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GSK冠心病药物darapladib第二个III期试验失败

来源:生物谷 2014-05-14 08:42

2014年5月13日讯 /生物谷BIOON/ --葛兰素史克(GSK)5月13日公布了实验性冠心病(CHD)药物darapladib III期项目中第2个III期试验SOLID-TIMI 52的研究数据。SOLID-TIMI 52是一项随机、安慰剂对照、双盲、平行组多中心研究,调查了darapladib作为一种长期疗法,用于30天内发生急性冠脉综合征(ACS)患者的疗效和安全性。数据表明,与安慰剂相比,darapladib未能达到显著降低主要不良心血管事件(包括心血管死亡,心肌梗死和中风)的主要终点。研究中的安全数据与此前报道的一致。该项研究的进一步数据分析正在进行中。

此前,GSK于2013年11月公布了darapladib III期项目首个III期研究STABILITY的数据。该项研究在冠心病(CHD)成人患者中开展,数据表明,与安慰剂相比,darapladib未能降低心脏病发作和中风的整体风险,未能达到研究的主要终点。

darapladib是GSK最寄予厚望的药物之一,该药2项III期试验接连失败,对GSK而言是一个重大打击。

GSK于2012年耗资30亿美元收购人类基因组科学公司(HGS)后,获得了狼疮药物Benlysta,同时获得了darapladib的全部权利。尽管一些业内分析师认为,darapladib如果取得成功,将有望成为一个年销售额达100亿美元的重磅药物。但根据汤姆森路透药业,目前的共识预测指出,darapladib在2018年的年销售额将仅为6.05亿美元。

(注:急性冠脉综合征(ACS)是冠心病的一种急症,发病时情况最为危急,是导致冠心病死亡的主要原因,且有极高复发风险。)

关于darapladib:

darapladib是一种选择性、口服有效的脂蛋白相关磷脂酶A2(lipoprotein-associated phospholipase A2, Lp-PLA2)抑制剂,目前正调查作为一种潜在的药物,用于降低冠心病(CHD)患者的心血管事件。Lp-PLA2是一种蛋白酶,存在于血液和动脉粥样斑块中。动脉粥样硬化的发生和发展与升高的Lp-PLA2活性相关。(生物谷Bioon.com)

英文原文:GSK announces phase III study with darapladib did not meet primary endpoint in patients following an acute coronary syndrome

Issued: Tuesday 13 May 2014, London UK – LSE announcement

GlaxoSmithKline (LSE/NYSE: GSK) today announced headline results from its second phase III study with darapladib, SOLID-TIMI 52, evaluating the efficacy of its investigational Lp-PLA2 inhibitor in adults following an acute coronary syndrome.

In the study, darapladib did not achieve the primary endpoint of a reduction of major coronary events versus placebo when added to standard of care. The overall safety profile for darapladib showed no major safety concerns and was generally consistent with the safety data seen in the previously reported phase III study, STABILITY. Further analysis of the data is ongoing. Darapladib is not approved for use anywhere in the world.

Acute coronary syndrome is a term used to describe situations or events, including heart attack, where there is a sudden reduction of blood flow to the heart. Initial presentation by a patient with acute coronary syndrome results in a diagnosis of coronary heart disease.

The primary endpoint measure in the SOLID-TIMI 52 study was time to first occurrence of any event from the composite of coronary heart disease death, myocardial infarction (heart attack) and urgent coronary revascularisation (medical procedures performed to restore normal blood flow in patients with atherosclerosis) for myocardial ischemia. Full results of the SOLID-TIMI 52 study will be presented at a scientific meeting.

About the SOLID-TIMI 52 trial and the phase III programme

SOLID-TIMI 52 (Stabilisation Of pLaques usIng Darapladib – Thrombolysis In Myocardial Infarction 52) is the second of two event-driven phase III studies with darapladib in coronary heart disease.

In November 2013, GSK announced results of the first study, STABILITY, which showed that darapladib did not achieve a statistically significant reduction in the primary endpoint of major adverse cardiovascular events (comprised of cardiovascular death, myocardial infarction and stroke) versus placebo in patients with chronic coronary heart disease.

In SOLID-TIMI 52, darapladib was tested as a long-term therapy in patients within 30 days of an acute coronary syndrome. The randomised, placebo-controlled, double-blind, parallel group multi-centre study enrolled more than 13,000 patients across 36 countries. The study design of SOLID-TIMI 52 was published in the October 2011 edition of the American Heart Journal (M.L O’Donoghue et al).

The SOLID-TIMI 52 study was led by the TIMI Study Group, Brigham and Women's Hospital, Boston, Massachusetts.

About darapladib and atherosclerosis

Elevated Lp-PLA2 activity has been implicated in the development and progression of atherosclerosis. Darapladib is a selective and orally active inhibitor of Lp-PLA2 (lipoprotein-associated phospholipase A2).  Lp-PLA2 is an enzyme that is found in blood and in atherosclerotic plaques.  Atherosclerosis is an inflammatory condition characterised by the build-up of plaques of fat, cholesterol and other substances within the walls of arteries. When these plaques rupture they can block vital blood vessels, causing acute coronary syndromes (heart attacks) and strokes.  

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