Nitrogen mustard alkylating agent and prodrug. Phosphoramide mustard (active metabolite) forms DNA cross-links leading to cell death. Inhibits aldehyde dehydrogenase 1 (ALDH1) through its degradation product acrolein. Chemotherapeutic for the treatment of breast cancer; regulates Bax and Bcl-2 expression when administered with etoposide (Cat. No. 1226) in breast cancer cell lines.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 261.09. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.83 mL||19.15 mL||38.3 mL|
|5 mM||0.77 mL||3.83 mL||7.66 mL|
|10 mM||0.38 mL||1.92 mL||3.83 mL|
|50 mM||0.08 mL||0.38 mL||0.77 mL|
References are publications that support the products' biological activity.
Gibson et al (1999) Regulation of BAX and BCL-2 expression in breast cancer cells by chemotherapy. Breast Cancer Research and Treatment 55 107 PMID: 10481938
Hengstler et al (1992) DNA strand breaks and DNA cross-links in peripheral mononuclear blood cells of ovarian cancer patients during chemotherapy with cyclophosphamide/carboplatin. Cancer Res. 15 52 PMID:
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Keywords: Cyclophosphamide, supplier, chemotherapeutics, cross-links, alkylates, DNA, cytotoxic, inhibits, inhibitors, aldehyde, dehydrogenase, 1, ALDH1, Apoptosis, Inducers, DNA,, RNA, and, Protein, Synthesis, Apoptosis, Inducers, Tocris Bioscience
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.