Nuon Therapeutics, Inc., a privately held, clinical stage biopharmaceutical company, announced that the company is advancing its lead program, NU1618, into phase 2b development for the treatment of chronic hyperuricemia in patients with gout. Nuon anticipates releasing topline data from a completed proof-of-principle, phase 2a study of NU1618 in the second quarter of 2010.

A proprietary combination of the drugs tranilast and allopurinol, NU1618 decreases uric acid in the body through two mechanisms: by increasing its excretion by the kidney (via the uricosuric action of tranilast) and by decreasing its production (through inhibition of the enzyme xanthine oxidase, the mechanism of allopurinol). In addition, data demonstrate that tranilast is also an immune system modulator, potentially allowing NU1618 to address the chronic inflammatory component of gout. To the company's knowledge, no other drug in development or on the market possesses these three mechanisms for treating patients with gout.

"The tranilast component of NU1618 inhibits uric acid transport by both URAT1 and GLUT9, transporters in the kidney that regulate uric acid excretion from the body," said Tito Serafini, PhD, Nuon's Chief Scientific Officer. "Tranilast is also an anti-inflammatory, immune system modulator. We believe that NU1618 has the potential therefore to provide an improved therapy for gout both by lowering uric acid through two complementary mechanisms, and by addressing the chronic inflammation induced by the disease."

Nuon Therapeutics is also investigating tranilast as a monotherapy for rheumatoid arthritis.

Although new to the United States and Europe, tranilast has been marketed in Japan as a treatment for asthma, atopic dermatitis and other conditions for nearly three decades. Allopurinol is also well understood and was first introduced as a treatment for gout in 1966.

About Hyperuricemia and Gout

Gout is a chronic, progressive rheumatic disease, caused by an inflammatory response to uric acid crystals deposited in joints and soft tissues as a result of an excess of uric acid in the blood ("hyperuricemia"). The most common form of inflammatory arthritis, gout affects approximately 6-10 million people in the United States and Europe. The disease is characterized by acute episodes, or flares, in which uric acid crystals trigger an immune response in the body and produce painful and debilitating inflammation. Gout patients also have a chronic, systemic inflammation as a result of their disease and underlying uric acid crystal burden. This chronic, systemic inflammation associated with gout, as in other rheumatic diseases, has been identified as a risk factor for cardiovascular disease. Effective treatment of hyperuricemia in gout patients requires lifelong therapy to decrease uric acid in the body.

Source
Nuon Therapeutics, Inc.