pyruvate to oxaloacetate. Pyruvate carboxylase not only maintains tricarboxylic acid cycle activity and redox homeostasis, but also drives hepatic gluconeogenesis and fatty acid synthesis. The activity of Pyruvate carboxylase is upregulated in insulin-resistant states, exacerbating hepatic glucose production. Pyruvate carboxylase also shows significantly enhanced expression in early-stage non-small cell lung cancer (NSCLC). Pyruvate carboxylase promotes tumor proliferation by supporting nucleotide and lipid synthesis, and its functional deficiency cannot be compensated by glutaminolysis. Pyruvate carboxylase can be used in the research of prediabetes type 2 and NSCLC .
    Pyruvate carboxylase
  • HY-171030
    Pro-GA

    		Reactive Oxygen Species (ROS) Cancer
    Pro-GA is a γ-glutamyl cyclotransferase (GGCT) inhibitor. Pro-GA inhibits the enzymatic activity of GGCT, disrupts glutathione homeostasis, induces the production of mitochondrial ROS, and upregulates the expression of p21, p27 and p16 in cells. Pro-GA inhibits the growth of cancer cells, induces cell cycle arrest and cellular senescence. Pro-GA exerts anti-tumor effects in breast cancer xenograft mouse models. Pro-GA can be used in research related to bladder cancer and breast cancer .
    Pro-GA
  • 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-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-159004
    Se-DOPE

    		Reactive Oxygen Species (ROS) Metabolic Disease Inflammation/Immunology
    Se-DOPE is a phospholipid molecule with selenium. Se-DOPE can be used to synthesize the bifunctional Janus liposozyme. Se-DOPE promotes the production of ROS with induction of lights, scavenges the ROS with the presence of glutathione. Se-DOPE regulates redox and immune homeostasis in infected diabetic wounds .
    Se-DOPE
  • 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-183294
    GPX4-IN-24

    		Glutathione Peroxidase Ferroptosis Reactive Oxygen Species (ROS) Cancer
    GPX4-IN-24 is an orally active glutathione peroxidase 4 (GPX4) inhibitor with a human IC50 of 10.90 μM, human Kd of 10.04 μM. GPX4-IN-24 suppresses GPX4 enzymatic activity, disrupts redox homeostasis, drives lipid peroxidation, promotes lipid peroxidation, and induces ferroptosis. GPX4-IN-24 can be used for the research of triple-negative breast cancer .
    GPX4-IN-24
  • HY-181665
    Ferroptosis-IN-23

    		Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS) Apoptosis Neurological Disease
    Ferroptosis-IN-23 is an inhibitor of ferroptosis. Ferroptosis-IN-23 exerts a synergistic effect by simultaneously activating Steap4 and glutathione peroxidase 4 (GPX4), thereby maintaining iron metabolism homeostasis. Ferroptosis-IN-23 reverses neuronal ferroptosis and inhibits lipid ROS accumulation in cells. Ferroptosis-IN-23 inhibits ferroptosis in zebrafish, alleviates neuronal apoptosis, ROS accumulation, and dopaminergic neuron damage in a zebrafish model of Parkinson's disease. Ferroptosis-IN-23 can be used for research on Parkinson's disease .
    Ferroptosis-IN-23
  • HY-182052
    anti-NSCLC agent-2

    		Glutathione Peroxidase Reactive Oxygen Species (ROS) NO Synthase Ferroptosis Apoptosis Cancer
    anti-NSCLC agent-2 exhibits nanomolar anti-proliferative activity and acts on wild-type and drug-resistant non-small cell lung cancer (NSCLC) cells. anti-NSCLC agent-2 downregulates ferroptosis-related factors SLC7A11 and GPX4, disrupts cellular redox homeostasis, depletes glutathione, accumulates lipid peroxides, and simultaneously elevates mitochondrial nitric oxide and ROS levels to induce ferroptosis in tumor cells. anti-NSCLC agent-2 is applicable to research related to non-small cell lung cancer .
    anti-NSCLC agent-2
  • HY-183549
    Ferroptosis/apoptosis inducer-4

    		Apoptosis Ferroptosis Cancer
    Ferroptosis/apoptosis inducer-4 is a pyridine-hydrazone-derived Cu (II) complex and a synergistic inducer of ferroptosis and apoptosis. Ferroptosis/apoptosis inducer-4 exerts anti-tumor proliferation and anti-metastasis effects with extremely low systemic toxicity. Ferroptosis/apoptosis inducer-4 disrupts cellular redox homeostasis by depleting glutathione and generating hydroxyl radicals through the Cu 2+/Cu + redox cycle. Ferroptosis/apoptosis inducer-4 also triggers mitochondrial dysfunction and endoplasmic reticulum stress, which in turn lead to Ca 2+ release, mitochondrial Ca 2+ overload, and the formation of a ROS−Ca 2+ self-amplifying feedback loop. Ferroptosis/apoptosis inducer-4 can be used in studies related to cervical cancer .
    Ferroptosis/apoptosis inducer-4
  • HY-P2997B
    γ-glutamyltransferase, Human (HEK293)

    		Biochemical Assay Reagents Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    γ-glutamyltransferase, Human (HEK293) is a γ-glutamyltransferase expressed in HEK293 cells. γ-glutamyltransferase participates in glutathione metabolism. Serum γ-glutamyltransferase activity is identified as a predictor of atherosclerotic complications, and has prognostic value for cardiovascular diseases and stroke. γ-glutamyltransferase also serves as a biomarker for carcinogenesis and tumor progression .
    γ-glutamyltransferase, Human (HEK293)

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