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dfmo  (Lonza)


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Bioz Manufacturer Symbol Lonza manufactures this product  
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    Structured Review

    Lonza dfmo
    Dfmo, supplied by Lonza, 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/dfmo/dfmo/pm22640800-161-9-13
    Average 90 stars, based on 1 article reviews
    dfmo - by Bioz Stars, 2026-11
    90/100 stars

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    Related Articles

    Incubation:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.

    Inhibition:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.

    Concentration Assay:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.

    MTT Assay:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.

    Saline:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.

    Expressing:

    Article Title: Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formation.
    Article Snippet: We thank Tony Pegg and Lisa Shantz for providing ODC antibody, Lonza Biochemicals for providing DFMO, Martine Roussel and Charles Sherr for providing ArfGFP/GFP mice, and Elsie White for technical assistance.



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    (A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of <t>DFMO</t> (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).
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    (A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of <t>DFMO</t> (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).
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    Image Search Results


    (A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of DFMO (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).

    Journal: Molecular cancer therapeutics

    Article Title: QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp–overexpressing cancer models

    doi: 10.1158/1535-7163.MCT-25-1013

    Figure Lengend Snippet: (A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of DFMO (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).

    Article Snippet: Paclitaxel was purchased from LC Laboratories; colchicine and verapamil from Sigma; and Q-VD-OPh (QVD), tariquidar, DFMO (eflornithine), and MLN8237 from MedChemExpress.

    Techniques: Activity Assay, MTS Assay, Western Blot, Marker, Control