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BioCryst Presents Results from Its BCX4208 Gout Program at the Annual European Congress of Rheumatology
Three posters summarize pharmacokinetic (PK), safety and efficacy results from BioCryst's Phase 2b trial of BCX4208 added to allopurinol in patients with gout who had failed to reach the serum uric acid (sUA) therapeutic goal of < 6.0 mg/dL on allopurinol alone. Positive 24-week results were reported from this trial earlier this year.
In addition, the abstract "Effect of BCX4208 Add-On Therapy to Allopurinol 300 mg on Plasma Hypoxanthine and Xanthine Concentrations in Gout Patients" was accepted as an oral presentation and concludes that BCX4208 in combination with allopurinol resulted in dose-dependent mean reductions in plasma xanthine and hypoxanthine concentrations in gout patients. These results confirm the mechanism of action of BCX4208. (Abstract OP0106)
"The conclusions from these trials further validate BCX4208's potential
to be a preferred treatment option for physicians and a large portion of
their gout patients. We believe BCX4208 offers important differentiating
characteristics in comparison to other treatment options," said Dr.
Copies of all abstracts are available online through the EULAR website
at www.eular.org.
The poster and oral presentations will be made available on BioCryst's BCX4208
publications page once they have been presented on About BCX4208 BCX4208 is a novel enzyme inhibitor with the potential for once-a-day oral dosing suitable for chronic administration to treat gout. It acts upstream of xanthine oxidase in the purine metabolism pathway to reduce sUA in patients with gout and has a mechanism of action that complements xanthine oxidase inhibitors, such as allopurinol and febuxostat, in reducing uric acid production. With its unique mechanism of action, clinical activity and safety in clinical studies to date, BCX4208 is a Phase-3-ready asset in development as an add-on therapy to xanthine oxidase inhibitors to address unmet medical needs in patients with gout. To date, BCX4208 has been studied in over 500 patients in clinical trials. About Gout Gout is a chronic inflammatory arthritis caused by monosodium urate crystal deposits in joints and the kidneys resulting from elevated sUA levels in the blood, a condition known as hyperuricemia. The consequences of gout may include intense, painful flares affecting one or more joints, impaired kidney function and joint destruction. Gout continues to grow in prevalence and severity, affecting over 17 million people in major markets, including 8.3 million in the U.S. A majority of gout patients are also treated to manage other chronic conditions, including hypertension, diabetes and/or high cholesterol. Decreasing sUA to the recommended level (less than 6 mg/dL) can reduce the risk of gout attacks over the long-term. A minority of patients treated with the current standard of care, allopurinol, achieve this therapeutic goal. There is a need for new therapies that effectively and safely get a larger portion of gout suffers to goal without the risk of drug-drug interactions. More information regarding gout and hyperuricemia is available on the CDC website at www.cdc.gov/arthritis/basics/gout.htm.
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