Xanthine oxidase !

Performs the last two steps of purine breakdown and makes uric acid; it is the target of allopurinol and febuxostat.

Updated 2026-11-01

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Key facts

Hypoxanthine → xanthine → uric acid, using O₂ (oxidase form) or NAD⁺ (dehydrogenase form).
Cofactors: molybdenum (molybdopterin), FAD and two iron–sulfur clusters.
Allopurinol: a hypoxanthine analogue; its metabolite oxypurinol stays bound to the molybdenum. Febuxostat: not a purine; it plugs the substrate channel.
It also inactivates 6-mercaptopurine: with allopurinol, azathioprine and 6-MP accumulate and become toxic.

The dehydrogenase form converts to the oxidase by cysteine oxidation or proteolysis (ischaemia).
The oxidase form produces superoxide and H₂O₂, contributing to reperfusion injury.

Xanthine oxidase inhibitors are the mainstay for lowering urate in chronic gout and preventing urate nephropathy.
On allopurinol, hypoxanthine and xanthine accumulate; in Lesch-Nyhan syndrome they can form xanthine stones.
Its inherited deficiency is xanthinuria: almost undetectable uric acid and xanthine stones.
Carriers of the HLA-B*58:01 allele have a higher risk of severe skin reactions to allopurinol.

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Which metal sits in the active site of xanthine oxidase?

Molybdenum, bound to molybdopterin; it also has FAD and iron–sulfur clusters.

Why is combining allopurinol and azathioprine avoided without adjustment?

Xanthine oxidase inactivates 6-mercaptopurine; blocking it lets the drug build up and can cause severe myelosuppression.

How do allopurinol and febuxostat differ?

Allopurinol is a purine analogue (oxypurinol binds the molybdenum); febuxostat is not a purine and blocks the substrate channel.

Educational information, not medical advice. For any symptom, see a health professional.

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Representative model, for educational purposes only.