Terminal degradation of purine nucleotides (AMP, GMP) to uric acid. Hypoxanthine and guanine flow through xanthine on the way to uric acid via xanthine oxidase (XO) — the target of allopurinol + febuxostat for gout. Humans lack uricase (lost in primate evolution), so uric acid is the endpoint; in most other mammals uricase converts it to allantoin (the basis for pegloticase therapy in refractory gout — uricase enzyme replacement). Renal tubular reabsorption via URAT1 controls plasma urate setpoint — uricosurics (probenecid, lesinurad) inhibit URAT1.
Organ Systems
renal
musculoskeletal
Pathway Steps
hypoxanthine → xanthine — via xanthine oxidase (XO) — ALLOPURINOL TARGET. Xanthine oxidase oxidizes hypoxanthine to xanthine, generating reactive oxygen species as a byproduct. It is the target of allopurinol (and its active metabolite oxypurinol) and febuxostat in gout/hyperuricemia.
xanthine → uric-acid — via xanthine oxidase (XO) — same enzyme, second step. The same enzyme oxidizes xanthine to uric acid, the end product of purine catabolism in humans (who lack uricase). Poor urate solubility drives gout (monosodium-urate crystals) and uric-acid stones; rasburicase is recombinant uricase for tumor-lysis syndrome.
Known Modulators
allopurinol (inhibitor) — xanthine oxidase. Hypoxanthine analog; xanthine oxidase converts it to oxypurinol (active metabolite) which then inhibits the enzyme — suicide-inhibitor logic.
febuxostat (inhibitor) — xanthine oxidase. Non-purine XO inhibitor; reserved for allopurinol intolerance (FDA boxed warning for CV mortality 2019).