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Further Information
Erastin is a ferroptosis activator acting on mitochondrial VDAC. It induces ferroptotic cell death in vitro.
RSL3 and Erastin, as activators of ferroptosis, can induce cellular ferroptosis. Ferroptosis can be employed to eliminate problematic cell types, such as cancer cells, inflammatory cells, or activated fibroblasts. Abundant research indicates that ferroptosis plays a crucial role in various conditions such as tumor suppression, immunity, neurodegenerative diseases, tissue and organ damage, inflammatory and infectious diseases. Scientists widely believe that targeting ferroptosis holds the potential to advance the development and clinical translation of therapies based on ferroptosis.
571203-78-6
Erastin is a ferroptosis activator acting on mitochondrial VDAC. It induces ferroptotic cell death in vitro. The product is unstable in solution and is recommended to be dispensed now.
C30H31ClN4O4
Ferroptosis is a type of programmed cell death different from apoptosis and necrotic cell death. Actually, ferroptosis is characterized by the depletion of glutathione (GSH), a reduction in the activity of glutathione peroxidase 4 (GPX4), and the iron-dependent accumulation of reactive oxygen species (ROS) and lipid ROS.
Ferroptosis can be triggered by various small molecules, including RSL3 and Erastin, which directly inhibit the cystine/glutamate reverse transporter protein (System Xc-) on the cell surface and GPX4. The cystine/glutamate reverse transporter protein is a heterodimer on the cell membrane responsible for the intracellular and extracellular transport of cystine and glutamate. It facilitates a 1:1 exchange of cystine and glutamate in and out of the cell. Absorbed cystine is reduced to cysteine within the cell, and cysteine, along with glutamate, is utilized in the biosynthesis of reduced glutathione (GSH). GSH, under the action of GPX4, reduces lipid hydroperoxides to lipid alcohols, thereby reducing ROS. Inhibiting the activity of System Xc- can affect GSH synthesis, leading to reduced GPX4 activity, diminished cellular antioxidant capacity, accumulation of lipid ROS, and ultimately resulting in oxidative damage and ferroptosis.
547.05
Membrane transporter/Ion channel; Apoptosis; Cell Cycle/Checkpoint
0.9975
Tumour suppression and immunity; Neurodegenerative diseases; Tissue and organ damage; Inflammatory and infectious diseases
CCOc1ccccc1-n1c(nc2ccccc2c1=O)C(C)N1CCN(CC1)C(=O)COc1ccc(Cl)cc1
Ferroptosis; VDAC