TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Clin Cardiol. 2012;35(7):385-91. doi: 10.1002/clc.22014. Epub 2012 Jun 19.
Lowering low-density lipoprotein cholesterol (LDL-C) is a cornerstone for the prevention of atherosclerotic heart disease, improving clinical outcomes and reducing vascular mortality in patients with hypercholesterolemia. The clinical benefits of LDL-C reduction appear to extend even to patients starting with LDL-C as low as 60-80 mg/dL prior to initiating therapy. Statins are the first-line agents for treating hypercholesterolemia and are effective in reducing LDL-C, but many patients are unable to achieve their optimal lipid targets despite intensive statin therapy. Therefore, there has been a strong impetus for the development of novel pharmacologic agents designed to lower LDL-C further in patients already on statin therapy. Genetic mutations resulting in altered cholesterol homeostasis provide valuable information regarding novel approaches for treating hypercholesterolemia. To that end, mutations in proprotein convertase subtilisin/kexin type 9 (PCSK9) were linked to altered levels of LDL-C, illustrating this protein's role in lipid metabolism. PCSK9 promotes degradation of the LDL receptor, preventing its transport back to the cell surface and thereby increasing circulating LDL-C. Conversely, inhibition of PCSK9 can profoundly decrease circulating LDL-C, and thus is an attractive new target for LDL-C-lowering therapy. AMG 145 is a fully human monoclonal immunoglobulin G2 antibody that binds specifically to human PCSK9 and inhibits its interaction with the low-density lipoprotein receptor. In this manuscript, we describe the rationale and design of LDL-C Assessment with PCSK9 Monoclonal Antibody Inhibition Combined With Statin Therapy-Thrombolysis In Myocardial Infarction 57 (LAPLACE-TIMI 57; NCT01380730), a 12-week, randomized, double-blind, dose-ranging, placebo-controlled study designed to assess the safety and efficacy of AMG 145 when added to statin therapy in patients with hypercholesterolemia.
降低低密度脂蛋白胆固醇(LDL-C)是预防动脉粥样硬化性心脏病的基石,可以改善高胆固醇血症患者的临床结局并降低血管死亡率。降低 LDL-C 的临床益处似乎甚至延伸到那些在开始治疗前 LDL-C 已经低至 60-80mg/dL 的患者。他汀类药物是治疗高胆固醇血症的一线药物,可有效降低 LDL-C,但许多患者尽管接受了强化他汀类药物治疗,仍无法达到最佳的血脂目标。因此,人们强烈希望开发新型药物来进一步降低已经接受他汀类药物治疗的患者的 LDL-C。导致胆固醇稳态改变的基因突变提供了有关治疗高胆固醇血症新方法的有价值信息。为此,前蛋白转化酶枯草溶菌素/糜蛋白酶 9(PCSK9)的突变与 LDL-C 水平的改变有关,说明了该蛋白在脂质代谢中的作用。PCSK9 促进 LDL 受体的降解,阻止其转运回细胞表面,从而增加循环 LDL-C。相反,抑制 PCSK9 可以显著降低循环 LDL-C,因此是降低 LDL-C 治疗的一个有吸引力的新靶点。AMG 145 是一种完全人源化单克隆 IgG2 抗体,特异性结合人 PCSK9 并抑制其与 LDL 受体的相互作用。在本文中,我们描述了 LDL-C 评估与 PCSK9 单克隆抗体抑制联合他汀类药物治疗-心肌梗死溶栓治疗 57 期(LAPLACE-TIMI 57;NCT01380730)的原理和设计,这是一项为期 12 周的随机、双盲、剂量范围、安慰剂对照研究,旨在评估 AMG 145 联合他汀类药物治疗高胆固醇血症患者的安全性和疗效。