THOUSAND OAKS, Calif.,
June 10, 2015 /PRNewswire/
-- Amgen (NASDAQ: AMGN) today announced that the Company will
discuss the data supporting the
RepathaTM (evolocumab) Biologics License
Application (BLA) for the treatment of high cholesterol with the
U.S. Food and Drug Administration's (FDA) Endocrinologic and
Metabolic Drugs Advisory Committee (EMDAC). Repatha is an
investigational fully human monoclonal antibody that inhibits
proprotein convertase subtilisin/kexin type 9 (PCSK9), a protein
that reduces the liver's ability to remove low-density lipoprotein
cholesterol (LDL-C), or "bad" cholesterol, from the
blood.1
At today's FDA advisory committee meeting, Amgen will present
Repatha clinical trial data from approximately 6,800 patients,
including more than 4,500 patients with high cholesterol in 10
Phase 3 trials. The Phase 3 studies evaluated the efficacy and
safety of Repatha in patients with elevated cholesterol, including
patients on statins with or without other lipid-lowering therapies;
patients who cannot tolerate statins; patients with heterozygous
familial hypercholesterolemia (HeFH) and patients with homozygous
familial hypercholesterolemia (HoFH), a rare and serious genetic
disorder.2
"We look forward to discussing the efficacy and safety data from
our clinical program with the FDA advisory committee as there
remains a significant unmet medical need for patients who, despite
currently available therapies, are unable to control their high
cholesterol," said Sean E. Harper, M.D., executive vice
president of Research and Development at Amgen. "If approved,
Repatha would provide patients and physicians with an important new
treatment option for managing high cholesterol."
The FDA has set a Prescription Drug User Fee Act (PDUFA) target
action date of Aug. 27, 2015, for the Repatha BLA.
High cholesterol, particularly elevated LDL-C, is the most
common form of dyslipidemia, which is an abnormality of cholesterol
and/or fats in the blood.3,4 Nearly one in three
Americans have elevated LDL-C,5 which is recognized as a
major risk factor for cardiovascular disease.6,7
Familial hypercholesterolemia (FH) is an inherited condition caused
by genetic mutations which lead to high levels of LDL-C at an early
age,2 and it is estimated that less than one percent of
people with FH (heterozygous and homozygous forms) in the U.S. are
diagnosed.8
PROFICIO Clinical Program Results
PROFICIO, which
stands for the Program to Reduce LDL-C and Cardiovascular Outcomes
Following Inhibition of PCSK9 In Different POpulations, is a large
and comprehensive clinical trial program evaluating Repatha.
PROFICIO includes 22 clinical trials, with a combined planned
enrollment of approximately 35,000 patients.
In data from the clinical program to date, Repatha has
demonstrated consistent, significant and durable reduction in LDL-C
levels with favorable effects on other lipid parameters in
approximately 6,000 patients with primary hyperlipidemia and mixed
dyslipidemia.9 In these studies, Repatha reduced LDL-C
by approximately 55 percent to 75 percent compared with
placebo10-13 and by approximately 35 percent to 45
percent compared with ezetimibe.10,11,13 In patients
with HoFH, Repatha reduced LDL-C by approximately 30 percent
compared with placebo.14 Reduction of LDL-C was
maintained with long-term treatment.15
The adverse event profile for Repatha was similar overall to
that of the control groups.10-16 The most common adverse
events that occurred in greater than or equal to 2 percent of the
Repatha group, and more frequently than in the control group, were
nasopharyngitis (5.9 percent Repatha; 4.8 percent any control),
upper respiratory tract infection (3.2 percent Repatha; 2.7 percent
any control), back pain (3.0 percent Repatha; 2.7 percent any
control), arthralgia (2.3 percent Repatha; 2.2 percent any
control), influenza (2.1 percent Repatha; 2.0 percent any control)
and nausea (2.1 percent Repatha; 1.8 percent any control).
About RepathaTM
(evolocumab)
RepathaTM (evolocumab) is a fully
human monoclonal antibody that inhibits proprotein convertase
subtilisin/kexin type 9 (PCSK9).1 PCSK9 is a protein
that targets LDL receptors for degradation and thereby reduces the
liver's ability to remove LDL-C, or "bad" cholesterol, from the
blood.17 Repatha, being developed by Amgen scientists,
is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL
receptors on the liver surface. In the absence of PCSK9, there are
more LDL receptors on the surface of the liver to remove LDL-C from
the blood.1
The FDA has provisionally approved the use of the trade name
Repatha.
About Amgen Cardiovascular
Building on more than three
decades of experience in developing biotechnology medicines for
patients with serious illnesses, Amgen is dedicated to addressing
important scientific questions to advance care and improve the
lives of patients with cardiovascular disease, the leading cause of
morbidity and mortality worldwide.18 Amgen's research
into cardiovascular disease, and potential treatment options, is
part of a growing competency at Amgen that utilizes human genetics
to identify and validate certain drug targets. Through its own
research and development efforts, as well as partnerships, Amgen is
building a robust cardiovascular pipeline consisting of several
investigational molecules in an effort to address a number of
today's important unmet patient needs, such as high cholesterol and
heart failure.
About Amgen
Amgen is committed to unlocking the
potential of biology for patients suffering from serious illnesses
by discovering, developing, manufacturing and delivering innovative
human therapeutics. This approach begins by using tools like
advanced human genetics to unravel the complexities of disease and
understand the fundamentals of human biology.
Amgen focuses on areas of high unmet medical need and leverages
its biologics manufacturing expertise to strive for solutions that
improve health outcomes and dramatically improve people's lives. A
biotechnology pioneer since 1980, Amgen has grown to be one of the
world's leading independent biotechnology companies, has reached
millions of patients around the world and is developing a pipeline
of medicines with breakaway potential.
For more information, visit www.amgen.com and follow us on
www.twitter.com/amgen.
Forward-Looking Statements
This news release contains
forward-looking statements that are based on management's current
expectations and beliefs and are subject to a number of risks,
uncertainties and assumptions that could cause actual results to
differ materially from those described. All statements, other than
statements of historical fact, are statements that could be deemed
forward-looking statements, including estimates of revenues,
operating margins, capital expenditures, cash, other financial
metrics, expected legal, arbitration, political, regulatory or
clinical results or practices, customer and prescriber patterns or
practices, reimbursement activities and outcomes and other such
estimates and results. Forward-looking statements involve
significant risks and uncertainties, including those discussed
below and more fully described in the Securities and Exchange
Commission (SEC) reports filed by Amgen, including Amgen's most
recent annual report on Form 10-K and any subsequent periodic
reports on Form 10-Q and Form 8-K. Please refer to Amgen's most
recent Forms 10-K, 10-Q and 8-K for additional information on the
uncertainties and risk factors related to our business. Unless
otherwise noted, Amgen is providing this information as of
June 10, 2015, and expressly
disclaims any duty to update information contained in this news
release.
No forward-looking statement can be guaranteed and actual
results may differ materially from those we project. Discovery or
identification of new product candidates or development of new
indications for existing products cannot be guaranteed and movement
from concept to product is uncertain; consequently, there can be no
guarantee that any particular product candidate or development of a
new indication for an existing product will be successful and
become a commercial product. Further, preclinical results do not
guarantee safe and effective performance of product candidates in
humans. The complexity of the human body cannot be perfectly, or
sometimes, even adequately modeled by computer or cell culture
systems or animal models. The length of time that it takes for us
to complete clinical trials and obtain regulatory approval for
product marketing has in the past varied and we expect similar
variability in the future. We develop product candidates internally
and through licensing collaborations, partnerships and joint
ventures. Product candidates that are derived from relationships
may be subject to disputes between the parties or may prove to be
not as effective or as safe as we may have believed at the time of
entering into such relationship. Also, we or others could identify
safety, side effects or manufacturing problems with our products
after they are on the market. Our business may be impacted by
government investigations, litigation and products liability
claims. We depend on third parties for a significant portion of our
manufacturing capacity for the supply of certain of our current and
future products and limits on supply may constrain sales of certain
of our current products and product candidate development.
In addition, sales of our products are affected by the
reimbursement policies imposed by third-party payors, including
governments, private insurance plans and managed care providers and
may be affected by regulatory, clinical and guideline developments
and domestic and international trends toward managed care and
healthcare cost containment as well as U.S. legislation affecting
pharmaceutical pricing and reimbursement. Government and others'
regulations and reimbursement policies may affect the development,
usage and pricing of our products. In addition, we compete with
other companies with respect to some of our marketed products as
well as for the discovery and development of new products. We
believe that some of our newer products, product candidates or new
indications for existing products, may face competition when and as
they are approved and marketed. Our products may compete against
products that have lower prices, established reimbursement,
superior performance, are easier to administer, or that are
otherwise competitive with our products. In addition, while we
routinely obtain patents for our products and technology, the
protection offered by our patents and patent applications may be
challenged, invalidated or circumvented by our competitors and
there can be no guarantee of our ability to obtain or maintain
patent protection for our products or product candidates. We cannot
guarantee that we will be able to produce commercially successful
products or maintain the commercial success of our existing
products. Our stock price may be affected by actual or perceived
market opportunity, competitive position, and success or failure of
our products or product candidates. Further, the discovery of
significant problems with a product similar to one of our products
that implicate an entire class of products could have a material
adverse effect on sales of the affected products and on our
business and results of operations. Our efforts to integrate the
operations of companies we have acquired may not be successful. We
may experience difficulties, delays or unexpected costs and not
achieve anticipated benefits and savings from our recently
announced restructuring plan. Our business performance could affect
or limit the ability of our Board of Directors to declare a
dividend or their ability to pay a dividend or repurchase our
common stock.
The scientific information discussed in this news release
related to our product candidates is preliminary and investigative.
Such product candidates are not approved by the U.S. Food and Drug
Administration (FDA), and no conclusions can or should be drawn
regarding the safety or effectiveness of the product
candidates.
CONTACT: Amgen, Thousand
Oaks
Kristen Davis, 805-447-3008
(media)
Trish Hawkins, 805-447-5631
(media)
Arvind Sood, 805-447-1060
(investors)
References
- Amgen Data on File, Investigator Brochure.
- National Human Genome Research Institute. Learning About
Familial Hypercholesterolemia. http://www.genome.gov/25520184.
Accessed June 2015.
- World Health Organization. Quantifying Selected Major Risks to
Health. In: The World Health Report 2002 - Reducing Risks,
Promoting Healthy Life. Geneva.
2002:49-97.
- Merck Manuals website.
http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/lipid_disorders/dyslipidemia.html.
Accessed June 2015.
- Mozaffarian D, Benjamin EJ, Go AS, et al. Heart Disease and
Stroke Statistics—2015 Update: A Report From the American Heart
Association. Circulation. 2014;131;e1-e295.
- American Heart Association (2014). Why cholesterol matters.
http://www.heart.org/HEARTORG/Conditions/Cholesterol/WhyCholesterolMatters/Why-Cholesterol-Matters_UCM_001212_Article.jsp.
Accessed June 2015.
- World Health Organization. Global status report on
noncommunicable diseases 2014. Geneva, 2014.
- Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial
Hypercholesterolaemia is Underdiagnosed and Undertreated in the
General Population: Guidance for Clinicians to Prevent Coronary
Heart Disease. Eur Heart J. 2013;34:3478-3490.
- Sabatine MS, Giugliano RP, Wiviott SD, et al. Efficacy and
Safety of Evolocumab in Reducing Lipids and Cardiovascular Events.
N Engl J Med. 2015;372:1500-1509.
- Koren MJ, Lundqvist P, Bolognese M, et al. Anti-PCSK9
monotherapy for hypercholesterolemia: the MENDEL-2 randomized,
controlled phase III clinical trial of evolocumab. J Am Coll
Cardiol. 2014;63:2531-2540.
- Robinson JG, Nedergaard BS, Rogers WJ, et al. Effect of
evolocumab or ezetimibe added to moderate or high-intensity statin
therapy on LDL-C lowering in patients with hypercholesterolemia.
The LAPLACE-2 randomized clinical trial. JAMA.
2014;311:1870-1882.
- Raal FJ, Stein EA, Dufour R, et al. PCSK9 inhibition with
evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia
(RUTHERFORD-2): a randomised, double-blind, placebo-controlled
trial. Lancet. 2015;385:331-340.
- Stroes E, Colquhoun D, Sullivan D, et al. Anti-PCSK9 antibody
effectively lowers cholesterol in patients with statin intolerance:
the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial
of evolocumab. J Am Coll Cardiol. 2014;63:2541-2548.
- Raal FJ, Honarpour N, Blom DJ, et al. Inhibition of PCSK9 with
evolocumab in homozygous familial hypercholesterolaemia (TESLA Part
B): a randomised, double-blind, placebo-controlled trial.
Lancet. 2015;385:341-50.
- Blom DJ, Hala T, Bolognese M. A 52-week placebo-controlled
trial of evolocumab in hyperlipidemia. N Engl J Med.
2014;370:1809-1819.
- Koren MJ, Giugliano RP, Raal FJ, et al. Efficacy and
Safety of Longer-Term Administration of Evolocumab (AMG 145) in
Patients With Hypercholesterolemia: 52-Week Results from the
Open-Label Study of Long-Term Evaluation Against LDL-C (OSLER)
Randomized Trial. Circulation. 2014;129:234-243.
- Qian Y-W, Schmidt RJ, Zhang Y, et al. Secreted PCSK9
downregulates low density lipoprotein receptor through
receptor-mediated endocytosis. J. Lipid Res.
2007;48:1488-1498.
- World Health Organization. Cardiovascular diseases (CVDs) fact
sheet. http://www.who.int/mediacentre/factsheets/fs317/en/.
Accessed June 2015.
Logo - http://photos.prnewswire.com/prnh/20081015/AMGENLOGO
To view the original version on PR Newswire,
visit:http://www.prnewswire.com/news-releases/amgen-to-discuss-details-of-repatha-evolocumab-biologics-license-application-for-the-treatment-of-high-cholesterol-300096889.html
SOURCE Amgen