Novartis' canakinumab, which is already approved for the rare autoinflammatory disease CAPS, has impressed in late-stage trials for gout.

The Swiss major is unveiling data at the European League Against Rheumatism congress in London from two Phase III trials in patients with severe gouty arthritis. It shows that ACZ885 (canakinumab), a fully human monoclonal antibody, provided superior pain relief and reduced the risk of suffering new attacks by up to 68% compared to an injectable steroid, triamcinolone acetonide, currently used to treat such attacks.

The studies involved more than 450 patients for whom standard anti-inflammatories, non-steroidal anti-inflammatory drugs or colchicine were inadequate or inappropriate. 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.

Novartis quoted Naomi Schlesinger of the Robert Wood Johnson University Hospital in New Jersey as saying that "patients describe gouty arthritis as agonisingly painful,". However, ACZ885, which inhibits interleukin-1 beta, effectively treated and extended the time to new attacks".

David Epstein, head of pharma at Novartis, said "we are very excited about these results, which indicate that ACZ885 may become a significant new alternative for gouty arthritis". He added that the company is committed to further investigating the potential of the drug "in a number of other conditions where interleukin-1 beta may play a role." These include diabetes and chronic obstructive pulmonary disease.

Regulatory filings for the use of ACZ885 in gouty arthritis patients with limited treatment options were submitted in the European Union in 2010 and in the USA, Canada and Switzerland in the first quarter this year.

Canakinumab is already approved (and sold as Ilaris) in Europe, the USA and elsewhere for cryopyrin-associated periodic syndrome (CAPS). The latter disorder is caused by a single gene mutation that leads to overproduction of interleukin-1 beta,