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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.
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 392.4. 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|
|0.5 mM||5.1 mL||25.48 mL||50.97 mL|
|2.5 mM||1.02 mL||5.1 mL||10.19 mL|
|5 mM||0.51 mL||2.55 mL||5.1 mL|
|25 mM||0.1 mL||0.51 mL||1.02 mL|
References are publications that support the biological activity of the product.
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-Secr.g bulky tumors. Cancer Res. 66 10048 PMID: 17047068
If you know of a relevant reference for SN 38, please let us know.
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Keywords: SN 38, SN 38 supplier, DNA, topoisomerase, I, inhibitors, inhibits, antitumor, Isomerases, SN38, chemotherapeutics, 7-Ethyl-10-hydroxycamptothecin, Topoisomerase, 2684, Tocris Bioscience
10 Citations for SN 38
Citations are publications that use Tocris products. Selected citations for SN 38 include:
Duff et al (2018) Regulation of senescence escape by the cdk4-EZH2-AP2M1 pathway in response to chemotherapy. Cell Death Dis 9 199 PMID: 29415991
Wolff et al (2018) Camptothecin exhibits topoisomerase1-independent KMT1A suppression and myogenic differentiation in alveolar rhabdomyosarcoma cells. Oncotarget 9 25796 PMID: 29899822
Guillon et al (2019) Regulation of senescence escape by TSP1 and CD47 following chemotherapy treatment. Cell Death Dis 10 199 PMID: 30814491
Prill et al (2019) Tumor-associated macrophages and individual chemo-susceptibility are influenced by iron chelation in human slice cultures of gastric cancer. Oncotarget 10 4731 PMID: 31413815
Ni et al (2011) Identification of proline residues in or near the transmembrane helices of the human breast cancer resistance protein (BCRP/ABCG2) that are important for transport activity and substrate specificity. Biochemistry 50 8057 PMID: 21854076
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 irino. treatment and prevents cell emergence by switching the senescence response to apoptosis. Exp Neurol 6 43342 PMID: 26485768
Kathawala et al (2014) Masitinib antagonizes ATP-binding cassette subfamily G member 2-mediated multidrug resistance. Int J Oncol 44 1634 PMID: 24626598
Chen et al (2014) Enzymatic methylation and structure-activity-relationship studies on polycarcin V, a gilvocarcin-type antitumor agent. Chembiochem 15 2729 PMID: 25366963
Ni et al (2010) Transmembrane helices 1 and 6 of the human breast cancer resistance protein (BCRP/ABCG2): identification of polar residues important for drug transport. Am J Physiol Cell Physiol 299 C1100 PMID: 20739628
Do you know of a great paper that uses SN 38 from Tocris? Please let us know.
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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.