Ferroptosis-IN-26
Ferroptosis-IN-26 is a CEPT1-targeting ferroptosis inhibitor. Ferroptosis-IN-26 enhances CEPT1-dependent phosphatidylcholine remodeling to enrich cellular membranes with monounsaturated fatty acid-containing phosphatidylcholine (PC-MUFA). Ferroptosis-IN-26 suppresses lipid peroxidation. Ferroptosis-IN-26 can be used for the research of acute liver injury.
For research use only. We do not sell to patients.
- Formula: C24H16N2O2
- Molecular Weight:364.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Ferroptosis-IN-26 (Compound 4g) potently inhibits RSL3 (HY-100218A)-induced ferroptosis in 786-O cells with an EC50 of 0.16 μM[1].
Ferroptosis-IN-26 potently inhibits RSL3-induced ferroptosis in HT-1080 cells with an EC50 of 0.15 μM[1].
Ferroptosis-IN-26 potently inhibits RSL3-induced ferroptosis in H9c2 cells with an EC50 of 93 nM[1].
Ferroptosis-IN-26 potently inhibits RSL3-induced ferroptosis in SK-HEP-1 cells with an EC50 of 102 nM[1].
Ferroptosis-IN-26 potently inhibits Erastin (HY-15763)-induced ferroptosis in HT-1080 cells with an EC50 of 0.27 μM[1].
Ferroptosis-IN-26 potently inhibits FIN56 (HY-103087)-induced ferroptosis in HT-1080 cells with an EC50 of 0.32 μM[1].
Ferroptosis-IN-26 (1 μM) suppresses RSL3-induced lipid ROS accumulation in 786-O and H9c2 cells[1].
Ferroptosis-IN-26 (1 μM) suppresses Erastin- and FIN56-induced lipid ROS accumulation in HT-1080 cells[1].
Ferroptosis-IN-26 (1 μM; 24 h) does not protect SK-HEP-1 or 786-O cells against STS-induced apoptosis[1].
Ferroptosis-IN-26 (1 μM; 24 h) does not protect SK-HEP-1 or 786-O cells against H2O2-induced necrosis[1].
Ferroptosis-IN-26 (up to 1.5 μM; 24 h) has low inherent cytotoxicity in HEK293T cells, with a CC50 greater than 20 μM[1].
Ferroptosis-IN-26 (1-2 μM; 0-180 min) does not inhibit AAPH (HY-Y0525)-induced lipid peroxidation in EggPC liposomes[1].
Ferroptosis-IN-26 (50 μM) does not exhibit DPPH radical scavenging activity[1].
Ferroptosis-IN-26 does not alter cellular glutathione levels in cells treated with Erastin[1].
Ferroptosis-IN-26 does not alter cellular total free thiol levels in cells treated with Erastin[1].
Ferroptosis-IN-26 (0.5-10 μM) does not alter the expression of ferroptosis-associated proteins in cells[1].
Ferroptosis-IN-26 inhibits RSL3-induced ferroptosis in SK-HEP-1 and 786-O cells independently of the FSP1/CoQ10 system[1].
Ferroptosis-IN-26 inhibits RSL3-induced ferroptosis in GPX4-knockout HT-1080 cells, demonstrating activity independent of GPX4 function[1].
Ferroptosis-IN-26 (3 μM; 72 h) increases cellular levels of MUFA-enriched phosphatidylcholine species in 786-O cells[1].
The antiferroptotic activity of Ferroptosis-IN-26 in SCD1-knockout 786-O and HT-1080 cells is independent of SCD1-mediated MUFA generation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SK-HEP-1 cells; 786-O cells
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Concentration:1 μM
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Incubation Time:24 h
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Result:Did not protect SK-HEP-1 or 786-O cells against STS-induced apoptosis.
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Cell Line:SK-HEP-1 cells; 786-O cells
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Concentration:1 μM
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Incubation Time:24 h
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Result:Did not protect SK-HEP-1 or 786-O cells against H2O2-induced necrosis.
Ferroptosis-IN-26 (5-10 mg/kg) ameliorates ConA (HY-P2149)-induced acute liver injury in mice by suppressing ferroptosis and hepatocellular damage[1].
Ferroptosis-IN-26 (5 mg/kg) ameliorates APAP (HY-66005)-induced acute liver injury in C57 mice by improving liver function and reducing hepatocellular damage[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 mice (male; eight weeks old; intravenously injected with 15 mg/kg ConA to establish an acute liver injury model)[1]
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Dosage:5 mg/kg; 10 mg/kg
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Administration:i.p.; 2 doses administered 24 h apart
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Result:Significantly alleviated hepatocellular lesions.
Markedly reduced serum levels of the liver injury markers ALT and AST.
Substantially decreased 4-HNE adducts.
Significantly reduced serum MDA levels.
Downregulated the mRNA expression of the ferroptosis-associated gene Ptgs2 in mice livers.
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Animal Model:C57BL/6 mice (male; six weeks old; 18-22 g; intraperitoneally injected with 400 mg/kg APAP to establish an acute liver injury model)[1]
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Dosage:5 mg/kg; 10 mg/kg
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Administration:i.p.; 2 doses administered 24 h apart
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Result:Markedly reduced serum levels of the liver injury markers ALT and AST.
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Animal Model:C57BL/6 mice (male; eight weeks old; hepatic ischemia-reperfusion injury)[1]
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Dosage:10 mg/kg
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Administration:i.p.; 2 doses at 36 h and again
at 12 h prior to surgery -
Result:Markedly ameliorated extensive ischemic areas and inflammatory infiltration.
Significantly attenuated the HIRI-induced elevation in serum ALT and AST levels.
Significantly reduced serum MDA levels.
Chemical Information
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Molecular Weight 364.40
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Formula C24H16N2O2
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SMILES
CC1=CC2=C(C=C1O)OC3=NC4=C(C(C=CC=C5)=C5N4)C(C6=CC=CC=C6)=C32
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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