Pfizer Inc, Drug Safety Research and Development, La Jolla Laboratories, 10646 Science Center Drive, San Diego, CA 92121, USA.
J Appl Toxicol. 2012 Dec;32(12):1008-20. doi: 10.1002/jat.2801. Epub 2012 Aug 31.
PF-04254644 is a selective kinase inhibitor of mesenchymal epithelial transition factor/hepatocyte growth factor receptor with known off-target inhibitory activity against the phosphodiesterase (PDE) family. Rats given repeated oral doses of PF-04254644 developed a mild to moderate myocardial degeneration accompanied by sustained increase in heart rate and contractility. Investigative studies were conducted to delineate the mechanisms of toxicity. Microarray analysis of Sprague-Dawley rat hearts in a 6 day repeat dose study with PF-04254644 or milrinone, a selective PDE3 inhibitor, revealed similar perturbation of the cyclic adenosine monophosphate (c-AMP) pathway. PDE inhibition and activation of c-AMP were further substantiated using PDE3B immunofluorescence staining and through a c-AMP response element reporter gene assay. The intracellular calcium and oxidative stress signaling pathways were more perturbed by treatment with PF-04254644 than milrinone. The rat cardiomyocytes calcium assay found a dose-dependent increase in intracellular calcium with PF-04254644 treatment. These data suggest that cardiotoxicity of PF-04254644 was probably due to activation of c-AMP signaling, and possibly subsequent disruption of intracellular calcium and oxidative stress signaling pathways. The greater response with PF-04254644 as compared with milrinone in gene expression and micro- and ultrastructural changes is probably due to the broader panel of PDEs inhibition.
PF-04254644 是一种间充质上皮转化因子/肝细胞生长因子受体的选择性激酶抑制剂,已知对磷酸二酯酶 (PDE) 家族具有非靶点抑制活性。给予重复口服 PF-04254644 的大鼠出现轻度至中度心肌变性,伴有心率和收缩力持续增加。进行了研究以阐明毒性的机制。在重复剂量研究中,使用 PF-04254644 或米力农(一种选择性 PDE3 抑制剂)对 Sprague-Dawley 大鼠心脏进行的微阵列分析显示,环腺苷酸 (c-AMP) 途径的类似扰动。使用 PDE3B 免疫荧光染色和 c-AMP 反应元件报告基因测定进一步证实了 PDE 抑制和 c-AMP 激活。与米力农相比,PF-04254644 处理更扰乱细胞内钙和氧化应激信号通路。大鼠心肌细胞钙测定发现,PF-04254644 处理时细胞内钙呈剂量依赖性增加。这些数据表明,PF-04254644 的心脏毒性可能是由于 c-AMP 信号的激活,以及随后可能破坏细胞内钙和氧化应激信号通路。与米力农相比,PF-04254644 在基因表达和微观及超微结构变化方面的反应更大,这可能是由于更广泛的 PDE 抑制。