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PCSK9 Antibodies Safely Cut LDL in Phase II

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Antibodies Offer New Approach to LDL Reduction

In these studies, the antibodies showed quite good lipid-lowering effects and quite good safety. They seemed as potent as moderate- to high-potency statins. Some of the antibodies also lower lipoprotein(a), an added plus.

Medicine has been bumping up against statin intolerance in typical post–myocardial infarction patients. We have aggressive LDL cholesterol goals for these patients, and we get frustrated that we often can’t get them to their goal level. We need to do better for patients at moderate and high cardiovascular disease risk.

Mitchel L. Zoler/IMNG Medical Media


Dr. Peter W.F. Wilson

High-potency statins reduce LDL cholesterol by about 50%, which leaves room for improvement, plus not every patient does well on a statin. Some patients have myalgia or a liver-function abnormality; roughly 5%-15% of patients prescribed a statin are unable to take the most appropriate dose because of an adverse effect. We have a clear need for different and better ways to lower LDL cholesterol.

The other major target for a new LDL-lowering drug is patients with heterozygous familial hypercholesterolemia. About 500,000-1,000,000 of these patients are American, with a worldwide prevalence of about 10 million. More than half of these patients don’t know they have the disease. Because they start with very high LDL levels, conventional treatment with a potent statin and ezetimibe often does not provide enough LDL reduction.

The phase II results indicate that the antibodies produced a low rate of myalgias. A few patients had large creatinine kinase elevations, and this effect needs further assessment in larger studies, plus more scrutiny is needed of immunologic effects and triggering of antibody reactions to the administered antibody protein. And the impact of treatment with these antibodies needs testing in large studies with cardiovascular disease end points. But so far the results are extremely encouraging for effective lowering of LDL cholesterol, non-HDL cholesterol, and apoprotein B.

Peter W.F. Wilson, M.D., is a professor of medicine in the Clinical Cardiovascular Research Institute of Emory University in Atlanta. Dr. Wilson said that he had no relevant disclosures. He made these comments as the invited discussant, and in an interview.


 

AT THE ANNUAL SCIENTIFIC SESSIONS OF THE AMERICAN HEART ASSOCIATION

• A third study of the Amgen 145 antibody, RUTHERFORD (Reduction of LDL-C with PCSK9 Inhibition in Heterozygous Familial Hypercholesterolemia Disorder), enrolled 167 patients with heterozygous familial hypercholesterolemia who had LDL cholesterol levels of at least 100 mg/dL despite a stable lipid-lowering regimen. The highest dosage of the antibody tested, 420 mg delivered subcutaneously every 4 weeks, led to an average 55% reduction in LDL cholesterol during 12 weeks of treatment in 56 patients, reported Dr. Frederick Raal, head of the division of endocrinology and metabolism at the University of Witwatersrand in Johannesburg, South Africa. Two-thirds of the patients who received this tested dosage achieved an LDL cholesterol level of less than 70 mg/dL.

Two patients treated with the highest dosage had serious adverse events, compared with none of the 56 placebo-treated patients. Four of the patients on the highest dosage had muscle-related adverse events, compared with two of the placebo patients. In addition, two patients in the highest-dosage group had a creatine kinase elevation greater than five times the upper limit of normal, compared with none of the placebo patients. Results from the study were published online concurrent with Dr. Raal’s report (Circulation 2012;126:2408-17).

• The fourth Amgen 145 study, GAUSS (Goal Achievement after Utilizing an Anti-PCSK9 Antibody in Statin Intolerant Subjects), enrolled 157 patients at cardiovascular risk who were unable to tolerate effective statin doses because of muscle-related adverse effects. The highest dosage of the antibody administered alone tested, 420 mg given subcutaneously every 4 weeks, lowered LDL cholesterol by an average of 51% in 31 patients, reported Dr. Evan A. Stein, director of the Metabolic and Atherosclerosis Research Center in Cincinnati. Among 29 patients who received the same antibody dosage plus 10 mg of ezetimibe daily, average LDL cholesterol fell by 63%.

Three patients who received the antibody stopped treatment because of an adverse effect, compared with two placebo patients. Two of the patients on antibody treatment had creatine kinase elevations greater than 10 times the upper limit of normal. Results from the study were published online concurrent with Dr. Stein’s report (JAMA 2012;308 [doi: 10.1001/jama.2012.25790]).

• The fifth phase II study report at the meeting dealt with an antibody under development by Pfizer, RN316. That study enrolled 135 patients with primary hypercholesterolemia who were not at their goal LDL cholesterol level despite high- or maximal-dosage statin regimens. Patients received one of four dosages of the antibody or placebo as an intravenous infusion every 4 weeks. After 12 weeks of treatment, patients on the highest tested dosage had an average 60% reduction in their LDL cholesterol level, reported Dr. Barry Gumbiner, an endocrinologist and executive director of clinical research for Pfizer in South San Francisco, Calif.

Three patients who received RN316 had a serious adverse event, and one patient stopped the study medication because of an adverse event. Five patients who received the antibody developed myalgia, and one patient had a significant rise in creatinine kinase to greater than 10 times the upper limit of normal. No patients had a clinically significant rise in liver enzymes.

The Amgen 145 studies were sponsored by Amgen. The RN316 study was sponsored by Pfizer. Dr. Giugliano said that he has been a consultant to Amgen. Dr. Koren said that he has received research grants from Amgen. Dr. Raal said that he has received research funding from Amgen and Sanofi. Dr. Stein said that he has been a consultant to Amgen, Adnexus Therapeutics, and Sanofi, and that he has received research support from Amgen, Sanofi, and Regeneron. Dr. Gumbiner said that he is an employee of Pfizer.

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