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Results for "

GSH Depletion

" in MedChemExpress (MCE) Product Catalog:

7

Inhibitors & Agonists

1

Biochemical Assay Reagents

2

Natural
Products

1

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-17363
    Dimethyl fumarate
    35+ Cited Publications

    Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite Infection Neurological Disease Inflammation/Immunology Cancer
    Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .
    Dimethyl fumarate
  • HY-17363R

    Keap1-Nrf2 Reactive Oxygen Species HIV Autophagy Endogenous Metabolite Infection Neurological Disease Inflammation/Immunology Cancer
    Dimethyl fumarate (Standard) is the analytical standard of Dimethyl fumarate. This product is intended for research and analytical applications. Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research .
    Dimethyl fumarate (Standard)
  • HY-17363S1

    Autophagy HIV Keap1-Nrf2 Endogenous Metabolite Reactive Oxygen Species Cancer
    Dimethyl fumarate-d2 is the deuterium labeled Dimethyl fumarate[1]. Dimethyl fumarate (DMF) is an orally active and brain-penetrant Nrf2 activator and induces upregulation of antioxidant gene expression. Dimethyl fumarate induces necroptosis in colon cancer cells through GSH depletion/ROS increase/MAPKs activation pathway, and also induces cell autophagy. Dimethyl fumarate can be used for multiple sclerosis research[2][3].
    Dimethyl fumarate-d2
  • HY-151940

    Reactive Oxygen Species Cancer
    Mal-Pc is a versatile molecular photosensitizer designed based phthalocyanine and maleimides. Mal-Pc can react with GSH to deplete GSH and reduce aggregation, thereby improving ROS (Reactive Oxygen Species)-mediated effect of photodynamic therapy (PDT) in cancer cells .
    Mal-Pc
  • HY-162944

    Ferroptosis Mitochondrial Metabolism STING Autophagy Cancer
    NA-Ir is a Ferroptosis inducer. NA-Ir targets mitochondrial DNA (mtDNA) and activates the cGAS-STING pathway to induce ferritinophagy (Autophagy), while also generating reactive oxygen species (ROS) through photodynamic therapy (PDT), depleting glutathione (GSH), and downregulating glutathione peroxidase 4 (GPX4), thereby triggering lipid peroxidation and Ferroptosis. NA-Ir exhibits higher anticancer activity under light exposure and selectively inhibits cancer cells with high H2S levels .
    NA-Ir
  • HY-161521

    Polo-like Kinase (PLK) Cancer
    PLK1-IN-10 (Compound 4Bb) is an orally active PLK1 PBD (polo-box domain) inhibitor. PLK1-IN-10 blocks the interaction of PLK1 with the cell division regulator protein 1 (PRC1) and decreases the protein expression of the CDK1-Cyclin B1 complex. PLK1-IN-10 reacts with glutathione (GSH) to increase cellular oxidative stress, ultimately leading to cell death .
    PLK1-IN-10

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