1. Apoptosis Metabolic Enzyme/Protease NF-κB Immunology/Inflammation
  2. Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS) Apoptosis
  3. Ferroptosis-IN-23

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.

For research use only. We do not sell to patients.

Ferroptosis-IN-23

Ferroptosis-IN-23 Chemical Structure

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Description

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[1].

In Vitro

Ferroptosis-IN-23 (Compound 8h) (10 μM; 48 h) potently reverses ferroptosis in HT-22 hippocampal neurons induced by RSL3 (HY-100218A), Erastin (HY-15763), and Ammonium iron (III) citrate (FAC) (HY-B1645)[1].
Ferroptosis-IN-23 (5-20 μM; 48 h) inhibits RSL3-induced lipid ROS accumulation in HT-22 hippocampal neuron cells in a dose-dependent manner[1].
Ferroptosis-IN-23 (10-20 μM; 48 h) reverses RSL3-induced ferroptosis in Steap4-silenced HT-22 hippocampal neurons, with the 10 μM concentration restoring cell viability to 60.4%, indicating that Steap4 contributes to, but is not essential for, its anti-ferroptotic activity[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Cell Line: RSL3-treated HT-22 hippocampal neuronal cells
Concentration: 10 μM (after 4 h pre-treatment with 0.1 μM RSL3)
Incubation Time: 48 h
Result: Reversed RSL3-induced ferroptosis, restoring HT-22 cell viability to 74.3% relative to the control group.

Cell Viability Assay[1]

Cell Line: erastin-treated HT-22 hippocampal neuronal cells
Concentration: 10 μM (after 4 h pre-treatment with 0.3 μM erastin)
Incubation Time: 48 h
Result: Significantly reversed erastin-induced ferroptosis in HT-22 cells, with superior activity relative to a comparator compound.

Cell Viability Assay[1]

Cell Line: FAC-treated HT-22 hippocampal neuronal cells
Concentration: 10 μM (after 4 h pre-treatment with 6 mM FAC)
Incubation Time: 48 h
Result: Reversed FAC-induced ferroptosis in HT-22 cells.

Cell Viability Assay[1]

Cell Line: Steap4-silenced, RSL3-treated HT-22 hippocampal neuronal cells
Concentration: 10-20 μM (after 4 h pre-treatment with 0.1 μM RSL3 in Steap4-silenced cells)
Incubation Time: 48 h
Result: Restored cell viability to 60.4% relative to the control group at 10 μM, while 20 μM showed further improved viability.
In Vivo

Ferroptosis-IN-23 (2-8 μM; 72 h) dose-dependently inhibits RSL3-induced ferroptosis in wild-type AB strain zebrafish by reducing ROS accumulation and lipid peroxidation, as well as restoring iron homeostasis and GPX4 function[1].
Ferroptosis-IN-23 (2-8 μM; 72 h) dose-dependently alleviates 6-OHDA (HY-B1081A)-induced neuronal apoptosis and ROS accumulation in wild-type AB strain zebrafish (a Parkinson's disease model)[1].
Ferroptosis-IN-23 (2-8 μM; 96 h) dose-dependently protects Tg (vmat2: GFP) zebrafish, a Parkinson's disease model, against MPTP (HY-15608)-induced dopaminergic neuron damage[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: wild-type AB strain (2 hours post-fertilization)[1]
Dosage: 2 μM; 4 μM; 8 μM
Administration: 72 h
Result: Significantly reduced the number of apoptotic brain cells induced by RSL3.
Dose-dependently reduced RSL3-induced reactive oxygen species (ROS) accumulation in zebrafish brains.
Dose-dependently decreased RSL3-induced increases in lipid peroxidation (LPO) and malondialdehyde (MDA) levels.
Dose-dependently reduced RSL3-induced upregulation of hepcidin (HEPC) expression and restored ferroportin (FPN) expression.
Dose-dependently reversed RSL3-induced downregulation of glutathione peroxidase 4 (GPX4a and GPX4b) expression.
Dose-dependently restored RSL3-induced downregulation of Steap4 expression.
Animal Model: wild-type AB strain (2 hours post-fertilization)[1]
Dosage: 2 μM; 4 μM; 8 μM
Administration: immersion; daily replenishment; 72 hours, followed by 24 hours of co-exposure with 6-OHDA
Result: Significantly reduced the number of apoptotic brain cells induced by 6-OHDA.
Dose-dependently reduced 6-OHDA-induced ROS accumulation in zebrafish brains.
Animal Model: Tg(vmat2: GFP) strain (1 day post-fertilization)[1]
Dosage: 2 μM; 4 μM; 8 μM
Administration: immersion; daily replenishment; 96 hours with concurrent MPTP exposure
Result: Dose-dependently reversed MPTP-induced shortening of dopaminergic neuron regions, with recovery toward control levels.
Molecular Weight

370.36

Formula

C19H18N2O6

SMILES

O=C1NC(C(C2=CC=CC(OC)=C2)=O)=NC3=C1C(OC)=C(OC)C(OC)=C3

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Please store the product under the recommended conditions in the Certificate of Analysis.

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Product Name:
Ferroptosis-IN-23
Cat. No.:
HY-181665
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