ULORICrx

Efficacy and safety profile

ULORIC powerfully lowers serum uric acid to target levels <6 mg/dL 5,6

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Efficacy data

ULORIC 80 mg was proven superior to allopurinol at lowering serum uric acid in 3 head-to-head studies.5,6

The 40-mg starting dose of ULORIC effectively lowered serum uric acid similar to allopurinol.5

Individual results may vary based on factors such as baseline serum uric acid levels.

* Based on results combined across three phase 3 studies; ULORIC 40 mg was included only in one of the studies, and ULORIC 80 mg and allopurinol were included in each of the studies.

† p<0.001 vs allopurinol.

‡ In APEX, allopurinol patients (n=10) with serum creatinine >1.5 mg/dL and ≤2 mg/dL were dosed at 100 mg daily. In CONFIRMS, allopurinol patients (n=145) with estimated ClCr ≥30 mL/min and Clcr ≤59 mL/min were dosed at 200 mg daily. All other patients received 300 mg daily.

Watch a video about John Find out more about patients like John

Consider ULORIC for your gout patients like John,* who has high serum uric acid:

  • Serum uric acid level: 8.2 mg/dL
  • Flares per year: 2–3
  • Current treatment: Allopurinol 300 mg daily

*Not an actual patient.

Watch as rheumatologist Dr. Chad Boomershine and family practitioner Dr. Gary Ruoff discuss the treatment of hyperuricemia in patients with gout.

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Efficacy data in patients with mild to moderate renal impairment†

ULORIC was superior to allopurinol in gout patients with mild to moderate renal impairment.*†5

Patients with mild to moderate renal impairment can be treated with either dose of ULORIC.5

Individual results may vary based on factors such as baseline serum uric acid levels.

There are insufficient data in patients with severe renal impairment and no data in patients with severe hepatic impairment. Caution should be exercised in these patients.

* CONFIRMS study.

† Clcr 30-89 mL/min.

‡ p<0.05 vs allopurinol and ULORIC 40 mg.

§ p<0.05 vs allopurinol.

|| Allopurinol patients (n=145) with estimated Clcr ≥30 mL/min and ClCr ≤59 mL/min were dosed at 200 mg daily.

Watch a video about Mary Find out more about patients like Mary

Consider ULORIC for your gout patients like Mary,* who has moderate renal impairment:

  • Serum uric acid level: 9.2 mg/dL
  • Flares per year: 2–3
  • Renal function: Chronic renal dysfunction (Clcr 42 mL/min)
  • Current treatment: Allopurinol 200 mg daily

*Not an actual patient.

Watch as nephrologist Dr. Anthony Bleyer discusses the treatment of hyperuricemia in gout patients who also have mild to moderate renal impairment.†

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†Clcr 30-89 mL/min.

The safety profile of ULORIC has been evaluated in more than 4000 patients.6

Review the safety profile of ULORIC

Indication

ULORIC is a xanthine oxidase (XO) inhibitor indicated for the chronic management of hyperuricemia in patients with gout. ULORIC is not recommended for the treatment of asymptomatic hyperuricemia.

Important Safety Information

  • ULORIC is contraindicated in patients being treated with azathioprine or mercaptopurine.
  • An increase in gout flares is frequently observed during initiation of anti-hyperuricemic agents, including ULORIC. If a gout flare occurs during treatment, ULORIC need not be discontinued. Prophylactic therapy (i.e. – NSAIDs or colchicine) upon initiation of treatment may be beneficial for up to six months.
  • Cardiovascular Events: In randomized controlled studies, there was a higher rate of cardiovascular thromboembolic events (cardiovascular deaths, non-fatal myocardial infarctions, and non-fatal strokes) in patients treated with ULORIC [0.74 per 100 P-Y (95% CI 0.36-1.37)] than allopurinol [0.60 per 100 P-Y (95% CI 0.16-1.53)]. A causal relationship with ULORIC has not been established. Monitor for signs and symptoms of MI and stroke.
  • Liver Enzyme Elevations: In randomized controlled studies, transaminase elevations greater than 3 times the upper limit of normal (ULN) were observed (AST: 2%, 2%, and ALT: 3%, 2% in ULORIC and allopurinol-treated patients, respectively). No dose-effect relationship for these transaminase elevations was noted. Laboratory assessment of liver function is recommended at, for example, 2 and 4 months following initiation of ULORIC and periodically thereafter.
  • Adverse reactions occurring in at least 1% of ULORIC-treated patients, and, at least 0.5% greater than placebo, are liver function abnormalities, nausea, arthralgia, and rash.

Please click here for complete Prescribing Information.

Show references
  1. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65:1312-1324.
  2. Edwards NL. Clinical gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 5th ed. Philadelphia, PA: Mosby Elsevier; 2011:1859-1865.
  3. Schumacher HR Jr. The pathogenesis of gout. Cleve Clin J Med. 2008;75(suppl 5):S2-S4.
  4. Shoji A, Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum. 2004;51:321-325.
  5. ULORIC (febuxostat) full prescribing information, January 2011.
  6. Data on file, Takeda Pharmaceuticals North America, Inc.
  7. McLean L, Becker MA. Etiology and pathogenesis of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 5th ed. Philadelphia, PA: Mosby Elsevier; 2011:1841-1857.
  8. Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheum. 1972;15:189-192.
  9. Wortmann RL. Gout and hyperuricemia. In: Firestein GS, Budd RC, Harris ED Jr, McInnes IB, Ruddy S, Sergent JS, eds. Kelley’s Textbook of Rheumatology. Vol 2. 8th ed. Philadelphia, PA: Saunders Elsevier; 2009:1481-1506.
  10. Becker MA, Jolly M. Clinical gout and the pathogenesis of hyperuricemia. In: Koopman WJ, Moreland LW, eds. Arthritis and Allied Conditions: A Textbook of Rheumatology. Vol 2. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:2303-2339.
  11. Pascual E, Pedraz T. Gout. Curr Opin Rheumatol. 2004;16:282-286.
  12. Pascual E, Batlle-Gualda E, Martínez A, Rosas J, Vela P. Synovial fluid analysis for diagnosis of intercritical gout.
    Ann Intern Med. 1999;131:756-759.
  13. McCarthy GM, Barthelemy CR, Veum JA, Wortmann RL. Influence of antihyperuricemic therapy on the clinical and radiographic progression of gout. Arthritis Rheum. 1991;34:1489-1494.
  14. Edwards NL. Gout. A. Clinical features. In: Klippel JH, Stone JH, Crofford LJ, White PH, eds. Primer on the Rheumatic Diseases. 13th ed. New York, NY: Springer Science+Business Media, LLC; 2008:241-249.
  15. Li-Yu J, Clayburne G, Sieck M, et al. Treatment of chronic gout. Can we determine when urate stores are depleted enough to prevent attacks of gout? J Rheumatol. 2001;28:577-580.
  16. Perez-Ruiz F, Calabozo M, Pijoan JI, Herrero-Beites AM, Ruibal A. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002;47:356-360.
  17. Allopurinol full prescribing information, October 2009.
  18. Schumacher HR, Becker MA, Wortmann RL, et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum. 2008;59:1540-1548.
  19. Becker MA, Schumacher HR, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353:2450-2461.
  20. Becker MA, Schumacher HR, Espinoza LR, et al. The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. Arthritis Res. 2010;12:R63.

Important Safety Information

  • ULORIC is contraindicated in patients being treated with azathioprine or mercaptopurine.
  • An increase in gout flares is frequently observed during initiation of anti-hyperuricemic agents, including ULORIC. If a gout flare occurs during treatment, ULORIC need not be discontinued. Prophylactic therapy (i.e. – NSAIDs or colchicine) upon initiation of treatment may be beneficial for up to six months.
  • Cardiovascular Events: In randomized controlled studies, there was a higher rate of cardiovascular thromboembolic events (cardiovascular deaths, non-fatal myocardial infarctions, and non-fatal strokes) in patients treated with ULORIC [0.74 per 100 P-Y (95% CI 0.36-1.37)] than allopurinol [0.60 per 100 P-Y (95% CI 0.16-1.53)]. A causal relationship with ULORIC has not been established. Monitor for signs and symptoms of MI and stroke.
  • Liver Enzyme Elevations: In randomized controlled studies, transaminase elevations greater than 3 times the upper limit of normal (ULN) were observed (AST: 2%, 2%, and ALT: 3%, 2% in ULORIC and allopurinol-treated patients, respectively). No dose-effect relationship for these transaminase elevations was noted. Laboratory assessment of liver function is recommended at, for example, 2 and 4 months following initiation of ULORIC and periodically thereafter.
  • Adverse reactions occurring in at least 1% of ULORIC-treated patients, and, at least 0.5% greater than placebo, are liver function abnormalities, nausea, arthralgia, and rash.