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

For research use only. We do not sell to patients.

Fentomycin-1

Fentomycin-1 Chemical Structure

CAS No. : 3095435-04-1

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Fentomycin-1 Related Antibodies

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Description

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[1][2][3].

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.

Fentomycin-1 Related Antibodies

Immunofluorescence[1]

Cell Line: HT-1080 fibrosarcoma cells
Concentration: 1 μM
Incubation Time: 1 h
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.

Cell Viability Assay[1]

Cell Line: HT-1080 fibrosarcoma cells, human primary pancreatic ductal adenocarcinoma (PDAC) cells, human primary sarcoma cells, mouse 4T1 breast cancer cells
Concentration: 1 μM; 2 μM; 10 μM
Incubation Time: 1 h; 6 h; 24 h; 48 h
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.

Cell Proliferation Assay[1]

Cell Line: Doxorubicin-induced drug-tolerant persister (DTP) SUM159 triple-negative breast cancer cells
Concentration: 5 μM
Incubation Time: 72 h
Result: Eradicated doxorubicin-induced DTP SUM159 cells, significantly reducing the number of colonies formed compared to vehicle treatment.
In Vivo

Fentomycin-1 (0.003 mg per animal; intralymphatic; every other day) reduces intranodal tumour growth and increases tumour-size-based survival in a mouse model of triple-negative breast cancer metastasis by targeting CD44high iron-rich cancer cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Balb/c (female, 6-8 weeks old, syngeneic 4T1 triple-negative breast cancer intranodal metastasis model)[1]
Dosage: 0.003 mg per animal
Administration: intralymphatic; every other day
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.
Molecular Weight

947.17

Formula

C56H66N8O6
CAS No.
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
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
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References
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Fentomycin-1 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:

Fentomycin-13095435-04-1Fentomycin1Fentomycin 1FerroptosisReactive Oxygen Species (ROS)UPS cellssarcomapancreatic ductal adenocarcinomaHT-1080 cellsSUM159 triple-negative breast cancer cellsCD44high cancer cellslysosomal iron(II)murine breast cancer modelsferroptosis4T1 cellsInhibitorinhibitorinhibit

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