II01401 伊立替康(10mM in DMSO,无菌) 抑制剂/拮抗剂/激动剂 索莱宝

II01401 伊立替康(10mM in DMSO,无菌)

抑制剂/拮抗剂/激动剂 索莱宝
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  • ¥380
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  • 北京
  • II01401
  • 2025年07月23日
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    • 详细信息
    • 技术资料
    • 保存条件

      Stroe at -20℃,6 months.

    • 保质期

      Stroe at -20℃,6 months.

    • 英文名

      Irinotecan(10mM in DMSO,Sterile)

    • 库存

      现询

    • 供应商

      北京索莱宝科技有限公司

    • CAS号

      97682-44-5

    • 规格

      1ml

    基本信息
    CASNo.97682-44-5
    中文名称伊立替康(10mM in DMSO,无菌)
    英文名称Irinotecan(10mM in DMSO,Sterile)
    分子式C33H38N4O6
    分子量586.68
    溶解性请根据自己的实验要求使用。
    外观(性状)无菌溶液
    储存条件Stroe at -20℃,6 months.
    靶点Topoisomerase
    通路DNA Damage/DNA Repair
    背景说明Irinotecan是拓扑异构酶I抑制剂,通过与拓扑异构酶I-DNA复合物结合来防止DNA链的再连接。
    生物活性Irinotecan ((+)-Irinotecan) is a topoisomerase I inhibitor, preventing religation of the DNA strand by binding to topoisomerase I-DNA complex.[1-5]
    In VitroIrinotecan is a topoisomerase I inhibitor. Irinotecan inhibits the growth of LoVo and HT-29 cells, with IC50s of 15.8 ± 5.1 and 5.17 ± 1.4 μM, respectively, and induces similar amounts of cleavable complexes in both in LoVo and HT-29 cells[2]. Irinotecan suppresses the proliferation of human umbilical vein endothelial cells (HUVEC), with an IC50 of 1.3 μM[3].
    细胞实验Irinotecan (CPT-11, 5 mg/kg) significantly inhibits the growth of tumors by intratumoral injection daily for 5 days, on two consecutive weeks in rats, and such effects also occur via continuous intraperitoneal infusion by osmotic minipump into mice. However, Irinotecan (10 mg/kg) shows no effect on the growth of tumor by i.p[1]. Irinotecan (CPT-11, 100-300 mg/kg, i.p.) apparently suppresses tumor growth of HT-29 xenografts in athymic female mice by day 21. The two groups of Irinotecan (125 mg/kg) plus TSP-1 (10 mg/kg per day) or Irinotecan (150 mg/kg) in combination TSP-1 (20 mg/kg per day) are nearly equally effective and inhibit tumor growth 84% and 89%, respectively, and both are more effective than Irinotecan alone at doses of 250 and 300 mg/kg[3].
    细胞实验Exponentially growing cells are seeded in 20 cm2 dishes with an optimal cell number for each cell line (20,000 for LoVo cells, 100,000 for HT-29 cells). They are treated 2 days later with increasing concentrations of irinotecan or SN-38 for one cell doubling time (24 h for LoVo cells, 40 h 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 drug concentrations responsible for 50% growth inhibition as compared with cells incubated without drug[2].
    动物实验Irinotecan has been administered by intratumoral injection at 0.1 cc volume of the appropriate solution, for a doses of 5 mg/kg daily for 5 days, on two consecutive weeks, followed by a 7-days rest period, referred to as one cycle of therapy. Rats receive three cycles over a period of 8 weeks. Control animals receive 0.1 cc of sterile 0.9% sodium chloride solution by intratumoral injection in the same rule of administration as that of animals of group II[1].
    数据来源文献[1]. Morales C, et al. Antitumoral effect of irinotecan (CPT-11) on an experimental model of malignant neuroectodermal tumor. J Neurooncol. 2002 Feb;56(3):219-26.
    [2]. Pavillard V, et al. Determinants of the cytotoxicity of irinotecan in two human colorectal tumor cell lines. Cancer Chemother Pharmacol. 2002 Apr;49(4):329-35. Epub 2002 Jan 30.
    [3]. Allegrini G, et al. Thrombospondin-1 plus irinotecan: a novel antiangiogenic-chemotherapeutic combination that inhibits the growth of advanced human colon tumor xenografts in mice. Cancer Chemother Pharmacol. 2004 Mar;53(3):261-6. Epub 2003 Dec 5.
    [4]. Dela Cruz FS, et al. A case study of an integrative genomic and experimental therapeutic approach for rare tumors: identification of vulnerabilities in a pediatric poorly differentiated carcinoma. Genome Med. 2016 Oct 31;8(1):116.
    [5]. Huang MY, et al. Chemotherapeutic agent CPT-11 eliminates peritoneal resident macrophages by inducing apoptosis. Apoptosis. 2016 Feb;21(2):130-42.
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