Ac-MtFluNox
Ac-MtFluNox is a mitochondria-targeted Fluorescent probe that can be used for the selective detection of labile Fe (II). Ac-MtFluNox can enter living cells, where intracellular esterases cleave its acetyl protecting group to generate activated MtFluNox. Ac-MtFluNox functions through an Fe (II)-mediated deoxygenation mechanism of its amine N-oxide group, which eliminates the fluorescence quenching effect and oxidizes Fe (II) to Fe (III) to deplete the catalytically active Fe (II) pool. A FITC filter set (excitation 465-500 nm, emission 516-556 nm) is used for live-cell imaging. Ac-MtFluNox can be applied to studies related to myocardial ferroptosis.
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- Formel: C48H42F6N2O7P2
- Molecular Weight:934.79
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
Guide (The following is our recommended protocol. This protocol is for guidance only and should be modified according to your specific needs).
1. Stock Solution Preparation
1.1 Solvent: DMSO.
1.2 Concentration recommendation: 1 mM.
2. Working Solution Preparation
2.1 Diluent: HBSS; MEM without FBS.
2.2 Working concentration: 1 μM, 2 μM, 5 μM.
2.3 Note: Adjust working solution concentration as needed; prepare fresh before use.
3. Staining Procedure
3.1 Sample type descriptions
3.1.1 For adherent cultured cells[1][2]: Includes HepG2 cells, HEK293 cells, HT1080 cells; no trypsinization required prior to staining.
3.2 Incubation conditions
3.2.1 For adherent cultured cells[1]: Incubate with 1-5 μM Ac-MtFluNox in HBSS or MEM without FBS at 37°C for 30 min-3 h; co-staining with 0.5 μM MitoTracker® Deep Red FM is optional during incubation.
3.3 Washing steps
3.3.1 For adherent cultured cells[1]: Wash once with MEM without FBS before incubation; wash once with HBSS after incubation.
4. Controls
4.1 Set up negative controls using equal volumes of vehicles instead of Fe(II), succinylacetone, or NOC-5.
4.2 Set up competitive inhibition controls with Fe(II) chelator 2,2′-bipyridyl or iron scavenger deferroxamine.
5. Detection & Analysis
5.1 Instrument type: Confocal fluorescence microscope; fluorescence microscope.
5.2 Ex/Em wavelengths: Excitation 465-500 nm, emission 516-556 nm (FITC filter set).
5.3 Result analysis
5.3.1 Fluorescence intensity changes: Turn-on fluorescence enhancement upon reaction with mitochondrial labile Fe(II); intensity is reduced in the presence of Fe(II) chelators.
5.3.2 Fluorescence localization: Fluorescence colocalizes with mitochondria (confirmed by co-staining with MitoTracker® Deep Red FM).
5.3.3 Color changes: Green fluorescence; fluorescence emission specific to labile Fe(II) detection via N-oxide deoxygenation mechanism.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Molecular Weight 934.79
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Formel C48H42F6N2O7P2
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SMILES
CC(OC1=CC=C2C(OC3=C(C24OC(C5=C4C=CC=C5)=O)C=CC([N+]6(CCN(CC6)C(CCC[P+](C7=CC=CC=C7)(C8=CC=CC=C8)C9=CC=CC=C9)=O)[O-])=C3)=C1)=O.F[P-](F)(F)(F)(F)F
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)