Active metabolite of CPT-11 (Cat. No. 2688) that inhibits DNA topoisomerase I (IC50 values are 0.74 and 1.9 μM in P388 and Ehrlich cells respectively). Inhibits DNA and RNA synthesis (IC50 values are 0.077 and 1.3 μM respectively) but does not affect protein synthesis. Displays potent antitumor activity against a range of human tumor cell lines (IC50 values are 3.3, 13, 19 and 22 nM for HCT-116, BEL-7402, HL60 and HELA cells respectively).
|Storage||Store at +4°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 392.4. 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||2.55 mL||12.74 mL||25.48 mL|
|5 mM||0.51 mL||2.55 mL||5.1 mL|
|10 mM||0.25 mL||1.27 mL||2.55 mL|
|50 mM||0.05 mL||0.25 mL||0.51 mL|
References are publications that support the products' biological activity.
Kawato et al (1991) Intracellular roles of SN-38, a metabolite of the camptothecin derivative CPT-11, in the antitumor effect of CPT-11. Cancer Res. 51 4187 PMID: 1651156
Gao et al (2005) Synthesis and antitumor activity of the hexacyclic camptothecin derivatives. Bioorg.Med.Chem.Lett. 15 3233 PMID: 15913996
Koizumi et al (2006) Novel SN-38-incorporating ploymeric micelles, NK012, eradicate vascular endothelial growth factor-secreting bulky tumors. Cancer Res. 66 10048 PMID: 17047068
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Keywords: SN 38, supplier, DNA, topoisomerase, I, inhibitors, inhibits, antitumor, Isomerases, SN38, chemotherapeutics, 7-Ethyl-10-hydroxycamptothecin, DNA, Topoisomerase, DNA, Topoisomerase, Tocris Bioscience
2 Citations for SN 38
Citations are publications that use Tocris products. Selected citations for SN 38 include:
Jonchère et al (2015) Irinotecan treatment and senescence failure promote the emergence of more transformed and invasive cells that depend on anti-apoptotic Mcl-1. Oncotarget 6 409 PMID: 25565667
Vétillard et al (2015) Akt inhibition improves irinotecan treatment and prevents cell emergence by switching the senescence response to apoptosis. Exp Neurol 6 43342 PMID: 26485768
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