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Art. -Nr.: HY-182390

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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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Formel: C₁₈H₁₅NO₃
Molecular Weight:293.32

Speicherung:

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

Ferroptosis-IN-24 Chemical Structure

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

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.

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	C_max	T_max	AUC_0-∞	T_1/2	V	CL	AUC_0-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.

Chemical Information

Molecular Weight 293.32
Formel C₁₈H₁₅NO₃
SMILES

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

Room temperature in continental US; may vary elsewhere.
Speicherung

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

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Shu Y, et al. Design, Synthesis, and Evaluation of Indolizine Derivatives as Nonclassical Ferroptosis Inhibitors with Efficacy in Acute Liver Injury and Ischemic Stroke Models. J Med Chem. Published online March 19, 2026. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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100 mg

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