This study demonstrates uric acid reduction in gout via cyclodextrins and HBCD-Pol, indicating improved treatment strategies.
Gout, which affects 3-6 % of Western populations, has well-established therapies but still lacks agents that directly target monosodium urate (MSU) deposits. This study investigates a novel strategy employing cyclodextrins (CDs) and hyperbranched cyclodextrin-based polymers (HBCD-Pol) to both mobilize and prevent MSU formation. Among the CDs tested, HPβ-CD exhibited the strongest uric acid (UA) complexation at 25 °C, while HBCD-Pol showed superior performance by chelating Na+ ions. Complex formation was confirmed through TGA, FTIR, and molecular docking analyses. In a murine model of MSU-induced knee inflammation, treatment with HPβ-CD and HBCD-Pol-either alone or in combination with standard anti-gout drugs (allopurinol, probenecid, colchicine, febuxostat) and bioactive compounds (resveratrol, oxyresveratrol)-significantly reduced inflammation, restored biochemical markers, and produced synergistic effects. HBCD-Pol demonstrated greater efficiency as a carrier, further enhancing drug activity. These findings indicate that CDs and HBCD-Pol, both based on authorized excipients, could provide a promising avenue for improving gout therapy and supporting the development of innovative treatment strategies.
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Matencio et al. (2025) studied this question.
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