Catalog No.S1212 Synonyms: SDX-105 (Cytostasane) HCl
Molecular Weight(MW): 394.72
Bendamustine HCL is a DNA-damaging agent with IC50 of 50 μM in cell-free assay.
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Cells were grown for 6-8 days in presence of increasing concentrations of (I) bendamustine. Relative toxicity of the drugs was determined by the WST-8 cell proliferation assay, Dashed lines with open circles or triangles indicate cell proliferation in absence of an anti-lymphoma drug. Other curves represent the cells grown in increasing concentrations (indicated by the associated number) of the tested drug. Maximal absorbance (highest number of viable cells) of cells grown without an anti-lymphoma agent in each experiment was set as 100%. Standard deviations were < 5% for all measurements.
PLoS One, 2015, 10(8):e0135314.. Bendamustine HCl purchased from Selleck.
Inhibition of DNA Synthesis by SGI-1776 (S) and Bendamustine (B) and Their Combination in JeKo-1 Cells. JeKo-1 Cells Were Treated With Dimethyl Sulfoxide (DMSO), 5 μM or 10 m M Bendamustine, 5 μM SGI-1776, or 5 μM or 10 m M Bendamustine Combined With 5 μM SGI-1776 for 24 Hours. Cells were Then Incubated With [Methyl-3H]-Thymidine at 0.8 m Ci/mL Concentration for 45 Minutes. Radioactive Incorporation Was Then Measured by Scintillation Count, and Values Were Recorded as Disintegration per Minute per Cell and Normalized to DMSO Controls. Experiments Were Performed in Triplicate and Presented as Mean ± Standard Error of the Mean.
Clin Lymphoma Myeloma Leuk 2013 13 Suppl 2, S355-62. Bendamustine HCl purchased from Selleck.
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Choose Selective DNA/RNA Synthesis Inhibitors
|Description||Bendamustine HCL is a DNA-damaging agent with IC50 of 50 μM in cell-free assay.|
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.  Using Bendamustine alone in concentrations from 1 μg/mL to 50 μg/mL, a dose- and time-dependent manner of cytotoxicity from 30.4% to 94.8% after 48 hours could be observed. The LD50 for untreated and pretreated CLL cells is 7.3 or 4.4 μg /mL, respectively.  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. 
|In vivo||A single dose of Bendamustine at 25 mg/kg demonstrates significant activity in all three tumor lines (DoHH-2, Granta 519 and RAMOS). DoHH-2 is the most sensitive, with 30% ORR and a 69% inhibition in tumor growth. Growth of Granta 519 and RAMOS is also inhibited by Bendamustine (%TGI of 74% and 81%, respectively), and the effect is more durable in Granta 519 (%TGD of 124%) than for DoHH-2 or RAMOS (69% and 43%, respectively). |
-  Leoni LM, et al. Clin Cancer Res. 2008, 14(1), 309-317.
-  Schw?nen C, et al. Leukemia. 2002, 16(10), 2096-2105.
-  Konstantinov SM, et al. J Cancer Res Clin Oncol. 2002, 128(5), 271-278.
|In vitro||DMSO||78 mg/mL (197.6 mM)|
|Ethanol||17 mg/mL (43.06 mM)|
|Water||2 mg/mL (5.06 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% DMSO+30% polyethylene glycol+1% Tween 80
For best results, use promptly after mixing.
* 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.
|Synonyms||SDX-105 (Cytostasane) HCl|
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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|
|NCT02477215||Active not recruiting||Multiple Myeloma||Parameswaran Hari|Medical College of Wisconsin||October 9 2015||Phase 1|Phase 2|
|NCT02008006||Recruiting||Follicular Lymphoma||Centre Leon Berard||July 9 2014||Phase 2|
|NCT02071225||Active not recruiting||Chronic Lymphocytic Leukemia||Hoffmann-La Roche||April 9 2014||Phase 2|
|NCT01886872||Active not recruiting||CD19 Positive|CD20 Positive|CD5 Positive|Stage I Chronic Lymphocytic Leukemia|Stage II Chronic Lymphocytic Leukemia|Stage III Chronic Lymphocytic Leukemia|Stage IV Chronic Lymphocytic Leukemia||National Cancer Institute (NCI)||December 9 2013||Phase 3|
|NCT01891227||Completed||Breast Cancer||Arbeitsgemeinschaft medikamentoese Tumortherapie||August 9 2013||Phase 2|
|NCT01535924||Active not recruiting||Adult Lymphocyte Depletion Hodgkin Lymphoma|Adult Lymphocyte Predominant Hodgkin Lymphoma|Adult Mixed Cellularity Hodgkin Lymphoma|Adult Nodular Lymphocyte Predominant Hodgkin Lymphoma|Adult Nodular Sclerosis Hodgkin Lymphoma|Recurrent Adult Hodgkin Lymphoma||Beth Christian|Ohio State University Comprehensive Cancer Center||February 9 2012||Phase 1|Phase 2|
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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