2. Apoptosis NF-κB Metabolic Enzyme/Protease Immunology/Inflammation
  3. Ferroptosis Reactive Oxygen Species (ROS) Keap1-Nrf2
  4. 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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Ferroptosis-IN-24

Ferroptosis-IN-24 Chemical Structure

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Ferroptosis-IN-24 Related Antibodies

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Description

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[1].

In Vitro

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.

Ferroptosis-IN-24 Related Antibodies

Cell Viability Assay[1]

Cell Line: PC12 cells (RSL3-induced ferroptosis)
Concentration: 6.25 μM; 12.5 μM
Incubation Time: 24 h
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.

Western Blot Analysis[1]

Cell Line: PC12 cells (RSL3-treated)
Concentration: 1 μM
Incubation Time: 6 h
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.
Parmacokinetics
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
In Vivo

Ferroptosis-IN-24 (10-20 mg/kg; i.p.; single pretreatment) dose-dependently alleviates liver necrosis, restores levels of liver enzymes and antioxidants, and improves histological manifestations in a mouse model of acetaminophen-induced acute liver injury[1].
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.

Animal Model: C57BL/6 (male, APAP-induced acute liver injury model)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: i.p.; single pretreatment (1 h before APAP challenge)
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.
Animal Model: SD (male, MCAO-induced cerebral ischemia-reperfusion injury model)[1]
Dosage: 10 mg/kg
Administration: i.v.; single pretreatment (1 h before MCAO, followed by 24 h reperfusion)
Result: Reduced cerebral infarct volume.
Improved neurological deficits.
Molecular Weight

293.32

Formula

C18H15NO3
SMILES

O=C(C1=CC(OC(C)=O)=C2N1C=CC=C2)C3=CC=CC=C3C
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Ferroptosis-IN-24 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Ferroptosis-IN-24FerroptosisReactive Oxygen Species (ROS)Keap1-Nrf2ferroptosisRSL3ratoxidative stresslipid peroxidationacetaminophenacute liver injurycerebral ischemia-reperfusion injuryredox homeostasiserastinblood-brain barrierInhibitorinhibitorinhibit

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