Catalog No.S1198 Synonyms: CPT-11
Molecular Weight(MW): 586.68
Irinotecan is a topoisomerase I inhibitor for LoVo cells and HT-29 cells with IC50 of 15.8 μM and 5.17 μM, respectively.
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Growth inhibitory effects of Irinotecan in human pancreatic cancer cells. Panc1 cells were plated in triplicates into 48-well plates at a density of 10,000 cells/ml. After 24 hours, complete culture medium was changed into fresh low-serum-containing medium (1% FBS) containing DMSO (control) or indicated doses of Irinotecan (Selleckchem). Cell viability 72 hours after treatment was determined by AlamarBlue assay (Invitrogen) according to manufacturer's instructions. Results are expressed as percentages of control, which was arbitrarily assigned 100% viability, and represented as the mean ± standard deviation (SD) of the tripicate wells.
Dr. Mikhail Menshikov of Cardiology Research Center. Irinotecan purchased from Selleck.
Purity & Quality Control
Choose Selective Topoisomerase Inhibitors
|Description||Irinotecan is a topoisomerase I inhibitor for LoVo cells and HT-29 cells with IC50 of 15.8 μM and 5.17 μM, respectively.|
|Features||Irinotecan is a prodrug that is used to treat metastatic colorectal cancer.|
Irinotecan is activated to SN-38 by carboxylesterases to become able to interact with its target, topoisomerase I. Irinotecan induces similar amounts of cleavable complexes at its IC50 in LoVo cells and HT-29 cell lines. SN-38 induces a concentration-dependent formation of cleavable complexes, which is not significantly different in LoVo cells and HT-29 cell lines. Cell accumulation of Irinotecan is markedly different, reaching consistently higher levels in HT-29 cells than in LoVo cells.  The lactone E-ring of Irinotecan and SN-38 hydrolyses reversibly in aqueous solutions, and the interconversion between the lactone and carboxylate forms is dependent on pH and temperature. Liver is primarily responsible for the activation of Irinotecan to SN-38. At equal concentrations of Irinotecan and SN-38 glucuronide, the rate of beta-glucuronidase-mediated SN-38 production is higher than that formed from Irinotecan in both tumour and normal tissue.  Irinotecan is also converted to SN-38 in intestines, plasma and tumor tissues.  Irinotecan is significantly more active in SCLC than in NSCLC cell lines, whereas no significant difference between histological types is observed with SN-38. 
|In vivo||In COLO 320 xenografts, Irinotecan induces a maximum growth inhibition of 92%.  A single dose of Irinotecan significantly increases amounts of topoisomerase I covalently bound to DNA in stomach, duodenum, colon and liver. Concomitantly, the Irinotecan-treated group shows significantly higher amounts of DNA strand breaks in colon mucosa cells compared to the control group. |
-  Pavillard V, et al. Cancer Chemother Pharmacol. 2002, 49(4), 329-335.
-  Tobin P, et al. Br J Clin Pharmacol. 2006, 62(1), 122-129.
-  Shingyoji M, et al. Cancer Sci. 2004, 95(6), 537-540.
|In vitro||DMSO||7 mg/mL (11.93 mM)|
|In vivo||30% propylene glycol, 5% Tween 80, 65% D5W||30 mg/mL|
* 1 mg/ml means slightly soluble or insoluble.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01928290||Recruiting||Stomach Neoplasms|Esophageal Neoplasms||Washington University School of Medicine||November 8, 2013||Phase 2|
|NCT01336985||Terminated||Neoplasm Metastases|Melanoma|Colorectal Neoplasms||National Institutes of Health Clinical Center (CC)||March 28, 2011||Phase 1|
|NCT02316496||Terminated||Colorectal Cancer Metastatic||Groupe Cooperateur Multidisciplinaire en Oncologie (GERCOR)||September 23, 2015||Phase 2|
|NCT02975882||Not yet recruiting||Childhood Solid Neoplasm|Recurrent Central Nervous System Neoplasm|Recurrent Solid Neoplasm|Refractory Central Nervous System Neoplasm||Childrens Oncology Group|National Cancer Institute (NCI)||September 2017||Phase 1|
|NCT03009058||Not yet recruiting||Metastatic Cancer||Immodulon Therapeutics Ltd||January 2017||Phase 1|Phase 2|
|NCT03017326||Not yet recruiting||Hepatoblastoma|Carcinoma, Hepatocellular||University of Birmingham|Fundació Institut Germans Trias i Pujol|University of Padua|University of Newcastle Upon-Tyne|University Hospital Munich|University Hospital, Bonn|University of Kiel|University Hospital Tuebingen|Medical University of Gdansk||January 2017||Phase 3|
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