Uric Acid Reducing Therapies – Target Pipeline List 03/2019
Targets: Uric Acid, Urate, Xanthine Oxidase, Uric Acid Transporter 1, URAT1
This Target Pipeline List provides an overview of biologic and chemical entities on the market or in development for treatment of hyperuricemia associated with gout and tumor lysis syndrome
Hyperuricemia may occur because of decreased excretion (underexcretors), increased production (overproducers), or a combination of these two mechanisms. Uric acid in the blood is saturated at 6.4-6.8 mg/dL at ambient conditions, with the upper limit of solubility placed at 7 mg/dL. Worldwide, the prevalence of hyperuricemia has increased substantially in recent decades. The progressive increase in serum levels of uric acid levels may be linked to the rising prevalence of overweight and obesity, as well as the increase in consumption of sugar-sweetened beverages, foods rich in purines, and alcohol.
Symptoms of hyperuricemia are those of gout and nephrolithiasis. Gout typically manifests as an acute monoarthritis, most commonly in the great toe and less frequently in the tarsal joint, knee, and other joints. Uric acid nephrolithiasis may manifest as hematuria; pain in the flank, abdomen, or inguinal region; and/or nausea and vomiting
The choice of urate-lowering medications includes uric acid depletion, inhibition of uric acid production or selective uric acid reabsorption inhibition. Treatment with uric acid reducing molecules is indicated for severe, refractory gout and treatment or prophylaxis of acute hyperuricemia in patients with hematological malignancies at high or potential risk for tumor lysis syndrome (TLS).
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