DNA alkylating agent; induces cytotoxicity through the formation of stable interstrand and intrastrand crosslinks within DNA. Inhibits growth of PC-3 cells (IC50 values are 0.074 and 0.77 μg/ml for sequential dosing and single dosing respectively).
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 305.2. 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|
|0.2 mM||16.38 mL||81.91 mL||163.83 mL|
|1 mM||3.28 mL||16.38 mL||32.77 mL|
|2 mM||1.64 mL||8.19 mL||16.38 mL|
|10 mM||0.33 mL||1.64 mL||3.28 mL|
References are publications that support the biological activity of the product.
Blumberg et al (1965) An alkylating agent for multiple myeloma: melphalan. JAMA. 191 547 PMID: 14239026
Merck Index 12 5872
Bauer and Povirk (1997) Specificity and kinetics of interstrand and intrastrand bifunctional alkylation by nitrogen mustards at a G-G-C sequence. Nucleic Acids Res. 25 1211 PMID: 9092631
Mougenot et al (2006) In vitro cytotoxic effect of melphalan and pilot phase II study in hormone-refractory prostate cancer. Anticancer Res. 26 2197 PMID: 16821586
If you know of a relevant reference for Melphalan, please let us know.
Keywords: Melphalan, Melphalan supplier, antineoplastics, alkylating, DNA, agents, chemotherapeutics, cytotoxic, crosslinks, Other, Apoptosis, 4619, 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.