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gemcitabine  (MedChemExpress)


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    Structured Review

    MedChemExpress gemcitabine
    A-B . Clofarabine treatment effectively reversed AC220 (A) and gilteritinib (B) resistance in SPRY3 KO/ FLT3 ITD + MV4-11 AML cells. C-D. Clofarabine treatment effectively reversed AC220 (C) and gilteritinib (D) resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. E. Clofarabine alone exhibited minimal cytotoxicity in MV4-11 AML cells. F-H. Additional RNRis, including fludarabine, <t>gemcitabine,</t> and hydroxyurea, also effectively reversed gilteritinib resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. I . Cladribine, a clinically approved purine nucleoside analog and indirect RNR inhibitor, reversed FLT3i resistance in NRAS mut / FLT3 ITD + AML cells. J. Triapine, a potent RNRi, reversed FLT3i resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. K. Nelarabine, an RNR activator, induced FLT3i resistance in NRAS WT MV4-11 AML cells; this effect was reversed by clofarabine. Data represent the means ± SD of three replicates.
    Gemcitabine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 227 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gemcitabine/Gemcitabine/bio_rxiv__64898__2026__07__21__736123-206-9-28
    Average 97 stars, based on 227 article reviews
    gemcitabine - by Bioz Stars, 2026-09
    97/100 stars

    Images

    1) Product Images from "Ribonucleotide Reductase Inhibition Overcomes FLT3 Inhibitor Resistance in Acute Myeloid Leukemia"

    Article Title: Ribonucleotide Reductase Inhibition Overcomes FLT3 Inhibitor Resistance in Acute Myeloid Leukemia

    Journal: bioRxiv

    doi: 10.64898/2026.07.21.736123

    A-B . Clofarabine treatment effectively reversed AC220 (A) and gilteritinib (B) resistance in SPRY3 KO/ FLT3 ITD + MV4-11 AML cells. C-D. Clofarabine treatment effectively reversed AC220 (C) and gilteritinib (D) resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. E. Clofarabine alone exhibited minimal cytotoxicity in MV4-11 AML cells. F-H. Additional RNRis, including fludarabine, gemcitabine, and hydroxyurea, also effectively reversed gilteritinib resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. I . Cladribine, a clinically approved purine nucleoside analog and indirect RNR inhibitor, reversed FLT3i resistance in NRAS mut / FLT3 ITD + AML cells. J. Triapine, a potent RNRi, reversed FLT3i resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. K. Nelarabine, an RNR activator, induced FLT3i resistance in NRAS WT MV4-11 AML cells; this effect was reversed by clofarabine. Data represent the means ± SD of three replicates.
    Figure Legend Snippet: A-B . Clofarabine treatment effectively reversed AC220 (A) and gilteritinib (B) resistance in SPRY3 KO/ FLT3 ITD + MV4-11 AML cells. C-D. Clofarabine treatment effectively reversed AC220 (C) and gilteritinib (D) resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. E. Clofarabine alone exhibited minimal cytotoxicity in MV4-11 AML cells. F-H. Additional RNRis, including fludarabine, gemcitabine, and hydroxyurea, also effectively reversed gilteritinib resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. I . Cladribine, a clinically approved purine nucleoside analog and indirect RNR inhibitor, reversed FLT3i resistance in NRAS mut / FLT3 ITD + AML cells. J. Triapine, a potent RNRi, reversed FLT3i resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. K. Nelarabine, an RNR activator, induced FLT3i resistance in NRAS WT MV4-11 AML cells; this effect was reversed by clofarabine. Data represent the means ± SD of three replicates.

    Techniques Used:

    Related Articles

    Injection:

    Article Title: Methods and compositions for treating and diagnosing pancreatic cancers
    Article Snippet: .. In select experiments, mice were treated with intraperitoneal injection of gemcitabine (1.2 mg twice weekly; MedChemExpress). .. In other experiments, mice received a single intratumoral injection of recombinant mouse C3a (40 μg/kg; R&D) on day 14 after injections of orthotopic tumors.

    other:

    Article Title: Ribonucleotide Reductase Inhibition Overcomes FLT3 Inhibitor Resistance in Acute Myeloid Leukemia
    Article Snippet: Gilteritinib (HY-12432), AC220 (quizartinib, HY-13001), clofarabine (HY-A0005), fludarabine (HY-B0069), gemcitabine (HY-17026), hydroxyurea (HY-B0313), cladribine (HY-13599), triapine (HY-10082), nelarabine (HY-13701), doxycycline (HY-N0565), and D-luciferin potassium (HY-12591B) were purchased from MedChemExpress.

    Control:

    Article Title: Targeting PLOD2 induces epithelioid differentiation and improves therapeutic response in sarcomatoid renal cell carcinoma
    Article Snippet: Data acquisition and analysis were performed using FlowJo software version 10.8.1 (BD Biosciences, USA). .. Control and PLOD2-ko sccRCC cells were seeded in 96-well plates (2000 cells/well) and cultured in a humidified incubator with 5 % CO2, followed by treatment with varying concentrations of doxorubicin (MedChemExpress, China), gemcitabine (MedChemExpress, China), or everolimus (MedChemExpress, China) for 48 h, or with IFN-α (Genscript, USA) for 72 h prior to CCK8 analysis. .. For co-administration experiments, pre-cultured 786-O sccRCC cells (2000 cells/well) were treated with different concentrations of therapeutic drugs in combination with minoxidil at two mild doses (0.25 mM, 0.5 mM, MedChemExpress, China) for 48 h. For the subsequent CCK8 assay, cells were treated with a mixture of 10 μL CCK8 reagent (Lablead, China) and 90 μL RPMI-1640 medium at 37 °C for 1 h. Absorbance at 450 nm was then measured using a microplate reader (Thermo Fisher Scientific.

    Cell Culture:

    Article Title: Targeting PLOD2 induces epithelioid differentiation and improves therapeutic response in sarcomatoid renal cell carcinoma
    Article Snippet: Data acquisition and analysis were performed using FlowJo software version 10.8.1 (BD Biosciences, USA). .. Control and PLOD2-ko sccRCC cells were seeded in 96-well plates (2000 cells/well) and cultured in a humidified incubator with 5 % CO2, followed by treatment with varying concentrations of doxorubicin (MedChemExpress, China), gemcitabine (MedChemExpress, China), or everolimus (MedChemExpress, China) for 48 h, or with IFN-α (Genscript, USA) for 72 h prior to CCK8 analysis. .. For co-administration experiments, pre-cultured 786-O sccRCC cells (2000 cells/well) were treated with different concentrations of therapeutic drugs in combination with minoxidil at two mild doses (0.25 mM, 0.5 mM, MedChemExpress, China) for 48 h. For the subsequent CCK8 assay, cells were treated with a mixture of 10 μL CCK8 reagent (Lablead, China) and 90 μL RPMI-1640 medium at 37 °C for 1 h. Absorbance at 450 nm was then measured using a microplate reader (Thermo Fisher Scientific.



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    Image Search Results


    A-B . Clofarabine treatment effectively reversed AC220 (A) and gilteritinib (B) resistance in SPRY3 KO/ FLT3 ITD + MV4-11 AML cells. C-D. Clofarabine treatment effectively reversed AC220 (C) and gilteritinib (D) resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. E. Clofarabine alone exhibited minimal cytotoxicity in MV4-11 AML cells. F-H. Additional RNRis, including fludarabine, gemcitabine, and hydroxyurea, also effectively reversed gilteritinib resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. I . Cladribine, a clinically approved purine nucleoside analog and indirect RNR inhibitor, reversed FLT3i resistance in NRAS mut / FLT3 ITD + AML cells. J. Triapine, a potent RNRi, reversed FLT3i resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. K. Nelarabine, an RNR activator, induced FLT3i resistance in NRAS WT MV4-11 AML cells; this effect was reversed by clofarabine. Data represent the means ± SD of three replicates.

    Journal: bioRxiv

    Article Title: Ribonucleotide Reductase Inhibition Overcomes FLT3 Inhibitor Resistance in Acute Myeloid Leukemia

    doi: 10.64898/2026.07.21.736123

    Figure Lengend Snippet: A-B . Clofarabine treatment effectively reversed AC220 (A) and gilteritinib (B) resistance in SPRY3 KO/ FLT3 ITD + MV4-11 AML cells. C-D. Clofarabine treatment effectively reversed AC220 (C) and gilteritinib (D) resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. E. Clofarabine alone exhibited minimal cytotoxicity in MV4-11 AML cells. F-H. Additional RNRis, including fludarabine, gemcitabine, and hydroxyurea, also effectively reversed gilteritinib resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. I . Cladribine, a clinically approved purine nucleoside analog and indirect RNR inhibitor, reversed FLT3i resistance in NRAS mut / FLT3 ITD + AML cells. J. Triapine, a potent RNRi, reversed FLT3i resistance in NRAS mut / FLT3 ITD + MV4-11 AML cells. K. Nelarabine, an RNR activator, induced FLT3i resistance in NRAS WT MV4-11 AML cells; this effect was reversed by clofarabine. Data represent the means ± SD of three replicates.

    Article Snippet: Gilteritinib (HY-12432), AC220 (quizartinib, HY-13001), clofarabine (HY-A0005), fludarabine (HY-B0069), gemcitabine (HY-17026), hydroxyurea (HY-B0313), cladribine (HY-13599), triapine (HY-10082), nelarabine (HY-13701), doxycycline (HY-N0565), and D-luciferin potassium (HY-12591B) were purchased from MedChemExpress.

    Techniques: