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    Irinotecan (CPT-11)
    Irinotecan (CPT-11)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1393
    CAS #: 97682-44-5 Purity ≥98%

    Description: Irinotecan (also known as CPT-11; Camptosar; Irinophore C; CPT11; Irinotecan lactone; Irinotecanum), a semisynthetic analog of camptothecin and the prodrug of 7-ethyl-10-hydroxy-camptothecin (SN-38), is a topoisomerase I inhibitor approved for use as an anticancer drug. It inhibits topoisomerase I in LoVo and HT-29 cells with IC50s of 15.8 μM and 5.17 μM, respectively. 

    References: Cancer Chemother Pharmacol. 2002 Apr;49(4):329-35; Int J Cancer. 1997 Jan 27;70(3):335-40.

    Related CAS#: 136572-09-3 (HCl trihydrate); 100286-90-6 (HCl); 97682-44-5 (Free base) 

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    Molecular Weight (MW)586.68
    FormulaC33H38N4O6
    CAS No.97682-44-5 (Free base); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 7 mg/mL (11.9 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)30% Propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL 
    SynonymsCPT-11; (+)-Irinotecan; Camptosar; Irinophore C; CPT 11; CPT11; Irinotecan; Irinotecan lactone; Irinotecanum 


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    In Vitro

    In vitro activity: 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.


    Cell Assay: 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.

    In VivoIn 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.
    Animal modelFemale nude mice with COLO 320 and WiDr xenografts
    Formulation & DosageDissolved in 0.9% NaCl; 20 mg/mL; i.p. injection
    References

    Cancer Chemother Pharmacol. 2002 Apr;49(4):329-35; Br J Clin Pharmacol. 2006 Jul;62(1):122-9; Int J Cancer. 1997 Jan 27;70(3):335-40.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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