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carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (fccp) (uncoupling agent)  (Merck KGaA)

 
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    Merck KGaA carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (fccp) (uncoupling agent)
    Carbonyl Cyanide 4 (Trifluoromethoxy)phenylhydrazone (Fccp) (Uncoupling Agent), supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fccp+(uncoupling+agent)/carbonyl+cyanide+4++trifluoromethoxy++phenylhydrazone++fccp+/pmc08466145-87-22-32
    Average 90 stars, based on 1 article reviews
    carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (fccp) (uncoupling agent) - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Injection:


    Article Title: Dynasore Blocks Ferroptosis through Combined Modulation of Iron Uptake and Inhibition of Mitochondrial Respiration
    Article Snippet: Oligomycin (ATP synthase inhibitor) (Merck KGaA, Darmstadt, Germany) was injected into port A (20 μL) at a final concentration of 3 μM, FCCP (uncoupling agent) (22.5 μL into port B) (Merck KGaA, Darmstadt, Germany) at a concentration of 0.5 μM, rotenone/antimycin A (complex I/III inhibitors) (25 μL into port C) (Merck KGaA, Darmstadt, Germany) at a concentration of 100 nM and 1 μM and 2-deoxyglucose (Carl Roth GmbH, Karlsruhe, Germany) (glycolysis inhibitor) at a concentration of 50 mM (27.5 μL into port D), respectively.

    Concentration Assay:


    Article Title: Dynasore Blocks Ferroptosis through Combined Modulation of Iron Uptake and Inhibition of Mitochondrial Respiration
    Article Snippet: Oligomycin (ATP synthase inhibitor) (Merck KGaA, Darmstadt, Germany) was injected into port A (20 μL) at a final concentration of 3 μM, FCCP (uncoupling agent) (22.5 μL into port B) (Merck KGaA, Darmstadt, Germany) at a concentration of 0.5 μM, rotenone/antimycin A (complex I/III inhibitors) (25 μL into port C) (Merck KGaA, Darmstadt, Germany) at a concentration of 100 nM and 1 μM and 2-deoxyglucose (Carl Roth GmbH, Karlsruhe, Germany) (glycolysis inhibitor) at a concentration of 50 mM (27.5 μL into port D), respectively.



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    Metabolic flux analysis of TKI-treated T cells. Human T cells were treated with/without the TKIs asciminib (blue), imatinib (yellow), dasatinib (orange) or nilotinib (green), stimulated with/without αCD2/3/28-beads for 72 h and analyzed via metabolic flux analysis ( n = 3–4 different donors, n = 7–8 different donors for controls). a Metabolic phenotype. Measuring of OCR and ECAR before addition of metabolic inhibitors. b Mitochondrial stress test. Oligomycin (Oligo), carbonyl <t>cyanide-4</t> (trifluoromethoxy) phenylhydrazone (FCCP) and rotenone/antimycin A (Rot/AA) were successively added, OCR was measured and metabolic parameters (basal respiration, maximal respiration and spare respiratory capacity; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. c Glycolysis stress test. Glucose, Oligo and 2-deoxy- d -glucose (2-DG) were successively added, ECAR was measured and metabolic parameters (basal glycolysis, glycolytic capacity, and glycolytic reserve; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. Measurements were normalized to the respective TKI-untreated controls. Norm normalized, uc unstimulated control (no bead addition), OCR oxygen consumption rate, ECAR extracellular acidification rate, ** p < 0.01, * p < 0.05
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    Metabolic flux analysis of TKI-treated T cells. Human T cells were treated with/without the TKIs asciminib (blue), imatinib (yellow), dasatinib (orange) or nilotinib (green), stimulated with/without αCD2/3/28-beads for 72 h and analyzed via metabolic flux analysis ( n = 3–4 different donors, n = 7–8 different donors for controls). a Metabolic phenotype. Measuring of OCR and ECAR before addition of metabolic inhibitors. b Mitochondrial stress test. Oligomycin (Oligo), carbonyl <t>cyanide-4</t> (trifluoromethoxy) phenylhydrazone (FCCP) and rotenone/antimycin A (Rot/AA) were successively added, OCR was measured and metabolic parameters (basal respiration, maximal respiration and spare respiratory capacity; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. c Glycolysis stress test. Glucose, Oligo and 2-deoxy- d -glucose (2-DG) were successively added, ECAR was measured and metabolic parameters (basal glycolysis, glycolytic capacity, and glycolytic reserve; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. Measurements were normalized to the respective TKI-untreated controls. Norm normalized, uc unstimulated control (no bead addition), OCR oxygen consumption rate, ECAR extracellular acidification rate, ** p < 0.01, * p < 0.05
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    Metabolic flux analysis of TKI-treated T cells. Human T cells were treated with/without the TKIs asciminib (blue), imatinib (yellow), dasatinib (orange) or nilotinib (green), stimulated with/without αCD2/3/28-beads for 72 h and analyzed via metabolic flux analysis ( n = 3–4 different donors, n = 7–8 different donors for controls). a Metabolic phenotype. Measuring of OCR and ECAR before addition of metabolic inhibitors. b Mitochondrial stress test. Oligomycin (Oligo), carbonyl <t>cyanide-4</t> (trifluoromethoxy) phenylhydrazone (FCCP) and rotenone/antimycin A (Rot/AA) were successively added, OCR was measured and metabolic parameters (basal respiration, maximal respiration and spare respiratory capacity; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. c Glycolysis stress test. Glucose, Oligo and 2-deoxy- d -glucose (2-DG) were successively added, ECAR was measured and metabolic parameters (basal glycolysis, glycolytic capacity, and glycolytic reserve; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. Measurements were normalized to the respective TKI-untreated controls. Norm normalized, uc unstimulated control (no bead addition), OCR oxygen consumption rate, ECAR extracellular acidification rate, ** p < 0.01, * p < 0.05
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    Image Search Results


    Metabolic flux analysis of TKI-treated T cells. Human T cells were treated with/without the TKIs asciminib (blue), imatinib (yellow), dasatinib (orange) or nilotinib (green), stimulated with/without αCD2/3/28-beads for 72 h and analyzed via metabolic flux analysis ( n = 3–4 different donors, n = 7–8 different donors for controls). a Metabolic phenotype. Measuring of OCR and ECAR before addition of metabolic inhibitors. b Mitochondrial stress test. Oligomycin (Oligo), carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone (FCCP) and rotenone/antimycin A (Rot/AA) were successively added, OCR was measured and metabolic parameters (basal respiration, maximal respiration and spare respiratory capacity; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. c Glycolysis stress test. Glucose, Oligo and 2-deoxy- d -glucose (2-DG) were successively added, ECAR was measured and metabolic parameters (basal glycolysis, glycolytic capacity, and glycolytic reserve; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. Measurements were normalized to the respective TKI-untreated controls. Norm normalized, uc unstimulated control (no bead addition), OCR oxygen consumption rate, ECAR extracellular acidification rate, ** p < 0.01, * p < 0.05

    Journal: Cancer Immunology, Immunotherapy

    Article Title: Effects of the STAMP-inhibitor asciminib on T cell activation and metabolic fitness compared to tyrosine kinase inhibition by imatinib, dasatinib, and nilotinib

    doi: 10.1007/s00262-022-03361-8

    Figure Lengend Snippet: Metabolic flux analysis of TKI-treated T cells. Human T cells were treated with/without the TKIs asciminib (blue), imatinib (yellow), dasatinib (orange) or nilotinib (green), stimulated with/without αCD2/3/28-beads for 72 h and analyzed via metabolic flux analysis ( n = 3–4 different donors, n = 7–8 different donors for controls). a Metabolic phenotype. Measuring of OCR and ECAR before addition of metabolic inhibitors. b Mitochondrial stress test. Oligomycin (Oligo), carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone (FCCP) and rotenone/antimycin A (Rot/AA) were successively added, OCR was measured and metabolic parameters (basal respiration, maximal respiration and spare respiratory capacity; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. c Glycolysis stress test. Glucose, Oligo and 2-deoxy- d -glucose (2-DG) were successively added, ECAR was measured and metabolic parameters (basal glycolysis, glycolytic capacity, and glycolytic reserve; exemplarily illustrated for αCD2/3/28-bead-stimulated control) were calculated. Measurements were normalized to the respective TKI-untreated controls. Norm normalized, uc unstimulated control (no bead addition), OCR oxygen consumption rate, ECAR extracellular acidification rate, ** p < 0.01, * p < 0.05

    Article Snippet: For the mitochondrial stress test (Agilent Technologies, California, USA), the cartridge ports were loaded with 1 µM of the mitochondrial ATP synthase inhibitor oligomycin (Oligo, Sigma-Aldrich), 1.5 µM of the uncoupling agent carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone (FCCP, Sigma-Aldrich) and 3 µM of the complex I/III oxPhos inhibitors rotenone (Rot, Sigma-Aldrich) and antimycin A (AA, Sigma-Aldrich).

    Techniques: