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XORTX Announces Pioneering Research on Genome-Wide Pathogenic Pathways in Gout and Provides a Corporate Update
CALGARY, Alberta, Dec. 31, 2025 (GLOBE NEWSWIRE) -- XORTX Therapeutics Inc. (" XORTX " or the &#x...
About this update from Xortx Therapeutics, Inc.
[{"type":"text","content":"XORTX Announces Pioneering Research on Genome-Wide Pathogenic Pathways in Gout and Provides a Corporate UpdateClinical Data doubles known genetic factors associated with urate and Gout\nCALGARY, Alberta, Dec. 31, 2025 (GLOBE NEWSWIRE) -- XORTX Therapeutics Inc. (\"XORTX\" or the “Company”) (NASDAQ: XRTX | TSXV: XRTX | Frankfurt: ANU), a late-stage clinical pharmaceutical company focused on developing innovative therapies to treat gout and progressive kidney disease, highlights recent peer-reviewed, independent, published research reports that expand current knowledge that genetic factors are linked to the over-expression of xanthine oxidase (“XO”), high chronic uric acid concentrations in the blood and gout. These ground breaking findings further support the Company’s approach to treating gout, kidney and other diseases by inhibiting XO. Historically, high uric acid concentration in the blood has been associated with increased incidence of gout, inflammation and health consequences, attributed to diet and lifestyle choices. Xanthine oxidase is an essential enzyme within the uric acid metabolic pathway and is required for the breakdown of purine nucleotides. The breakdown products of XO, uric acid and reactive oxygen species, are released during the enzymatic reaction and may play a detrimental role in the circulatory system and within tissue during disease. XORTX-sponsored discoveries in rodent models of gout and polycystic kidney disease (“PKD”) implicate over-expression or over-activity of XO as a potentially important target in treating this disease. Gout is a chronic disease that is caused by an innate immune response to deposits of uric acid crystals when uric acid is high. Recent work by TJ Major and colleagues presented evidence that in a large clinical study of 2.6 million individuals that as many as 410 genetic factors (including 149 new factors) are associated with molecular mechanisms of the inflammatory component of gout1. This clinical study aligns closely with evidence for over-expression of XO in human2 and with work by Wang et al. suggests linkage of genetic factors to PKD2. Recently, new emerging discoveries link genetic factors to specific populations and show that higher XO expression is associated with a variety of conditions including hyperuricemia3, sepsis, o...