Fentomycin-1
Fentomycin-1 is a ferroptosis inducer. Fentomycin-1 activates lysosomal iron2+ under acidic conditions with hydrogen peroxide to form a reactive iron-oxo species, which induces oxidative degradation, oxidation, and lipolysis of membrane phospholipids, triggering ferroptosis. Fentomycin-1 can be used for the research of pancreatic ductal adenocarcinoma, breast cancer metastasis, and melanoma.
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- No. CAS: 3095435-04-1
- Fòrmula: C56H66N8O6
- Peso molecular:947.17
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
Descripciòn
In Vitro
Fentomycin-1 enhances iron-mediated oxidation of unsaturated phospholipids in a cell-free lysosome-like environment[1].
Fentomycin-1 (1 μM; 1 h) localizes to the plasma membrane under low endocytic flux conditions and accumulates in the endolysosomal compartment of HT-1080 cells at physiological temperature[1].
Fentomycin-1 (1-10 μM; 1-48 h) induces ferroptosis in HT-1080, primary PDAC, primary sarcoma, and 4T1 cells via membrane phospholipid oxidation[1].
Fentomycin-1 (Sublethal doses; 48 h) induces HT-1080 cells to acquire a ferroptosis-resistant, epithelial-like cell state characterized by upregulated ferroptosis suppressors, lysosome-associated proteins, and lipid metabolism pathways, alongside downregulated mesenchymal markers and iron homeostasis proteins[1].
Fentomycin-1 (5 μM; 72 h) eradicates Doxorubicin (HY-15142A)-induced drug-tolerant persister SUM159 triple-negative breast cancer cells in vitro[1].
Fentomycin-1 (1 μM; 24 h) reduces the CD44high subpopulation in primary human PDAC and UPS cells via ferroptosis[1].
Fentomycin-1 specifically activates lysosomal iron to induce ferroptosis and selectively targets iron-rich CD44high cancer cells[2].
Fentomycin-1 increases FSP1 mRNA levels in HT-1080 cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HT-1080 fibrosarcoma cells
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Concentration:1 μM
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Incubation Time:1 h
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Result:Localized to the plasma membrane under low endocytic flux conditions.
Accumulated in the endolysosomal compartment, colocalizing with LysoTracker, at 37°C.
Showed stronger endolysosomal accumulation than untethered Chen-White ligand, which had weak pan-cellular staining.
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Cell Line:HT-1080 fibrosarcoma cells, human primary pancreatic ductal adenocarcinoma (PDAC) cells, human primary sarcoma cells, mouse 4T1 breast cancer cells
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Concentration:1 μM; 2 μM; 10 μM
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Incubation Time:1 h; 6 h; 24 h; 48 h
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Result:Induced oxidation of membrane phospholipids in HT-1080 cells to a greater extent than well-established ferroptosis inducers.
Reduced phospholipid oxidation levels when co-treated with α-tocopherol, deferiprone, and liproxstatin-1.
Reduced cell viability, with cell death antagonized by ferroptosis inhibitors but not by apoptosis or necroptosis inhibitors.
Left residual toxicity despite ferroptosis inhibitor treatment.
Increased levels of lysophospholipids and glycerol, indicating oxidized phospholipid degradation.
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Cell Line:Doxorubicin-induced drug-tolerant persister (DTP) SUM159 triple-negative breast cancer cells
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Concentration:5 μM
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Incubation Time:72 h
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Result:Eradicated doxorubicin-induced DTP SUM159 cells, significantly reducing the number of colonies formed compared to vehicle treatment.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Balb/c (female, 6-8 weeks old, syngeneic 4T1 triple-negative breast cancer intranodal metastasis model)[1]
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Dosage:0.003 mg per animal
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Administration:intralymphatic; every other day
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Result:Reduced intranodal tumour volume compared with vehicle control on day 10 post-treatment initiation.
Increased tumour-size-based survival, with a Mantel-Cox log-rank test P value of 8.7×10-5 compared with vehicle.
Reduced abundance of CD44high cancer cells from 20.2% in vehicle-treated mice to 11.0% in treated mice.
Increased oxidation of membrane phospholipids in residual tumours.
Caused no adverse effects on body weight.
Chemical Information
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No. CAS 3095435-04-1
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Peso molecular 947.17
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Fòrmula C56H66N8O6
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SMILES
O=C(C1=C(C2=C(C=C(C=C2)C)C=C1)C3=O)C4=C3C=CC5=C4N[C@@]6(C)C(OC(CCC(NCCCCNC7=CC=NC(CN8CCC[C@H]8[C@@H]9CCCN9CC%10=CC(N(C)C)=CC=N%10)=C7)=O)=O)[C@H](C)O[C@]5([H])C6
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Cañeque T, et al. Activation of lysosomal iron triggers ferroptosis in cancer. Nature. 2025;642(8067):492-500. [Content Brief]
[2]. Ali Boubacar K, et al. Regulation of ferroptosis by BAP1. Cell Death Differ. 2026 Jan 23. [Content Brief]
[3]. Palma M, et al. Lymph node environment drives FSP1 targetability in metastasizing melanoma. Nature. 2026;649(8096):477-486. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Fentomycin-1 Related Classifications
HY-186196 Related Classifications
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Keywords
- Fentomycin-1
- 3095435-04-1
- Fentomycin1
- Fentomycin 1
- Ferroptosis
- Reactive Oxygen Species (ROS)
- UPS cells
- sarcoma
- pancreatic ductal adenocarcinoma
- HT-1080 cells
- SUM159 triple-negative breast cancer cells
- CD44high cancer cells
- lysosomal iron(II)
- murine breast cancer models
- ferroptosis
- 4T1 cells
- Inhibitor
- inhibitor
- inhibit