Fludarabine (Fludarabinum) is a fluorinated purine analog, an inhibitor of nucleic acid synthesis and an inhibitor of STAT1 activation. Fludarabine has antitumor activity and can be used for the treatment of leukemia and lymphoma.

MM.1S cells:13.48 µg/mL, HeLa cells:16 μM, MM.1R cells:33.79 µg/mL, HepG2 cells:20 μM, Mahlavu cells:10 μM, RPMI8226 cells:1.54 µg/mL, T47D cells:46.2 μM, PBMC cells:1.9 μM, MCF-7 cells:15 μM, A549 cells:47.44 μM, K562 cells:0.26 μM, CCRF-CEM cells:19.49 μM, HCT116 cells:6.6 μM

METHODS: Multiple myeloma cells RPMI8226, MM.1S and MM.1R were treated with Fludarabine (0-64 µg/mL) for 24-48 h. Cell viability was measured by MTT Assay.
RESULTS: Fludarabine dose-time-dependently inhibited the proliferation of RPMI8226 cells with an IC50 of 1.54 µg/mL at 24 h. At 48 h, the IC50 of Fludarabine on MM.1S and MM.1R cells was 13.48 µg/mL and 33.79 µg/mL, respectively. [1]
METHODS: Rat aortic VSMCs were treated with Fludarabine (50 µM) and FBS for 30 min, and the expression levels of target proteins were detected by Western Blot.
RESULTS: FBS stimulation produced progressive JAK2 and STAT-1 activation, and Fludarabine induced a significant reduction in STAT-1 phosphorylation, while it did not alter JAK2 activation. [2]

METHODS: To assay antitumor activity in vivo, Fludarabine (8-40 mg/kg) was injected intraperitoneally into SCID mice bearing multiple myeloma RPMI8226 once daily for three days.
RESULTS: The antitumor activity of Fludarabine in vivo was demonstrated by a less than 5-fold increase in tumors treated with 40 mg/kg of Fludarabine over 25 days compared to an approximately 10-fold increase in control tumors. [1]
METHODS: To study the effect on graft-versus-host disease (GVHD), Fludarabine (0.8 mg/kg) was administered intraperitoneally to (BALB/c x C57BL/6) F1 mice harboring B-cell leukemia (BCL-1) every two weeks for five days in two cycles, followed by intraperitoneal injection of cyclophosphamide (400 mg/kg).
RESULTS: Mice treated with a Fludarabine-containing regimen prior to transplantation also had much less GVHD clinically and at necropsy, while graft-versus-leukemia appeared to be increased in the same animals. [3]

VSMCs were isolated from the aorta of male Wistar rats weighing ～350–500 g, as previously described. For cell culture experiments, 2 × 10^5 rat VSMCs were plated in Dulbecco's modified Eagle's medium (DMEM) with 10% fetal bovine serum (FBS). Semiconfluent VSMCs were starved by incubation in 0.5% FBS/DMEM for 36–48 h and then serum-stimulated with normal growth medium (i.e., DMEM containing 10% FBS) in the presence or absence of fludarabine (50 μM) [2].

The animals in this study were handled according to the animal welfare regulation of the Magna Graecia University of Catanzaro, and the protocol was approved by the animal use committee of this institution. Fifty Wistar rats weighing 340 ± 40 g were anesthetized with an intramuscular injection of 100 mg/kg ketamine and 5 mg/kg xylazine. Angioplasty of the common carotid artery was performed using a balloon embolectomy catheter, as previously described and well validated in our laboratory. Fludarabine was dissolved in 30% pluronic F127 gel to the final concentrations of 2.5, 5, 15, or 25 mg/ml. At the time of balloon injury, gel containing fludarabine or vehicle was applied around the middle segment (2 cm in length) of the right injured carotid artery (0.1 ml per 1-cm length of the artery segment, equivalent to 0.5, 1, 3, or 5 mg of total fludarabine locally delivered), as previously described. As a control experiment, 200 μl of fludarabine/gel solution (25 mg/ml) were applied around the sham-operated carotid artery. To study the fludarabine toxicity, laboratory studies were performed at baseline and 2 wk after drug local delivery (25 mg/ml). Arterial pressure and heart rate were measured indirectly by a tail-cuff plethysmographic technique [2].

DMSO: 240 mg/mL (841.43 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 2.86 mg/mL (10.03 mM), Solution.