Ferroptosis inducer-17
Ferroptosis inducer-17 is a ferroptosis inducer that downregulates GPX4 and activates the CTSB and cGAS-STING pathways. Ferroptosis inducer-17 exhibits cytotoxicity against cancer cells but low toxicity toward normal cells. Ferroptosis inducer-17 accumulates in mitochondria and lysosomes, thereby inducing ROS production, lipid peroxidation, mitochondrial membrane depolarization, lysosomal iron accumulation, increased membrane permeability, and enhanced oxidative stress. Ferroptosis inducer-17 inhibits tumor growth in cisplatin-resistant xenograft models. Ferroptosis inducer-17 can be used for cancer-related research.
For research use only. We do not sell to patients.
- Formula: C37H41N3O7Zr
- Molecular Weight:730.96
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Cathepsin Isoforms
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Biological Activity
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GPX4 |
Cathepsin B |
Ferroptosis inducer-17 (compound 1t) (range of concentrations; 48 h) potently inhibits proliferation of Hep G2, Hep G2/DDP, SW620/DDP, and HeLa S3 cancer cells with IC50 values of 3.9 μM, 2.3 μM, 13.9 μM, and 51.8 μM respectively, while sparing normal LO2 liver cells[1].
Ferroptosis inducer-17 (compound 1t) (4 μM; 24 h, 48 h) potently inhibits migration of Hep G2/DDP cells after 24 h and 48 h of incubation[1].
Ferroptosis inducer-17 (compound 1t) (4 μM; 0.1-48 h) accumulates continuously in Hep G2/DDP cells over 48 h, reaching a maximum Zr content of 22.50 ng[1].
Ferroptosis inducer-17 (4 μM; 24 h) preferentially localizes to mitochondria and lysosomes in Hep G2/DDP cells after 24 h of incubation[1].
Ferroptosis inducer-17 (4 μM; 24 h) induces ferroptosis as the predominant mode of cell death in Hep G2/DDP cells, with a minor contribution from apoptosis[1].
Ferroptosis inducer-17 (4 μM) induces G1-phase cell cycle arrest in Hep G2/DDP cells[1].
Ferroptosis inducer-17 (4 μM) disrupts redox homeostasis in Hep G2/DDP cells and promotes membrane damage associated with lipid peroxidation; also increases ROS levels in Hep G2/DDP cells; causes mitochondrial membrane depolarization in Hep G2/DDP cells[1].
Ferroptosis inducer-17 (4 μM; 12 h) downregulates GPX4 protein expression in Hep G2/DDP cells[1].
Ferroptosis inducer-17 (4 μM; 24 h) increases lysosomal ironII levels and lysosomal pH in Hep G2/DDP cells[1].
Ferroptosis inducer-17 (4 μM; 24 h) upregulates NCOA4 and SLC7A11 protein expression in Hep G2/DDP cells[1].
Ferroptosis inducer-17 (4 μM; 24 h) modulates the expression of IFN-α, IFN-β, IFN-γ, IL-6, cGAS, and STING in Hep G2/DDP cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Hep G2/DDP (cisplatin-resistant hepatocellular carcinoma)
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Concentration:4 μM
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Incubation Time:24 h, 48 h
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Result:Markedly inhibited Hep G2/DDP cell migration, reducing wound closure rates from 26.42% (control) to 1.73% at 24 h.
Markedly inhibited Hep G2/DDP cell migration, reducing wound closure rates from 40.88% (control) to 7.87% at 48 h.
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Cell Line:Hep G2/DDP (cisplatin-resistant hepatocellular carcinoma)
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Concentration:4 μM; 10 μM (Ferrostatin-1, 3-MA), 20 μM (Z-VAD-FMK)
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Incubation Time:24 h (Ferroptosis inducer-17); 1 h (inhibitors pretreatment)
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Result:Only Ferrostatin-1 (HY-100579) (ferroptosis inhibitor) and Z-VAD-FMK (HY-16658B) (apoptosis inhibitor) substantially rescued cell viability, with Ferrostatin-1 showing the most significant rescue effect.
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Cell Line:Hep G2/DDP (cisplatin-resistant hepatocellular carcinoma)
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Concentration:4 μM
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Incubation Time:12 h
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Result:Markedly reduced GPX4 protein expression levels compared to untreated control cells.
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Cell Line:Hep G2/DDP (cisplatin-resistant hepatocellular carcinoma)
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Concentration:4 μM
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Incubation Time:24 h
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Result:Markedly increased NCOA4 protein expression levels compared to untreated control cells.
Markedly increased SLC7A11 protein expression levels compared to untreated control cells.
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Cell Line:Hep G2/DDP (cisplatin-resistant hepatocellular carcinoma)
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Concentration:4 μM
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Incubation Time:24 h
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Result:Modulated the expression of IFN-α, IFN-β, IFN-γ, IL-6, cGAS, and STING.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NOD/SCID (male, 5-6 weeks old)[1]
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Dosage:2.9 mg/kg
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Administration:i.v.; single dose
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Result:Significantly suppressed tumor growth in the cisplatin-resistant Hep G2/DDP orthotopic xenograft model.
Showed minimal systemic toxicity.
Chemical Information
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Molecular Weight 730.96
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Formula C37H41N3O7Zr
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SMILES
CC1=CC(C(C)(C)C)=C2O[Zr]34(OC5=O)(OC(C6=CC(O)=CC5=N6)=O)OC7=C(C(C)(C)C)C=C(C)C=C7C[N]3(CC8=CC=CC=[N]84)CC2=C1
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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)
- Ferroptosis inducer-17
- Ferroptosis inducer17
- Ferroptosis inducer 17
- Glutathione Peroxidase
- Cathepsin
- Cyclic GMP-AMP Synthase
- STING
- Ferroptosis
- Reactive Oxygen Species (ROS)
- lysosome-dependent cell death
- ferroptosis
- CTSB
- cisplatin-resistant hepatocellular carcinoma
- GPX4
- cGAS-STING pathway
- cervical cancer
- immunogenic cell death
- human colorectal adenocarcinoma
- Hep G2/DDP
- Inhibitor
- inhibitor
- inhibit