Nuon Therapeutics NU1618 phase 2a study in hyperuricemia meets primary endpoint

Jun 16 2010

Nuon Therapeutics, Inc., a privately held, clinical stage biopharmaceutical company, announced that a phase 2a study of NU1618, the company's lead program, met its primary endpoint of reduction in serum uric acid (sUA) levels in patients with hyperuricemia.

"This successful proof-of-principle study provides the basis to advance the NU1618 program rapidly," said Lee Rauch, president and chief executive officer of Nuon Therapeutics. "We have initiated a phase 2b study in patients with gout and expect to start enrollment within the next few weeks."

In the phase 2a randomized, double-blind, crossover study, twenty patients with hyperuricemia (mean sUA levels of 8.1 mg/dL) received 300 mg once daily (qd) tranilast, 300 mg qd allopurinol, 400 mg qd allopurinol, or one of two dosage strengths of a Nuon proprietary combination of tranilast and allopurinol. The proprietary combinations demonstrated greater percentage decreases in sUA than either single agent. The higher dosage combination showed a decrease in sUA of 49 percent compared to 38 percent for 400 mg qd allopurinol. In addition, a significantly greater percentage of patients taking the higher dose achieved reductions below a clinically relevant threshold of 4.0 mg/dL compared to those given 400 mg qd allopurinol (61 percent versus 11 percent).

"There is a need for therapeutic strategies to substantially reduce serum urate levels in patients with gout. The favorable responses achieved with the NU1618 program support further studies aimed toward demonstrating efficacy in achieving this therapeutic target," said John Sundy, M.D., Ph.D., director, Immunology and Inflammation Medicine, at the Duke Clinical Research Institute.

The Company plans to present a summary of the data from this study at an upcoming scientific congress.

The proprietary combination of tranilast and allopurinol decreases uric acid in the body through two mechanisms: by increasing uric acid excretion by the kidneys (via the uricosuric action of tranilast) and by decreasing its production (through inhibition of the enzyme xanthine oxidase, the mechanism of allopurinol). Tranilast is also an anti-inflammatory, immune system modulator, which may allow the NU1618 program to address the chronic inflammatory component of gout in addition to lowering urate levels.