Catalog No.S1491 Synonyms: FaraA, Fludarabinum
Molecular Weight(MW): 285.23
Fludarabine is a STAT1 activation inhibitor which causes a specific depletion of STAT1 protein (and mRNA) but not of other STATs. Also a DNA synthesis inhibitor in vascular smooth muscle cells.
Cited by 10 Publications
5 Customer Reviews
ERK signaling regulates STAT1 phosphorylation, and pSTAT1 modulates MHC II expression in the spinal cord under BCP conditions. AG490 (5 μg in 10 μL), Fludarabine (10 μg in 10 μL), or U0126 (5 μg in 10 μL) was intrathecally injected into cancer-bearing rats once a day for 14 days, beginning immediately after carcinoma cell inoculation (n = 3 in each group). (A) Representative western blot showing pSTAT1ser727, total STAT1, pERK42/44, total ERK42/44, CIITA, MHC II RTIB, and b actin protein levels in the spinal cords of BCP rats.
Brain Behav Immun, 2017, 60:161-173. Fludarabine purchased from Selleck.
Imatinib mesylate (IM) in combination of fludarabine phosphate (F-AMP) significantly inhibits Ki67 and c-KIT expression in GIST-T1 tumor xenografts. Tumors were collected on the day after the last treatment and were then subjected to immunohistochemical detection of Ki67 and c-KIT expression. Representative images of immunohistochemical staining of Ki67 and c-KIT in mice tumors.
Mol Cancer Ther, 2014, 13(10): 2276-87 . Fludarabine purchased from Selleck.
Bacterial infection in IPEC-J2 cells. The invasion and attachment of EHECO157:H7 was increased in the IPEC-J2 cells in the presence of 10 μM fludarabine. Data are expressed as the mean ± SEM (n= 6). Differences between groups were determined by paired samples t-test. *P<0.05 compared with the control.
Int Immunopharmacol, 2016, 36:199-204.. Fludarabine purchased from Selleck.
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|Description||Fludarabine is a STAT1 activation inhibitor which causes a specific depletion of STAT1 protein (and mRNA) but not of other STATs. Also a DNA synthesis inhibitor in vascular smooth muscle cells.|
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.  Fludarabine induces significant reduction of STAT-1 phosphorylation, whereas it does not change JAK2 activation. Interestingly, Fludarabine does not significantly affect the phosphorylation of these three STAT proteins. Fludarabine (1.5 mg) significantly prevents STAT-1 phosphorylation and also reduces the increased amount of this protein. No significant changes are demonstrated in JAK2 phosphorylation at 2 days, but Fludarabine inhibits JAK2-increased expression at 7 days. Fludarabine specifically inhibits STAT-1 activation without affecting other STAT proteins and consequently diminishes VSMC proliferation. 
|In vivo||Tumors 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. |
-  Meng H, et al. Eur J Haematol. 2007, 79(6), 486-493.
-  Brachwitz H, et al. Bioorg Med Chem. 1999, 7(6), 1195-1200.
-  Fernández-Calotti P, et al. Int Immunopharmacol. 2006, 6(5), 715-72
|In vitro||DMSO||57 mg/mL (199.83 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
|30 mg/mL (suspension)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01503242||Active not recruiting||Plasma Cell Myeloma|Refractory Plasma Cell Myeloma||Fred Hutchinson Cancer Research Center|National Cancer Institute (NCI)||January 9 2012||Phase 1|
|NCT03159702||Recruiting||Hematological Malignancy Undergoing a Related Donor Haploidentical HCT|Leukemia|Multiple Myeloma|Lymphoma||Medical College of Wisconsin||December 8 2017||Phase 2|
|NCT03333486||Recruiting||Accelerated Phase Chronic Myelogenous Leukemia BCR-ABL1 Positive|Acute Leukemia in Remission|Acute Lymphoblastic Leukemia|Acute Myeloid Leukemia|Acute Myeloid Leukemia With FLT3/ITD Mutation|Acute Myeloid Leukemia With Gene Mutations|Aplastic Anemia|B-Cell Non-Hodgkin Lymphoma|CD40 Ligand Deficiency|Chronic Granulomatous Disease|Chronic Leukemia in Remission|Chronic Lymphocytic Leukemia|Chronic Myelogenous Leukemia BCR-ABL1 Positive|Chronic Myelomonocytic Leukemia|Chronic Phase Chronic Myelogenous Leukemia BCR-ABL1 Positive|Congenital Amegakaryocytic Thrombocytopenia|Congenital Neutropenia|Congenital Pure Red Cell Aplasia|Glanzmann Thrombasthenia|Immunodeficiency Syndrome|Myelodysplastic Syndrome|Myelofibrosis|Myeloproliferative Neoplasm|Paroxysmal Nocturnal Hemoglobinuria|Plasma Cell Myeloma|Polycythemia Vera|Recurrent Non-Hodgkin Lymphoma|Refractory Non-Hodgkin Lymphoma|Secondary Acute Myeloid Leukemia|Secondary Myelodysplastic Syndrome|Severe Aplastic Anemia|Shwachman-Diamond Syndrome|Sickle Cell Disease|T-Cell Non-Hodgkin Lymphoma|Thalassemia|Waldenstrom Macroglobulinemia|Wiskott-Aldrich Syndrome||Roswell Park Cancer Institute|National Cancer Institute (NCI)||December 7 2017||Phase 2|
|NCT00448201||Completed||Chronic Myeloproliferative Disorders|Leukemia|Lymphoma|Multiple Myeloma and Plasma Cell Neoplasm|Myelodysplastic Syndromes||UNC Lineberger Comprehensive Cancer Center|National Cancer Institute (NCI)||January 7 2011||Phase 2|
|NCT00474747||Completed||Aplastic Anemia||M.D. Anderson Cancer Center|National Heart Lung and Blood Institute (NHLBI)|National Cancer Institute (NCI)||February 7 2006||Phase 1|Phase 2|
|NCT03494569||Recruiting||Acute Lymphoblastic Leukemia|Acute Lymphoblastic Leukemia in Remission|Acute Myeloid Leukemia|Acute Myeloid Leukemia in Remission|Hematopoietic Cell Transplantation Recipient|Minimal Residual Disease|Myelodysplastic Syndrome|Secondary Acute Myeloid Leukemia||City of Hope Medical Center|National Cancer Institute (NCI)||July 6 2018||Phase 1|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
how to re-suspend and deliver the inhibitor for in vivo experiments?
For S1491, Fludarabine, we tested a vehicle: 30% Propylene glycol, 5% Tween 80, 65% D5W that you can resuspend the compound in at up to 30mg/ml. It's a suspension and can only be given via oral gavage.