Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
J Pharm Biomed Anal. 2012 Dec;71:228-32. doi: 10.1016/j.jpba.2012.08.011. Epub 2012 Aug 19.
TP53 encodes for tumor protein p53. The suppression of p53 protein results in interruption of DNA repair mechanisms in dividing malignant cells thereby increasing the DNA damage and activating p53-independent mechanisms of apoptosis. This ultimately may translate into enhanced cytotoxic effects of standard chemotherapy. Based on this rationale, Cenersen, a phosphorothioate oligonucleotide antisense to p53-mRNA was synthesized and tested in clinical trials for patients with acute myeloid leukemia (AML). An important component of Cenersen clinical development is to develop a sensitive and specific method to quantify plasma and intracellular levels of Cenersen in different biologic matrices in order to determine tissue and intracellular distribution of the parent compound and its metabolites. Ultimately, this will allow us to determine pharmacokinetic and pharmacodynamic relationship for dose-effect correlation and design effective regimen to be rapidly translate into the clinic. An ELISA-based assay was adapted for assay development and validation of Cenersen in mouse plasma and cell lysate. Cellular uptake of Cenersen was studied in MV4-11 and KASUMI-1 AML cell lines. Real-time RT-PCR was used to measure P53-mRNA expression changes in treated cells. The assay had a limit of quantification of 35pmol/L in mouse plasma. Within-day and between-day precision of <15% and accuracy nearly 100% were observed in a linear range of 10-2000pmol/L (R(2)=0.99) in AML cell lysate. The selectivity of this assay examined as cross-reactivity with its 3'N-1, 3'N-2-metabolites, was 16.8% and 0.4%, respectively, and with its mismatch and the scramble oligonucleotides was 0.06% and 0.4%, respectively. Cenersen was stable in mouse plasma up to 8h at 37°C. When exposed to 0.1-1μmol/L Cenersen, MV4-11 and KASUMI-1 cells showed intracellular concentration in the range of 9.97-45.34nmol/mg protein and 0.1-2.1nmol/mg protein, respectively. Successful downregulation of p53-mRNA expression was observed in Cenersen treated cells. This ELISA-based assay was applicable to plasma and intracellular concentration measurement of Cenersen. Assessment of achievable concentration of Cenersen in different biologic matrices will be useful to elucidate the biological and clinical activity of this promising drug and define its recommended dose in future clinical trials.
TP53 编码肿瘤蛋白 p53。p53 蛋白的抑制导致分裂的恶性细胞中的 DNA 修复机制中断,从而增加 DNA 损伤并激活 p53 非依赖性凋亡机制。这最终可能转化为标准化疗的细胞毒性作用增强。基于这一原理,合成了一种针对 p53-mRNA 的磷硫代寡核苷酸反义药物 Cenersen,并在急性髓细胞白血病 (AML) 患者的临床试验中进行了测试。Cenersen 临床开发的一个重要组成部分是开发一种灵敏和特异的方法来定量不同生物基质中血浆和细胞内 Cenersen 的水平,以确定母体化合物及其代谢物的组织和细胞内分布。最终,这将使我们能够确定药代动力学和药效学关系,以进行剂量效应相关性分析,并设计有效的方案,迅速转化为临床应用。建立了一种 ELISA 检测法,用于在小鼠血浆和细胞裂解物中检测 Cenersen。在 MV4-11 和 KASUMI-1 AML 细胞系中研究了 Cenersen 的细胞摄取。实时 RT-PCR 用于测量处理细胞中 P53-mRNA 表达的变化。该测定法在小鼠血浆中的定量下限为 35pmol/L。在 AML 细胞裂解物中,在 10-2000pmol/L(R(2)=0.99)的线性范围内,日内和日间精密度均<15%,准确度接近 100%。该测定法的选择性,即与 3'N-1、3'N-2-代谢物的交叉反应性分别为 16.8%和 0.4%,与错配和乱序寡核苷酸的交叉反应性分别为 0.06%和 0.4%。Cenersen 在 37°C 下在小鼠血浆中稳定 8 小时。当暴露于 0.1-1μmol/L Cenersen 时,MV4-11 和 KASUMI-1 细胞的细胞内浓度分别为 9.97-45.34nmol/mg 蛋白和 0.1-2.1nmol/mg 蛋白。在 Cenersen 处理的细胞中观察到 p53-mRNA 表达的成功下调。这种基于 ELISA 的测定法适用于 Cenersen 的血浆和细胞内浓度测量。评估不同生物基质中 Cenersen 的可达到浓度将有助于阐明该有前途药物的生物学和临床活性,并确定其在未来临床试验中的推荐剂量。