Ferroptosis-IN-24
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.
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- Formule: C18H15NO3
- Masse moléculaire:293.32
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Ferroptosis-IN-24 (compound D12) (6.25-12.5 μM; 24 h) potently inhibits RSL3 (HY-100218A)-induced ferroptosis in PC12 cells, with an EC50 of 39.7 nM; at concentrations of 6.25 μM and 12.5 μM, it increases cell viability to 90.7% and 96.5%, respectively[1].
Ferroptosis-IN-24 (24 h) inhibits Erastin (HY-15763)-induced ferroptosis in PC12 cells, with an EC50 of 410.4 nM[1].
Ferroptosis-IN-24 (1 μM; 8 h) effectively reduces RSL3-induced intracellular ROS accumulation in PC12 cells[1].
Ferroptosis-IN-24 (1 μM; 8 h) effectively inhibits RSL3-induced lipid peroxidation in PC12 cells[1].
Ferroptosis-IN-24 (1 μM; 6 h) reverses the RSL3-induced downregulation of GPX4 and Nrf2 protein expression in PC12 cells[1].
Ferroptosis-IN-24 (1 μM) reduces the stress-induced overexpression of GPX4, Nrf2, HMOX1 and NQO1 mRNA in RSL3-treated PC12 cells, indicating that it alleviates upstream oxidative stress rather than directly activating the Nrf2 pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:PC12 cells (RSL3-induced ferroptosis)
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Concentration:6.25 μM; 12.5 μM
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Incubation Time:24 h
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Result:Increased PC12 cell viability to 90.7% under RSL3-induced ferroptosis conditions at 6.25 μM.
Increased cell viability to 96.5% under RSL3-induced ferroptosis conditions at 12.5 μM.
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Cell Line:PC12 cells (RSL3-treated)
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Concentration:1 μM
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Incubation Time:6 h
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Result:Reversed the RSL3-induced downregulation of GPX4 protein levels in PC12 cells, restoring expression to near-control levels.
Reversed the RSL3-induced downregulation of Nrf2 protein levels in PC12 cells, restoring expression to near-control levels.
| Species | Dose | Route | Cmax | Tmax | AUC0-∞ | T1/2 | V | CL | AUC0-t |
|---|---|---|---|---|---|---|---|---|---|
| Rat[1] | 10 mg/kg | i.v. | 8199.91 μg/L | 0.08 h | 4208.09 μg/L·h | 4.76 h | 0.53 L/kg | 2.38 L/h/kg | 3350.27 μg/L·h |
Ferroptosis-IN-24 (10 mg/kg; i.v.; single pretreatment) reduces the cerebral infarction volume and improves neurological deficits in a rat model of cerebral ischemia-reperfusion injury induced by MCAO[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, APAP-induced acute liver injury model)[1]
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Dosage:10 mg/kg; 20 mg/kg
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Administration:i.p.; single pretreatment (1 h before APAP challenge)
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Result:Reduced liver necrosis dose-dependently, with near-normal liver histology at 20 mg/kg.
Reduced serum alanine transaminase (ALT) level and aspartate transaminase (AST) level.
Restored hepatic glutathione (GSH) level.
Reduced malondialdehyde (MDA) level.
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Animal Model:SD (male, MCAO-induced cerebral ischemia-reperfusion injury model)[1]
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Dosage:10 mg/kg
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Administration:i.v.; single pretreatment (1 h before MCAO, followed by 24 h reperfusion)
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Result:Reduced cerebral infarct volume.
Improved neurological deficits.
Chemical Information
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Masse moléculaire 293.32
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Formule C18H15NO3
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SMILES
O=C(C1=CC(OC(C)=O)=C2N1C=CC=C2)C3=CC=CC=C3C
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)