THOUSAND OAKS, Calif., Nov. 15, 2016 /PRNewswire/ -- Amgen (NASDAQ:AMGN) today announced that adding Repatha ® (evolocumab) to optimized statin therapy resulted in statistically significant regression of atherosclerosis in patients with coronary artery disease (CAD). The detailed results from the GLAGOV Phase 3 coronary intravascular ultrasound imaging trial were presented at a Late-Breaking Clinical Trials Session of the American Heart Association (AHA) Scientific Sessions 2016 and simultaneously published in the Journal of the American Medical Association. To view the multimedia assets associated with this release, please click: http://www.multivu.com/players/English/74140513-amgen-repatha-glagov-study.
The GLAGOV study evaluated whether Repatha, a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor for the treatment of certain patients with elevated low-density lipoprotein cholesterol (LDL-C), would modify atherosclerotic plaque build-up in the coronary arteries of patients already treated with optimized statin therapy, as measured by intravascular ultrasound (IVUS) at baseline and week 78. "The cardiovascular community began conducting imaging studies with LDL-C therapies to measure slowing of atherosclerotic disease progression. This study shows that maximal LDL-C reduction with Repatha can actually regress coronary atherosclerotic disease compared to statins alone," said Sean E. Harper, M.D., executive vice president of Research and Development at Amgen. "In fact, nearly two-thirds of patients on Repatha in this trial, the vast majority of whom were already on high to moderate intensity statin therapy at baseline, experienced a reduction in plaque burden." The study met its primary objective showing that treatment with Repatha resulted in a statistically significant regression from baseline in percent atheroma volume (PAV), which is the proportion of arterial lumen occupied by plaque. Patients in the Repatha arm experienced a 0.95 percent decrease versus baseline in PAV compared with an increase of 0.05 percent versus baseline in patients receiving optimized statin therapy plus placebo (Repatha arm p<0.0001; placebo arm p=0.78). The difference between the two comparators was statistically significant ( p<0.0001). In addition, adding Repatha yielded plaque regression in PAV for a greater percentage of patients than for those receiving placebo (64.3 percent versus 47.3 percent, respectively, p<0.0001). At baseline, 98 percent of patients in both arms were on high to moderate intensity statin therapy. Patients in the Repatha arm experienced a mean decrease in normalized total atheroma volume (TAV), which is a measure of plaque volume, of 5.8mm³ compared with 0.9mm³ seen in the placebo arm (Repatha arm p<0.0001; placebo arm p=0.45). The difference between the two comparators was statistically significant ( p<0.0001). Additionally, adding Repatha yielded plaque regression in TAV for a greater percentage of patients than placebo (61.5 percent versus 48.9 percent, respectively, p=0.0002). "Based on previous studies, we did not know if GLAGOV would show additional plaque regression at LDL-C levels below 60 mg/dL," said Stephen J. Nicholls, M.D., Ph.D., professor of Cardiology and deputy director, South Australian Health & Medical Research Institute, Adelaide, Australia. "One of the most compelling results from GLAGOV is the continued reduction of plaque at LDL-C levels well below commonly accepted thresholds." At baseline, patients had a mean LDL-C of 92.5 mg/dL across both treatment arms. During 78 weeks of treatment, the time-weighted mean LDL-C level was 36.6 mg/dL in the Repatha arm, which represents a reduction of 59.8 percent, compared with 93.0 mg/dL in the placebo arm. At week 78, the mean LDL-C in the Repatha arm was 29 mg/dL, which represents a 68.0 percent decrease from baseline, and in the placebo arm was 90 mg/dL.