Modulation of ABCG2-mediated Urate Transport to Treat Hyperuricemia and Gout

Case ID:
C10666

C10666: Treatment of Hyperuricemia and Gout


Technical Details:

About 3 million people in U.S. are suffering from insufficiently treated gout. Incidence has more than tripled in the past 20 years, as the disease is correlated with being overweight, drinking too much alcohol, or having diets too high in meat or fish. It is well established that gout is a consequence of elevated serum urate levels. Yet, the medications to decrease serum urate levels are frequently not effective. It has been difficult to target renal urate secretion pharmacologically since the molecular identity of the transporters mediating secretion in humans was not known. JHU scientists have identified a new drug target, a secretory urate transporter, the activation of which will decrease serum urate levels. In addition, the JHU researchers have identified a common causal variant that accounts for more than 10% of gout in Caucasians. Activation of urate secretion through this new therapeutic target may decrease serum urate levels and therefore constitutes a promising drug target for hyperuricemia and gout.

Looking for Partners:

• Novel drugs for the treatment of hyperuricemia and gout.
• Diagnostic SNP chips for genotype-specific therapy.


Publications/Associated Cases:

Woodward O.M. et al (2009) Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout. PNAS. 106(25):10338-42.

Patent Information:
Title App Type Country Serial No. Patent No. File Date Issued Date Expire Date Patent Status
MODULATION OF ABCG2-MEDIATED URATE TRANSPORT TO TREAT HYPERURICEMIA AND GOUT PCT: Patent Cooperation Treaty United States 13/255,601 8,722,338 9/9/2011 5/13/2014 3/11/2030 Granted
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For Information, Contact:
Michael Woods
mwoods19@jh.edu
410-614-0300
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