Breakthrough Gout Therapy Rooted in Science, Designed for Life

Harness the power of targeted pharmacology to reduce uric acid levels, control inflammation, and prevent future flare-ups—because effective gout care begins at the molecular level

Gout

Gout is a rheumatic disease caused by the accumulation of monosodium urate (NaU) crystals in peripheral joints, most commonly the big toe’s metatarsophalangeal joint. These crystals trigger intense pain, swelling, and redness. Gout arises from elevated uric acid levels, due to increased production or reduced excretion, often linked to rapid cell turnover, certain medications, or alcohol use. Uric acid crystals activate the immune system, leading to neutrophil recruitment and inflammatory enzyme release, resulting in acute, painful joint inflammation. Globally, gout prevalence is projected to reach 95.8 million by 2050.

References

  1. Costa-Bauza A, Grases F. 7-Methylxanthine Inhibits the Formation of Monosodium Urate Crystals by Increasing Its Solubility. Biomolecules. 2023 Dec 10;13(12):1769. doi: 10.3390/biom13121769. PMID: 38136640; PMCID: PMC10742025 GBD 2021 Gout Collaborators. Global, regional, and national burden of gout, 1990-2020, and projections to 2050: a systematic analysis of the Global Burden of Disease Study 2021. Lancet Rheumatol. 2024 Aug;6(8):e507-e517. doi: 10.1016/S2665-9913(24)00117-6. Epub 2024 Jul 9. Erratum in: Lancet Rheumatol. 2024 Nov;6(11):e749. doi: 10.1016/S2665-9913(24)00303-5. PMID: 38996590; PMCID: PMC11263476 https://calgaryguide.ucalgary.ca/Gout-Pathogenesis-and-Clinical-Findings/