Irinotecan HCl Trihydrate

Catalog No.S2217 Synonyms: CPT-11 HCl Trihydrate

Irinotecan HCl Trihydrate Chemical Structure

Molecular Weight(MW): 677.18

Irinotecan prevents DNA from unwinding by inhibition of topoisomerase 1.

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In DMSO USD 190 In stock
USD 70 In stock
USD 210 In stock
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Cited by 8 Publications

1 Customer Review

  • 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 HCl Trihydrate purchased from Selleck.

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Biological Activity

Description Irinotecan prevents DNA from unwinding by inhibition of topoisomerase 1.
Features Irinotecan is a prodrug that is used to treat metastatic colorectal cancer.
Targets
Topo I [1]
In vitro

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. [1] 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. [2] Irinotecan is also converted to SN-38 in intestines, plasma and tumor tissues. [3] Irinotecan is significantly more active in SCLC than in NSCLC cell lines, whereas no significant difference between histological types is observed with SN-38. [4]
In vivo In COLO 320 xenografts, Irinotecan induces a maximum growth inhibition of 92%. [5] 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. [6]

Protocol

Cell Research:

[1]
+ Expand
  • Cell lines: LoVo and HT-29 cells
  • Concentrations: 0 μM -100 μM
  • Incubation Time: 48 hours
  • Method:

    Exponentially growing cells (LoVo and HT-29 cells) are seeded in 20 cm2 Petri dishes with an optimal cell number for each cell line (2 × 104 for LoVo cells, 105 for HT-29 cells). They are treated 2 days later with increasing concentrations of Irinotecan or SN-38 for one cell doubling time (24 hours for LoVo cells, 40 hours for HT-29 cells). After washing with 0.15 M NaCl, the cells are further grown for two doubling times in normal medium, detached from the support with trypsin-EDTA and counted in a hemocytometer. The IC50 values are then estimated as the Irinotecan or SN-38 concentrations responsible for 50% growth inhibition as compared with cells incubated without Irinotecan or SN-38.


    (Only for Reference)
Animal Research:

[5]
+ Expand
  • Animal Models: Female nude mice with COLO 320 and WiDr xenografts.
  • Formulation: 0.9% NaCl
  • Dosages: 20 mg/kg
  • Administration: Intraperitoneal injection
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (147.67 mM)
Ethanol 7 mg/mL (10.33 mM)
Water 1 mg/mL (1.47 mM)
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+saline
For best results, use promptly after mixing. 		20mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 677.18
Formula

C33H38N4O6.HCl.3H2O
CAS No. 136572-09-3
Storage powder
in solvent
Synonyms CPT-11 HCl Trihydrate

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03641313 Not yet recruiting Clinical Stage III Gastric Cancer AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IV Gastric Cancer AJCC v8|Clinical Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVA Gastric Cancer AJCC v8|Clinical Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVB Gastric Cancer AJCC v8|Clinical Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Metastatic Gastric Adenocarcinoma|Metastatic Gastroesophageal Junction Adenocarcinoma|Pathologic Stage III Gastric Cancer AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastric Cancer AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastric Cancer AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIC Gastric Cancer AJCC v8|Pathologic Stage IV Gastric Cancer AJCC v8|Pathologic Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage III Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IV Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|TP53 Gene Mutation|Unresectable Gastroesophageal Junction Adenocarcinoma National Cancer Institute (NCI) February 1 2019 Phase 2
NCT03709680 Not yet recruiting Solid Tumors|Ewing Sarcoma|Rhabdoid Tumor|Rhabdomyosarcoma|Neuroblastoma|Medulloblastoma Pfizer February 5 2019 Phase 1
NCT03739801 Not yet recruiting Locally Advanced Unresectable Gastric Adenocarcinoma|Metastatic Gastroesophageal Junction Adenocarcinoma|Metastatic Unresectable Gastric Adenocarcinoma|Unresectable Gastroesophageal Junction Adenocarcinoma|Gastric Adenocarcinoma|Gastroesophageal Junction Adenocarcinoma University of Southern California|National Cancer Institute (NCI)|Ipsen January 14 2019 Phase 1|Phase 2
NCT03722108 Not yet recruiting Adenocarcinoma of the Stomach|Adenocarcinoma of the Gastroesophageal Junction UNICANCER January 2019 Phase 1|Phase 2
NCT03697044 Not yet recruiting Colorectal Cancer Metastatic|Liver Metastases The Christie NHS Foundation Trust January 2019 --
NCT03607643 Not yet recruiting Cancer of Pancreas|Cancer of Liver|Cancer of Rectum|Cancer of Colon|Cancer Gall Bladder|Myeloma Multiple|Glioblastoma Multiforme Leaf Vertical Inc. January 15 2019 Phase 1|Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID