Marigold flavonoids are by-products of extracting lutein from marigold, accounting for 90% of the total content. Exploring the physiological functions of marigold flavonoids and repurposing processing byproducts are crucial for industrial applications. The purpose of this study was to investigate the effect of quercetagetin (QG) on hyperuricemia. A comparative study with quercetin (Que) revealed that both QG and Que significantly reduced cellular and serum uric acid (UA) levels, as well as creatinine (CRE), blood urea nitrogen (BUN), adenosine deaminase (ADA), and purine nucleotide phosphorylase (PNP) levels. Furthermore, QG and Que suppressed the activities of hepatic ADA, PNP, xanthine oxidase (XOD), and phosphate ribose pyrophosphate synthetase (PRPS) in mice. In renal tissues, QG down-regulated the mRNA expression of glucose transporter 9 (GLUT9) and urate anionic transporter 1 (URAT1) but up-regulated ATP-binding cassette subfamily G member 2 (ABCG2). Moreover, QG and Que also decreased oxidative stress markers including malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), and elevated anti-inflammatory mediators (nitric oxide (NO) and interleukin-10 (IL-10)) and antioxidant enzyme activities such as glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). QG also improved intestinal health via enhanced microbial diversity, lowering the microbiota dysbiosis index (MDI), and modulating gut microbiota composition. These changes promoted beneficial bacteria (e.g., Bifidobacterium, Faecalibaculum). These alterations suggest that QG alleviates hyperuricemia-induced oxidative stress, inflammation, and intestinal dysbiosis. QG and Que exhibit overlapping anti-hyperuricemic mechanisms.