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Biological Activity for Oxaliplatin
Oxaliplatin is an antitumor agent that forms platinum-DNA adducts. Causes intra- and interstrand DNA crosslinks blocking DNA replication and transcription. Displays higher cytotoxicity and lower nephrotoxicity than analog cisplatin (Cat. No. 2251) and shows antitumor activity in cell lines with acquired cisplatin resistance.
Technical Data for Oxaliplatin
|Storage||Store at +4°C|
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.
Solubility Data for Oxaliplatin
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|water||1.99||5 with gentle warming|
Preparing Stock Solutions for Oxaliplatin
The following data is based on the product molecular weight 397.29. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.05 mM||50.34 mL||251.71 mL||503.41 mL|
|0.25 mM||10.07 mL||50.34 mL||100.68 mL|
|0.5 mM||5.03 mL||25.17 mL||50.34 mL|
|2.5 mM||1.01 mL||5.03 mL||10.07 mL|
References for Oxaliplatin
References are publications that support the biological activity of the product.
Culy et al (2000) Oxaliplatin. A review of its pharmacological properties and clinical efficacy in metastatic colorectal cancer and its potential in other malignancies. Drugs 60 895 PMID: 11085200
Raymond et al (2002) Cellular and molecular pharmacology of oxalip. Mol.Cancer Ther. 1 227 PMID: 12467217
Mani et al (2002) Oxaliplatin: a review of evolving concepts. Cancer Invest. 20 246 PMID: 11901545
If you know of a relevant reference for Oxaliplatin, please let us know.
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Keywords: Oxaliplatin, Oxaliplatin supplier, DNA, cross-linking, antitumor, agent, inhibitors, inhibits, synthesis, Apoptosis, Inducers, platinum-DNA, adducts, chemotherapeutics, Eloxatin, DNA,, RNA, and, Protein, Synthesis, 2623, Tocris Bioscience
7 Citations for Oxaliplatin
Citations are publications that use Tocris products. Selected citations for Oxaliplatin include:
Li et al (2015) FBXW7-mutated colorectal cancer cells exhibit aberrant expression of phosphorylated-p53 at Serine-15. BMC Cancer 6 9240 PMID: 25860929
Rawlinson (2014) γH2AX and Chk1 phosphorylation as predictive pharmacodynamic biomarkers of Chk1 inhibitor-chemotherapy combination treatments. BMC Cancer 14 483 PMID: 24996846
Massey (2015) Multiparametric Cell Cycle Analysis Using the Operetta High-Content Imager and Harmony Software with PhenoLOGIC. PLoS One 10 e0134306 PMID: 26218638
Fukushima et al (2015) Atonal homolog 1 protein stabilized by tumor necrosis factor α induces high malignant potential in colon cancer cell line. Cancer Sci 106 1000 PMID: 26017781
Bryant et al (2014) Chk1 inhibition as a novel therapeutic strategy for treating triple-negative breast and ovarian cancers. Exp Neurol 14 570 PMID: 25104095
Boyette-Davis and Dougherty (2011) Protection against oxaliplatin-induced mechanical hyperalgesia and intraepidermal nerve fiber loss by MinCyc. Oncotarget 229 353 PMID: 21385581
Ibáñez et al (2012) A high throughput scintillation proximity imaging assay for protein methyltransferases. Comb Chem High Throughput Screen 15 359 PMID: 22256970
Do you know of a great paper that uses Oxaliplatin from Tocris? Please let us know.
Reviews for Oxaliplatin
Average Rating: 5 (Based on 2 Reviews.)
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HCT116 cells were treated with 600 uM of Oxaliplatin for 4 hours and up regulation of surface expression of calreticulin was measured.
Oxaliplatin was used at a 20 uM concentration for in vitro culture with SK-MEL-28 and cell viability was monitored over time with live imaging. Arrow indicates when compound was added to media.
Literature in this Area
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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.