Irinotecan

Catalog No.S1198 Batch:S119812

Technical Data

Formula

C₃₃H₃₈N₄O₆

Molecular Weight

586.68

CAS No.

97682-44-5

Solubility (25°C)*

In vitro

DMSO

25 mg/mL (42.61 mM)

Water

Insoluble

Ethanol

Insoluble

In vivo (Add solvents to the product individually and in order)

Clear solution	5% DMSO 1 95% Corn oil	0.5mg/ml	Taking the 1 mL working solution as an example, add 50 μL of 10 mg/ml clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results.
Clear solution	5%DMSO 1 40%PEG300 2 5%Tween80 3 50%ddH2O	6.0mg/ml	Taking the 1 mL working solution as an example, add 50 μL of 120 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results.

* <1 mg/ml means slightly soluble or insoluble.
* 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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

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.

Targets

Topo I ^[1]
(LoVo, HT-29 cells)

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]

Features

Irinotecan is a prodrug that is used to treat metastatic colorectal cancer.

Protocol (from reference)

Cell Assay:^{^[1]}	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.
Animal Study:^{^[5]}	Animal Models Female nude mice with COLO 320 and WiDr xenografts Dosages 20 mg/kg Administration Administered via i.p.

Cell Assay:^{^[1]}

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.

Animal Study:^{^[5]}

Animal Models
Female nude mice with COLO 320 and WiDr xenografts
Dosages
20 mg/kg
Administration
Administered via i.p.

References

+ Expand

Customer Product Validation

: , , Biomaterials, 2015, 72:74-89.

: Data independently produced by Dr. Edita Aksamitiene from Thomas Jefferson University, , Dr. Mikhail Menshikov of Cardiology Research Center

Selleck's Irinotecan has been cited by 46 publications

AMG 193, a Clinical Stage MTA-Cooperative PRMT5 Inhibitor, Drives Antitumor Activity Preclinically and in Patients With MTAP-Deleted Cancers [ Cancer Discov, 2024, 10.1158/2159-8290.CD-24-0887]	PubMed: 39282709
Developing Patient-Derived 3D-Bioprinting models of pancreatic cancer [ J Adv Res, 2024, S2090-1232(24)00413-2]	PubMed: 39278567
Targeting of mutant-p53 and MYC as a novel strategy to inhibit oncogenic SPAG5 activity in triple negative breast cancer [ Cell Death Dis, 2024, 15(8):603]	PubMed: 39164278
Discovery of non-genomic drivers of YAP signaling modulating the cell plasticity in CRC tumor lines [ iScience, 2024, 27(3):109247]	PubMed: 38439969
Transgelin-2, a novel cancer stem cell-related biomarker, is a diagnostic and therapeutic target for biliary tract cancer [ BMC Cancer, 2024, 24(1):357]	PubMed: 38509504
Visualization strategies to aid interpretation of high-dimensional genotoxicity data [ Environ Mol Mutagen, 2024, 10.1002/em.22604]	PubMed: 38757760
In-situ cryo-immune engineering of tumor microenvironment with cold-responsive nanotechnology for cancer immunotherapy [ Nat Commun, 2023, 14(1):392]	PubMed: 36693842
Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer [ Cell Rep Med, 2023, 4(9):101162]	PubMed: 37597521
Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer [ Cell Rep Med, 2023, S2666-3791(23)00315-4]	PubMed: 37597521
Thioparib inhibits homologous recombination repair, activates the type I IFN response, and overcomes olaparib resistance [ EMBO Mol Med, 2023, e16235.]	PubMed: 36652375

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.