Riebeseel Katja, Biedermann Elfi, Löser Roland, Breiter Norbert, Hanselmann Ralf, Mülhaupt Rolf, Unger Clemens, Kratz Felix
Tumor Biology Center, Department of Medical Oncology, Clinical Research, Breisacher Strasse 117, 79106 Freiburg, Germany.
Bioconjug Chem. 2002 Jul-Aug;13(4):773-85. doi: 10.1021/bc010098m.
Poly(ethylene glycol)s (PEGs) are potential drug carriers for improving the therapeutic index of anticancer agents. In this work, the anticancer drug methotrexate (MTX) was activated with N,N'-dicyclohexylcarbodiimide (DCC) and coupled to amino group bearing PEGs of MW 750, 2000, 5000, 10 000, 20,000, and 40,000. First, the activation process of MTX with DCC in the presence and absence of N-hydroxysuccinimide was analyzed through HPLC. Preincubation of methotrexate with DCC alone at 0 degrees C proved to be favorable with respect to the amount of activated species and the formation of byproducts. MTX-PEG conjugates were synthesized according to this procedure, isolated through size-exclusion chromatography, and characterized through analytical HPLC, MALDI-TOF spectrometry, and gel permeation chromatography. In a cell-free assay, all of the drug polymer conjugates inhibited the target enzyme of MTX, dihydrofolate reductase (DHFR), to a similar extent, but were not as active as free MTX. Additionally, incubation of the MTX-PEG40000 conjugate for 6 days at 37 degrees C in phosphate buffered saline (pH 7.4), in cell-conditioned medium, or in human serum revealed no significant release of methotrexate. These results, taken together, indicate that release of MTX from polymer conjugates is not necessary for an effective interaction with the active site of dihydrofolate reductase. Evaluation of the in vitro cytotoxicity of the MTX-PEG conjugates in two adherent and three suspension human tumor cell lines revealed that the IC(50) values of the tested compounds increased with the size of the drug-polymer conjugates. The most effective compound tested in these assays was the free drug MTX itself (IC(50) value ranging from approximately 0.01 to 0.05 microM), while the IC(50) values of the polymer conjugates were higher (IC(50) value for MTX-PEG750, 2000 and 5000: approximately 0.6-3 microM; for MTX-PEG10000 and 20000: approximately 2-7 microM; and for MTX-PEG40000: > 6 microM). Subsequently, MTX-PEG5000, MTX-PEG20000, and MTX-PEG40000 were evaluated in a human mesothelioma MSTO-211H xenograft model, and their antitumor effects were compared with free methotrexate and the albumin conjugate MTX-HSA, a conjugate that is currently in phase II clinical trials. In contrast to the in vitro results, the high molecular weight MTX-PEG conjugates exhibited the highest in vivo antitumor activity: At a dose of 40 and 80 mg/kg MTX-PEG5000 was less active than MTX at its optimal dose of 100 mg/kg; MTX-PEG20000 at a dose of 40 mg/kg showed antitumor efficacy comparable to MTX, but MTX-PEG40000 at a dose of 20 mg/kg was superior to MTX and demonstrated antitumor activity of the same order as MTX-HSA (20 mg/kg).
聚乙二醇(PEGs)是用于提高抗癌药物治疗指数的潜在药物载体。在本研究中,抗癌药物甲氨蝶呤(MTX)用N,N'-二环己基碳二亚胺(DCC)活化,并与分子量为750、2000、5000、10000、20000和40000且带有氨基的PEGs偶联。首先,通过高效液相色谱(HPLC)分析了在有和没有N-羟基琥珀酰亚胺存在的情况下MTX与DCC的活化过程。在0℃下单独用DCC对甲氨蝶呤进行预孵育,结果表明在活化物种的量和副产物的形成方面是有利的。按照此程序合成MTX-PEG缀合物,通过尺寸排阻色谱法分离,并通过分析型HPLC、基质辅助激光解吸电离飞行时间质谱(MALDI-TOF)和凝胶渗透色谱法进行表征。在无细胞试验中,所有药物聚合物缀合物对MTX的靶酶二氢叶酸还原酶(DHFR)的抑制程度相似,但活性不如游离MTX。此外,将MTX-PEG40000缀合物在37℃下于磷酸盐缓冲盐水(pH 7.4)、细胞条件培养基或人血清中孵育6天,未发现甲氨蝶呤有明显释放。综合这些结果表明,MTX从聚合物缀合物中的释放对于与二氢叶酸还原酶活性位点的有效相互作用不是必需的。对MTX-PEG缀合物在两种贴壁和三种悬浮人肿瘤细胞系中的体外细胞毒性进行评估,结果显示受试化合物的半数抑制浓度(IC50)值随药物-聚合物缀合物的尺寸增加而升高。在这些试验中测试的最有效的化合物是游离药物MTX本身(IC50值范围约为0.01至0.05 microM),而聚合物缀合物的IC50值更高(MTX-PEG750、2000和5000的IC50值:约0.6 - 3 microM;MTX-PEG一万和两万的IC50值:约2 - 7 microM;MTX-PEG40000的IC50值:> 6 microM)。随后,在人恶性间皮瘤MSTO-211H异种移植模型中评估了MTX-PEG5000、MTX-PEG20000和MTX-PEG40000,并将它们的抗肿瘤作用与游离甲氨蝶呤和白蛋白缀合物MTX-HSA(一种目前处于II期临床试验的缀合物)进行比较。与体外结果相反,高分子量MTX-PEG缀合物表现出最高的体内抗肿瘤活性:在40和80 mg/kg的剂量下,MTX-PEG5000的活性低于MTX的最佳剂量100 mg/kg;40 mg/kg剂量的MTX-PEG20000显示出与MTX相当的抗肿瘤疗效,但20 mg/kg剂量的MTX-PEG40000优于MTX,并显示出与MTX-HSA(该剂量为20 mg/kg)相同水平的抗肿瘤活性。
Chem Pharm Bull (Tokyo). 2010-2
Eur J Pharm Sci. 2000-5
Drug Des Devel Ther. 2018-10-5
Biochem Biophys Rep. 2021-10-23
RSC Med Chem. 2020-5-28
Nanomedicine (Lond). 2015
Clin Med Oncol. 2009-3-20