Inhibitor of DNA topoisomerase I that displays antitumor activity against a range of tumor types. Active metabolite available (SN 38, Cat. No. 2684).
|Storage||Store at RT|
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|
|water||3.12||5mM with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 623.14. 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||1.6 mL||8.02 mL||16.05 mL|
|5 mM||0.32 mL||1.6 mL||3.21 mL|
|10 mM||0.16 mL||0.8 mL||1.6 mL|
|50 mM||0.03 mL||0.16 mL||0.32 mL|
References are publications that support the products' biological activity.
Kawato et al (1993) Inhibitory activity of camptothecin derivatives against acetylcholinesterase in dogs and their binding activity to acetylcholine receptors in rats. J.Pharm.Pharmacol. 45 444 PMID: 8099964
Vassal et al (1996) Therapeutic activity of CPT-11, a DNA topoisomerase I inhibitor against peripheral primitive neuroectodermal tumour and neuroblastoma xenografts. Br.J.Cancer. 74 537 PMID: 8761367
If you know of a relevant reference for CPT 11, please let us know.
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Keywords: CPT 11, supplier, DNA, topoisomerase, I, inhibitors, inhibits, antitumor, Isomerases, CPT11, Camptothecin11, chemotherapeutics, Irinotecan, Camptothecin, 11, DNA, Topoisomerase, DNA, Topoisomerase, Tocris Bioscience
Citations for CPT 11
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Literature in this Area
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.