Bendamustine HCl

2 years -80 in solvent

Administered via i.v.

SU-DHL-1 and SU-DHL-9 cells

0-100 uM

Control

DNA single- and double-strand breaks caused by Bendamustine are more extensive and significantly more durable than those caused by cyclophosphamide, cisplatinum, or carmustine. Bendamustine specifically regulates, transcriptionally and posttranslationally, genes involved in apoptosis, DNA repair, and mitotic checkpoints. Bendamustine uniquely regulates DNA repair pathways in non–Hodgkin's lymphoma cells compared with other alkylators. Bendamustine inhibits mitotic checkpoints and induces mitotic catastrophe. Treatment with Bendamustine results in a 60% to 80% down-regulation of the mRNA expression of all three of these genes [polo-like kinase 1 (PLK-1), Aurora Kinase A, and cyclin B1] in SU-DHL-9 cells. Twenty-six percent of the Bendamustine-treated MCF-7/ADR cells showed micronucleation compared with only 6% in DMSO control cells. [1] Using Bendamustine alone in concentrations from 1 ug/mL to 50 ug/mL, a dose- and time-dependent manner of cytotoxicity from 30.4% to 94.8% after 48 hours could be observed. e LD50 for untreated and pretreated CLL cells is 7.3 or 4.4 ug /mL, respectively. [2] Myeloid and breast carcinoma cell lines are resistant towards Bendamustine with the exception of HL-60 cells which exhibit an intermediate sensitivity. Bendamustine is found to have a very low clastogenic effect as compared with equimolar doses of lomustine. [3]

72 hours

DMSO 79 mg/mL, Water 15 mg/mL, Ethanol 17 mg/mL