Approximately 10% of men and 6% of women over 70 years of age suffer from gout.

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New Phase II data show ACZ885 gave better pain relief and flare prevention for patients with chronic gout than an injectable corticosteroid

New results have shown that the novel biological therapy ACZ885 (canakinumab) is significantly more effective than an injectable corticosteroid at reducing pain and preventing recurrent attacks or ‘flares’ in patients with hard-to-treat gout, one of the most painful forms of arthritis.

The study met its primary endpoint by showing that during acute gout flares, ACZ885 reduced pain faster and more effectively than the injectable corticosteroid triamcinolone acetonide [1], a potent steroid with sustained effect used to treat severe inflammatory conditions (p<0.05) [2].

At the end of the eight-week study, the risk of flare recurrence was 94% less for patients on ACZ885 than for those on the steroid (p = 0.006) [1]. The results were presented recently at the American College of Rheumatology (ACR) Annual Scientific Meeting in Philadelphia, USA.

‘If not appropriately treated, gout can be a devastating condition. Current therapies can have limited efficacy and tolerability, and may be unsuitable for some patients,’ [3,4] said Professor Alexander So, MD, Department of Rheumatology at the University of Lausanne, Switzerland. ‘These results are important because they indicate that canakinumab might provide significant benefit in both the prevention and treatment of painful acute flares in these hard-to-treat patients.’

ACZ885 is a fully human monoclonal antibody that blocks the action of the inflammatory protein interleukin-1 beta (IL-1 beta). It has already been approved under the brand name Ilaris® in several countries for treating cryopyrin-associated periodic syndrome (CAPS), a rare life-long auto-inflammatory disease with debilitating symptoms and few treatment options.

Gout, also known as gouty arthritis, affects more than 1% of adults in Western countries [5,6]. It is more common in older people, with approximately 10% of men and 6% of women over 70 years old suffering from the disease [7,8,9]. Approximately one in ten patients have poorly controlled gout, resulting in more frequent flares [10]. They are regarded as being ‘hard-to-treat’ because they are often intolerant or unresponsive to standard medications, such as colchicine or non-steroidal anti-inflammatory drugs (NSAIDs) [11]. Corticosteroids have traditionally been given to these patients as a last resort to treat acute pain, but they can have substantial side-effects [2,12].

Gout is caused by the accumulation of uric acid crystals leading to severe inflammation in the joints and surrounding tissue [13,14]. Recent advances in the understanding of the disease have shown that uric acid crystals activate production of IL-1 beta, which is responsible for the inflammatory symptoms experienced by gout patients [7]. ACZ885 provides a selective blockade of IL-1 beta for a sustained period, neutralizing it and reducing inflammation [15,16,17].

The results presented at ACR were from a randomized, single-blind, double-dummy Phase II study involving 200 patients aged 18–80 years old with chronic gout, designed to assess the efficacy and optimum dose of ACZ885 in patients for whom current treatments (colchicine and/or NSAIDs) are ineffective or contraindicated [1].

The study showed that patients given ACZ885 150 mg experienced faster and more effective pain relief than those given the corticosteroid triamcinolone acetonide from 24 hours up to seven days [1]. ACZ885 was given by subcutaneous injection, and the steroid was given by intramuscular injection.

1 So, A. et al. Canakinumab (ACZ885) vs. triamcinolone acetonide for treatment of acute flares and prevention of recurrent flares in gouty arthritis patients refractory to or contraindicated to NSAIDs and/or colchicine. Abstract presented at the American College of Rheumatology Annual Meeting, Philadelphia, United States of America (US), October 17–21, 2009
2  KENALOG-10. Triamcinolone acetonide injection, suspension. US FDA label. Available at Accessed 13 October 2009
3  Harrold, L.R. et al. (2009) Adherence with urate-lowering therapies for the treatment of gout. Arthritis Res. Ther. 11, R46
4  Ganson, N.J. et al. (2006) Control of hyperuricemia in subjects with refractory gout, and induction of antibody against poly(ethylene glycol) (PEG), in a phase I trial of subcutaneous PEGylated urate oxidase. Arthritis Res. Ther. 8, R12
5  Terkeltaub, R.A. (2007) Learning how and when to employ uricase as bridge therapy in refractory gout. J. Rheumatol. 34, 1955–1958
6  Bieber, J.D. and Terkeltaub, R.A. (2004) Gout: on the brink of novel therapeutic options for an ancient disease. Arthritis and Rheumatism, 50, 2400–2414
7  So, A. (2008) Developments in the scientific and clinical understanding of gout. Arthritis Res. Ther. 10, 221–226
8  Kramer, H.M. and Curhan, G. (2002) The association between gout and nephrolithiasis: The National Health and Nutrition Examination Survey III, 1988–1994. Am. J. Kidney Dis. 40, 37–42
9  Mikuls, T.R. et al. (2005) Gout epidemiology: results from the UK General Practice Research Database, 1990–1999. Ann. Rheum. Dis. 64, 267–272
10  Halpern, R. et al. (2009) The effect of serum urate on gout flares and their associated costs. An administrative claims analysis. J. Clin. Rheumatol. 15, 3–7
11  Strand, V. et al. Oral presentation at the European League Against Rheumatism (EULAR) 2009 (Abstract 291)
12  Pascual, E. and Sivera, F. (2007) Therapeutic advances in gout. Curr. Opin. Rheumatol. 19, 122–7
13  Martinon, F. and Glimcher, L.H. Gout: new insights into an old disease. J. Clin. Invest. 116, 2073–2075
14  Choi, H.K. and Curhan, G. (2005) Gout: epidemiology and lifestyle choices. Curr. Opin. Rheumatol. 17, 341–345
15  Alten, R. et al. (2008) The human anti-interleukin-1ß (IL-1ß) monoclonal antibody ACZ885 is effective in joint inflammation models in mice and in a proof of concept study in rheumatoid arthritis patients. Arthritis Res. Ther. 10, R67
16  National Horizon Scanning Centre. Canakinumab for cryopyrin associated periodic syndrome. November 2008. Available at  Accessed 02 October 2009
17  Lachmann, H.J. et al. (2009) In vivo regulation of interleukin 1 in patients with cryopyrin-associated periodic syndromes. J. Exp. Med. Published online April 13 2009. Available at Accessed 02 October 2009


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