PDEPT:聚合物导向酶前药疗法。2. 以HPMA共聚物-β-内酰胺酶和HPMA共聚物-C-阿霉素作为模型组合

PDEPT: polymer-directed enzyme prodrug therapy. 2. HPMA copolymer-beta-lactamase and HPMA copolymer-C-Dox as a model combination.

作者信息

Satchi-Fainaro Ronit, Hailu Hanna, Davies John W, Summerford Clive, Duncan Ruth

机构信息

Department of Cell Research and Immunology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel.

出版信息

Bioconjug Chem. 2003 Jul-Aug;14(4):797-804. doi: 10.1021/bc020091k.

Abstract

Polymer-directed enzyme prodrug therapy (PDEPT) is a novel two-step antitumor approach that uses a combination of a polymeric prodrug and polymer-enzyme conjugate to generate a cytotoxic drug rapidly and selectively at the tumor site. Previously we have shown that N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-bound cathepsin B can release doxorubicin intratumorally from an HPMA copolymer conjugate PK1. Here we describe for the first time the synthesis and biological characterization of a PDEPT model combination that uses an HPMA-copolymer-methacryloyl-glycine-glycine-cephalosporin-doxorubicin (HPMA-co-MA-GG-C-Dox) as the macromolecular prodrug and an HPMA copolymer conjugate containing the nonmammalian enzyme beta-lactamase (HPMA-co-MA-GG-beta-L) as the activating component. HPMA-co-MA-GG-C-Dox had a molecular weight of approximately 31 600 Da and a C-Dox content of 5.85 wt %. Whereas free beta-L has a molecular weight of 45 kDa, the HPMA-co-MA-GG-beta-L conjugate had a molecular weight in the range of 75-150 kDa, and following purification no free enzyme was detectable. Against the cephalosporin C or HPMA-co-MA-GG-C-Dox substrates, the HPMA-co-MA-GG-beta-L conjugate retained 70% and 80% of its activity, respectively. In vivo (125)I-labeled HPMA-co-MA-GG-beta-L showed prolonged plasma concentration and greater tumor targeting than (125)I-labeled beta-L due to the enhanced permeability and retention (EPR) effect. Moreover, administration of HPMA-co-MA-GG-C-Dox iv to mice bearing sc B16F10 melanoma followed after 5 h by HPMA-co-MA-GG-beta-L led to release of free Dox. The PDEPT combination caused a significant decrease in tumor growth (T/C = 132%) whereas neither free Dox nor HPMA-co-MA-GG-C-Dox alone displayed activity. The PDEPT combination displayed no toxicity at the doses used, so further evaluation of this approach to establish the maximum tolerated dose (MTD) is recommended.

摘要

聚合物导向酶前药疗法(PDEPT)是一种新型的两步抗肿瘤方法,它使用高分子前药和聚合物 - 酶偶联物的组合,在肿瘤部位快速且选择性地产生细胞毒性药物。此前我们已经表明,与N -(2 - 羟丙基)甲基丙烯酰胺(HPMA)共聚物结合的组织蛋白酶B可以从HPMA共聚物偶联物PK1中在肿瘤内释放阿霉素。在此,我们首次描述了一种PDEPT模型组合的合成及生物学特性,该组合使用HPMA - 共聚物 - 甲基丙烯酰甘氨酸 - 甘氨酸 - 头孢菌素 - 阿霉素(HPMA - co - MA - GG - C - Dox)作为大分子前药,以及含有非哺乳动物酶β - 内酰胺酶的HPMA共聚物偶联物(HPMA - co - MA - GG - β - L)作为激活成分。HPMA - co - MA - GG - C - Dox的分子量约为31600 Da,C - Dox含量为5.85 wt%。游离的β - L分子量为45 kDa,而HPMA - co - MA - GG - β - L偶联物的分子量在75 - 150 kDa范围内,纯化后未检测到游离酶。针对头孢菌素C或HPMA - co - MA - GG - C - Dox底物,HPMA - co - MA - GG - β - L偶联物分别保留了其70%和80%的活性。在体内,由于增强的渗透和滞留(EPR)效应,(125)I标记的HPMA - co - MA - GG - β - L显示出比(125)I标记的β - L更长的血浆浓度和更高的肿瘤靶向性。此外,给携带皮下B16F10黑色素瘤的小鼠静脉注射HPMA - co - MA - GG - C - Dox,5小时后再注射HPMA - co - MA - GG - β - L,导致游离阿霉素的释放。PDEPT组合使肿瘤生长显著降低(T/C = 132%),而单独的游离阿霉素或HPMA - co - MA - GG - C - Dox均未显示活性。PDEPT组合在所使用的剂量下没有毒性,因此建议进一步评估该方法以确定最大耐受剂量(MTD)。

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