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    Fludarabine (NSC 118218)
    Fludarabine (NSC 118218)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1379
    CAS #: 21679-14-1Purity ≥98%

    Description: Fludarabine (also known as FaraA, Fludarabinum; NSC-118218; F-ara-A, HSDB6964; NSC118218; HSDB-6964) is a potent STAT1 activation inhibitor and a DNA synthesis inhibitor that has been approved as a chemotherapeutic drug for the treatment of leukemia and lymphoma. Fludarabine is a prodrug and is phosphorylated to the nucleoside triphosphate (F-ara-ATP) in cells to elicit biological activity. It affected a series of enzymes that required in DNA synthesis such as DNA primase, DNA polymerases, DNA ligase I, ribonucleotide reductase and 3'-5' exonuclease activity of DNA polymerases δ and ε. In human myeloma cell RPMI8226, fludarabine significantly inhibited cells growth and reduced phosphorylation of Akt.

    References: Eur J Haematol. 2007 Dec;79(6):486-93; Bioorg Med Chem. 1999 Jun;7(6):1195-200.

    Related CAS#: 75607-67-9 (Fludarabine phosphate); 21679-14-1 (free base)

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    Molecular Weight (MW)285.23
    CAS No.21679-14-1 (Fludarabine free);
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 57 mg/mL (199.8 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)30% propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
    SynonymsFaraA, Fludarabinum; HSDB 6964; F-ara-A, HSDB6964; NSC118218; HSDB-6964; NSC 118218; F-ara A, NSC-118218

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    In Vitro

    In vitro activity: Fludarabine efficiently inhibits the proliferation of RPMI 8226 cells with IC50 of 1.54 μg/mL. The IC50 of Fludarabine against MM.1S and MM.1R cells is 13.48 μg/mL and 33.79 μg/mL, respectively. In contrast, U266 cells are resistant to Fludarabine with IC50 of 222.2 μg/mL. Fludarabine treatment results in increased number of cells in the G1 phase of cell cycle, accompanied with a concomitant reduction of cells at the S phase of cell cycle in a time-dependent manner. Fludarabine induces a cell cycle block and triggers apoptosis in MM cells. Fludarabine triggers time-dependent cleavage of caspase-8, -9, and -3, -7, followed by PARP cleavage. Fludarabine increases expression of Bax in a time-dependent fashion, while the expression of Bak doesn't change. After exposure to Fludarabine for 12 hours, RPMI 8226 cells shows a loss of membrane potential with 61.05% of the cells expressing low fluorescence of rhodamine 123 compared with 8.62% of cells in untreated control. To enhance solubility, Fludarabine is formulated as the monophosphate (F-ara-AMP, fudarabine), which is instantaneously and quantitatively dephosphorylated to the parent nucleoside upon intravenous infusion. Inside the cells rephosphorylation occurs which leads to fuoroadenine arabinoside triphosphate (F-ara-ATP), the major cytotoxic metabolite of F-ara-A. Fludarabine can also induce pro-inflammatory stimulation of monocytic cells, as evaluated by increased expression of ICAM-1 and IL-8 release. Fludarabine does not affect the growth of ovarian cancer cell lines, whereas it induces marked and dose-dependent inhibition of proliferation in melanoma cell lines.

    Cell Assay: After treated with Fludarabine or control, dexamethasone-sensitive (MM.1S) and -resistant (MM.1R) human MM cell lines, RPMI8226 and U266 cell lines (5 × 105 cells) are washed twice in phosphate-buffered saline (PBS) and fixed with 70% ice-cold ethanol, then centrifuged and suspended in PBS containing 100 μg/mL RNase A. After incubated for 30 minutes at 37 ºC, samples are resuspended in 25 μg/mL propidium iodide. Flow cytometry is performed on a FACSCalibur automated system. Apoptosis is determined by Annexin V-FITC apoptosis detection kit, according to the manufacturer's instructions. For TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling) assay, cells are analyzed by flow cytometry using the in situ cell death detection kit.

    In VivoTumors treated with PBS grow rapidly to approx-imately 10-fold their initial volume in 25 day, whereas, the tumors in the Fludarabine at 40 mg/kg increase less than 5-fold. A significant antitumor effect of 40 mg/kg Fludarabine on RPMI8226 tumor growth is demonstrated. RPMI8226 tumors treated with 40 mg/kg Fludarabine at day 10 increase apoptotic nuclei. Fludarabine is effective in suppressing RPMI8226 myeloma xenografts in SCID mice.
    Animal modelSevere combined immunodeficient (SCID) mice bearing RPMI 8226 cells
    Formulation & DosageDissolved in PBS; 40 mg/kg; i.p. injection

    Eur J Haematol. 2007 Dec;79(6):486-93; Bioorg Med Chem. 1999 Jun;7(6):1195-200.

    These protocols are for reference only. InvivoChem does not independently validate these methods.



    Effects of fludarabine on survival pathways. Eur J Haematol. 2007 Dec;79(6):486-93.
    Antitumoral efficacy of fludarabine in established RPMI8226 tumors in vivo. Eur J Haematol. 2007 Dec;79(6):486-93.


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