Novartis data shows ACZ885 for severe gouty arthritis provided better pain relief and reduced risk of new attacks by up to 68% vs. steroid
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Novartis International AG /
Novartis data shows ACZ885 for severe gouty arthritis provided better pain
relief and reduced risk of new attacks by up to 68% vs. steroid
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The issuer is solely responsible for the content of this announcement.
* Two pivotal Phase III studies( )showed ACZ885 may meet significant unmet
need for patients for whom many standard therapies are inadequate or
inappropriate[1],[2]
* Gouty arthritis, commonly referred to as gout, is an inflammatory disease
affecting 1-4% of adults, causing severe pain and long-term consequences[3]-
[7]
* Regulatory filings for the use of ACZ885 in gouty arthritis patients with
limited treatment options have been submitted in the EU, US, Canada and
Switzerland
Basel, May 25, 2011 - Novartis announced positive results of two pivotal Phase
III trials in patients with severe gouty arthritis, showing that ACZ885
(canakinumab) provided superior pain relief and reduced the risk of new attacks
by up to 68% compared to an injectable steroid (triamcinolone acetonide, TA)
used to treat gouty arthritis attacks[1],[2]. ACZ885 is an investigational,
fully human monoclonal antibody.
The studies involved more than 450 gouty arthritis patients for whom the
standard anti-inflammatory therapies, non-steroidal anti-inflammatory drugs
(NSAIDs) or colchicine, were inadequate or inappropriate[1],[2]. Results will be
presented for the first time at the 2011 European League Against Rheumatism
(EULAR) Congress in London.
"These findings show that ACZ885 may represent an important advance in the
treatment of gouty arthritis in sufferers whose disease cannot be appropriately
managed with currently available treatments," said Professor Alexander So,
Rheumatology Department, CHUV, Lausanne, Switzerland, and one of the studies'
investigators. "Scientists only recently learned that the root cause of the pain
in gouty arthritis is interleukin-1 beta. Through specifically targeting
interleukin-1 beta, these studies show ACZ885 can effectively treat painful
attacks while extending the time to new attacks."
Both trials used an internationally recognized pain scale to measure differences
in pain 72 hours after treatment, and found ACZ885 reduced pain by an additional
-11.4 millimeters (mm) (p=0.0005) in one study and -9.8 mm in the other
(p=0.0018), compared to TA[1]. ACZ885 also significantly reduced the risk of
suffering a new gouty arthritis attack within three months, by 55% in one study
(p=0.0014) and 68% in the other (p<0.0001), compared to TA[2].
Gouty arthritis, commonly referred to as gout, is a serious, chronic and
progressive inflammatory disease that affects 1-4% of adults[3]-[7]. In the UK,
an estimated 1.4% of the population suffers from gouty arthritis[6], while in
the US, 3.9% of the population has the condition[7]. Gouty arthritis is the most
common form of inflammatory arthritis in adults, with a prevalence comparatively
higher than rheumatoid arthritis, which is estimated to affect 0.5-1% of
adults[8].
"We are very excited about these results, which indicate that ACZ885 may become
a significant new alternative for gouty arthritis patients where many standard
anti-inflammatory treatments are inadequate or inappropriate," said David
Epstein, Head of the Pharmaceuticals Division of Novartis. "Novartis is
committed to meeting this unmet medical need and to further investigating the
potential of ACZ885 in a number of other conditions where interleukin-1 beta may
play a role."
Gouty arthritis attacks occur when the body has a strong inflammatory response
to uric acid crystals forming in the affected joint, typically of the toe, foot,
ankle or knee[9]-[11]. This intense inflammatory response causes the severe pain
associated with gouty arthritis attacks, which can last for a week or
more[3],[11]-[13]. Gouty arthritis may also result in chronic disability and
joint destruction[14]-[16].
Treatments currently available to manage the pain and inflammation of gouty
arthritis attacks, such as NSAIDs or colchicine, may be inadequate or
inappropriate in patients who have coexisting medical problems[17]-[19]. This
poses a significant unmet treatment need in gouty arthritis. New data presented
at EULAR today indicates nearly 90% of gouty arthritis patients in the EU and
the US have at least one coexisting disease[20], a portion of whom may be unable
to take these standard anti-inflammatory therapies.
Regulatory filings for the use of ACZ885 in gouty arthritis patients with
limited treatment options were submitted in the EU in 2010 and in the US, Canada
and Switzerland in the first quarter of 2011.
About the Studies
The two studies were Phase III, 12-week, randomized, multicenter, double-blind,
double dummy, active-controlled studies involving 228 and 226 patients who met
the American College of Rheumatology (ACR) criteria for acute gouty
arthritis[1],[2]. Patients had suffered from three or more gouty arthritis
attacks in the previous 12 months and were either unresponsive or intolerant to
common therapies such as NSAIDs or colchicine, or these treatments were
contraindicated. Patients were randomized to receive a single dose of ACZ885
150 milligrams (mg) via subcutaneous (s.c.) injection or TA 40 mg via
intramuscular (i.m.) injection[1],[2]. In the case of a new attack, patients
received a new dose of the same treatment they were randomized to at baseline.
Both studies had the same two primary endpoints: pain intensity at 72 hours
post-dose; and time to the first new gouty arthritis attack[1],[2]. Pain in the
affected joint was measured according to an internationally recognized pain
scale, the Visual Analog Scale (VAS).
In one study, patients treated with ACZ885 had significantly lower mean pain
scores from baseline compared to TA, pain intensity at 72 hrs was 28.1 mm for
ACZ885 and 39.5 mm for TA (p=0.0005)[1]. Similarly, patients in the other study
receiving ACZ885 had significantly lower mean pain scores from baseline compared
to TA, pain intensity at 72 hrs was 22.1 mm for ACZ885 and 31.9 mm for TA
(p=0.0018)[1]. In both studies, the respective decreases of 46 and 53 mm from
baseline with ACZ885 exceeded those of 35 and 43 mm seen with TA[1].
The number of patients with new attacks across both studies was also
significantly reduced with ACZ885 compared to TA[2]. In the first study, nearly
twice as many patients experienced a new gouty arthritis attack in the TA group
compared to ACZ885 (40 vs. 21 patients respectively [p=0.0061])[2]. In addition,
in the second study nearly three times as many patients in the TA group
experienced a new attack compared to ACZ885 (42 vs. 15 patients respectively
[p=0.0001])[2]. In the previous year, patients in both studies suffered an
average of at least six attacks (6.5 for ACZ885 and seven for TA in study one;
and 6.5 and 5.9 respectively in study two)[21],[22].
ACZ885 was generally well tolerated in the two studies. In one study, 55.8% of
patients had adverse events (AEs) with ACZ885 vs. 38.3% with TA[21]. In the
other study, 54.5% of patients had AEs with ACZ885 vs. 50.9% with TA[22].
Serious adverse events (SAEs), 10 for ACZ885 vs. five for TA in one study and
three for ACZ885 vs. one for TA in the other study, were not considered to be
related to study medication by the investigators[21],[22].
About ACZ885
ACZ885 is a fully human monoclonal antibody that provides selective inhibition
of interleukin-1 beta (IL-1 beta), which is part of the body's immune system
defenses[23]. Excessive production of IL-1 beta plays a major role in many
inflammatory diseases, including gouty arthritis[24]. ACZ885 works by
neutralizing IL-1 beta for a sustained period of time, therefore inhibiting
inflammation[23].
Under the brand name Ilaris(®), ACZ885 is approved in more than 45 countries,
including the EU, US and Switzerland for the treatment of adults and children as
young as four with Cryopyrin-Associated Periodic Syndromes (CAPS), a rare,
lifelong, inflammatory disorder with debilitating symptoms[24]. ACZ885 is also
being studied in other diseases in which IL-1 beta plays a key role in causing
inflammation, such as Systemic Juvenile Idiopathic Arthritis (SJIA),
cardiovascular disease and diabetes. Not all potential patients with these
diseases would be eligible for treatment with ACZ885, if approved.
Disclaimer
The foregoing release contains forward-looking statements that can be identified
by terminology such as "may", "will", "committed", "potential" or similar
expressions, or by express or implied discussions regarding potential new
indications or labeling for ACZ885 or regarding potential future revenues from
ACZ885. You should not place undue reliance on these statements. Such forward-
looking statements reflect the current views of management regarding future
events, and involve known and unknown risks, uncertainties and other factors
that may cause actual results with ACZ885 to be materially different from any
future results, performance or achievements expressed or implied by such
statements. There can be no guarantee that ACZ885 will be approved for any
additional indications or labeling in any market, or at any particular time. Nor
can there be any guarantee that ACZ886 will achieve any particular levels of
revenue in the future. In particular, management's expectations regarding ACZ885
could be affected by, among other things, unexpected regulatory actions or
delays or government regulation generally; unexpected clinical trial results,
including unexpected new clinical data and unexpected additional analysis of
existing clinical data; competition in general; government, industry and general
public pricing pressures; the company's ability to obtain or maintain patent or
other proprietary intellectual property protection, the impact that the
foregoing factors could have on the values attributed to the Novartis Group's
assets and liabilities as recorded in the Group's consolidated balance sheet,
and other risks and factors referred to in Novartis AG's current Form 20-F on
file with the US Securities and Exchange Commission. Should one or more of these
risks or uncertainties materialize, or should underlying assumptions prove
incorrect, actual results may vary materially from those anticipated, believed,
estimated or expected. Novartis is providing the information in this press
release as of this date and does not undertake any obligation to update any
forward-looking statements contained in this press release as a result of new
information, future events or otherwise.
About Novartis
Novartis provides healthcare solutions that address the evolving needs of
patients and societies. Focused solely on healthcare, Novartis offers a
diversified portfolio to best meet these needs: innovative medicines, eye care,
cost-saving generic pharmaceuticals, consumer health products, preventive
vaccines and diagnostic tools. Novartis is the only company with leading
positions in these areas. In 2010, the Group's continuing operations achieved
net sales of USD 50.6 billion, while approximately USD 9.1 billion (USD 8.1
billion excluding impairment and amortization charges) was invested in R&D
throughout the Group. Headquartered in Basel, Switzerland, Novartis Group
companies employ approximately 119,000 full-time-equivalent associates and
operate in more than 140 countries around the world. For more information,
please visithttp://www.novartis.com.
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http://twitter.com/novartis.
References
[1] So A, Alten R, Bardin T, et al. Canakinumab vs triamcinolone in the
treatment of acute flares in gouty arthritis patients contraindicated,
intolerant and unresponsive to NSAIDs and/or colchicines. Abstract at: The
2011 Annual European Congress of The European League Against Rheumatism;
2011 May 25-28; London, United Kingdom.
[2] Schlesinger N, Alten R, Bardin T, et al. Efficacy of canakinumab vs
triamcinolone acetonide in preventing recurrent flares in acute gouty
arthritis patients contraindicated, intolerated or unresponsive to NSAIDs
and/or colchicine. Oral presentation (OP0107) at: The 2011 Annual European
Congress of The European League Against Rheumatism; 2011 May 25-28; London,
United Kingdom.
[3] Schumacher HR Jr. The pathogenesis of gout. Cleve Clin J Med.
2008; 75(5):S2-4.
[4] Badley E, DesMeules M. Arthritis in Canada: an ongoing challenge. Ottawa:
Public Health Agency of Canada. 2003.
[5] Begg S, Vos T, Barker B, Stevenson C, Stanley L, Lopez AD, 2007. The burden
of disease and injury in Australia 2003. PHE 82. Canberra: AIHW.
[6] Annemans l, Spaepen E, Gaskin M, et al. Gout in the UK and Germany:
prevalence, comorbidities and management in general practice 2000-2005. Ann
Rheum Dis. 2008; 67(7):960-6.
[7] Zhu Y, Pandya B, Choi H. Increasing gout prevalence in the US over the last
two decades: The National Health and Nutrition Examination Survey (NHANES).
Presented at: The American College of Rheumatology Annual Scientific
Meeting; 2010 Oct; Atlanta, GA.
[8] Silman AJ, Pearson JE. Epidemiology and genetics of rheumatoid arthritis.
Arthritis Res. 2002;4 Suppl 3:S265-72.
[9] Martinon F, Glimcher LH. Gout: new insights into an old disease. J Clin
Invest. 2006; 116(8):2073-5.
[10] Martinon F, Petrilli V, Mayor A, Tardivel A, Tschopp J. Gout-associated
uric acid crystals activate the NALP3 inflammasome. Nature.
2006; 440(7081):237-41.
[11] Mandell BF. Clinical manifestations of hyperuricemia and gout. Cleve Clin J
Med. 2008; 75(5):S5-8.
[12] Busso N, So A. Mechanisms of inflammation in gout. Arthritis Res Ther.
2010; 12:206-13.
[13] So A, De Meulemeester M, Pikhlak EA, et al. Canakinumab for the treatment
of acute flares in difficult-to-treat gouty arthritis. Arthritis Rheum.
2010 October ; 62(10):3064-76.
[14] Edwards NL. Clinical gout. In: Hochberg MC, Silman AJ, Smolen JS,
Weinblatt ME, Weisman MH, eds. Rheumatology. 5(th) ed. Philadelphia, PA:
Elievier; 2011:1859-1865.
[15] Dalbeth N, Smith T, Nicolson B, et al. Enhanced osteoclastogenesis in
patients with tophaceous gout. Arthritis Rheum. 2008;58(6)1854-1865.
[16] Schlesinger N, Thiele RG. The pathogenesis of bone erosions in gouty
arthritis. Ann Rheum Dis. 2010;69(11):1907-1912.
[17] Terkeltaub R, Edwards NL. Gout: Diagnosis and Management of Gouty Arthritis
and Hyperuricemia. 1st ed. West Islip, NY: Professional Communications,
Inc; 2010.
[18] Schlesinger N, Dalbeth N, Perez-Ruiz F. Gout-what are the treatment
options? Expert Opin Pharmacother. 2009;10:1319-28.
[19] Jordan KM, Cameron JS, Snaith M, et al. British Society for Rheumatology
and British Health Professionals in Rheumatology guideline for the
management of gout. Rheumatology. 2007;46:1372-4.
[20] Gregson J, Ferreira A. Resource use and treatment patterns in difficult-to-
treat gout patients. Poster (#THU0040) presented at: The 2011 Annual
European Congress of The European League Against Rheumatism; 2011 May
25-28; London, United Kingdom.
[21] So A, Alten R, Bardin T, et al. A controlled trial of canakinumab vs
triamcinolone acetonide in acute gouty arthritis patients: results of the
Beta-RELIEVED study (REsponse in acute fLare and In prEVEntion of episoDes
of re-flare in gout). Oral presentation (OP0108) at: The 2011 Annual
European Congress of The European League Against Rheumatism; 2011 May
25-28; London, United Kingdom.
[22] Schlesinger N, Alten R, Bardin T, et al. Efficacy of canakinumab versus
triamcinolone acetonide in acute gouty arthritis patients: results of the
Beta-RELIEVED II study (REsponse in acute fLare and In prEVEntion of
episoDes of re-flare in gout). Poster (#THU0019) presented at: The 2011
Annual European Congress of The European League Against Rheumatism; 2011
May 25-28; London, United Kingdom.
[23] ILARIS [Prescribing Information]. East Hanover, NJ: Novartis
Pharmaceuticals Corp; 2009.
[24] Church LD, Cook GP, McDermott MF. Primer: inflammasomes and interleukin
1beta in inflammatory disorders. Nat Clin Pract Rheumatol.
2008; 4(1):34-42.
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