---
title: "Purine breakdown to uric acid Template | MolDraw"
url: https://www.moldraw.com/templates/biopath-purine-degradation/
description: "Purine breakdown to uric acid template: AMP → adenosine → inosine (adenosine deaminase) → hypoxanthine (purine nucleoside phosphorylase) → xanthine → uric…"
lang: en
publisher: Scidart Academy
generated: 2026-11-13
---
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# Purine breakdown to uric acid template

![Purine breakdown to uric acid template: AMP → adenosine → inosine (adenosine deaminase) → hypoxanthine (purine nucleoside phosphorylase) → xanthine → uric acid (xanthine oxidase); GMP → guanosine → guanine → xanthine (guanine deaminase); allopurinol → oxypurinol blocks xanthine oxidase in gout.](https://www.moldraw.com/templates/biopath-purine-degradation.webp)

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AMP → adenosine → inosine (adenosine deaminase) → hypoxanthine (purine nucleoside phosphorylase) → xanthine → uric acid (xanthine oxidase); GMP → guanosine → guanine → xanthine (guanine deaminase); allopurinol → oxypurinol blocks xanthine oxidase in gout.

## What the template shows

- AMP and GMP are stripped of phosphate and ribose and oxidised by xanthine oxidase; humans excrete the end product, uric acid
- From AMP
- R = β-D-ribose 5′-phosphate, R′ = β-D-ribose (N9-linked); PNP = purine nucleoside phosphorylase. Xanthine oxidase is a molybdenum enzyme (Mo, FAD, Fe–S) and works twice
- uric acid
- From GMP
- Guanine joins the same path at xanthine
- Allopurinol, a hypoxanthine analogue, treats gout
- Xanthine oxidase turns it into oxypurinol (alloxanthine), which stays bound to the reduced Mo(IV) centre
- oxypurinol (alloxanthine)
- Humans and apes lack urate oxidase, so uric acid (pKa ≈ 5.4, mostly urate in blood) is the end product; other mammals excrete allantoin.
- Gout: monosodium urate crystals deposit in joints when serum urate is high. Allopurinol (Elion and Hitchings, Nobel Prize 1988) and febuxostat inhibit xanthine oxidase; hypoxanthine and xanthine are more soluble and are excreted.
- Adenosine deaminase deficiency causes severe combined immunodeficiency (SCID); HGPRT deficiency (Lesch–Nyhan) stops salvage of hypoxanthine and guanine and raises uric acid.
- Each xanthine oxidase step adds an O at C2 or C8 from water; O₂ takes the electrons and leaves as H₂O₂. Tautomers are drawn as the oxo (lactam) forms.

Drawn with 133 atoms, 9 arrows, 3 shapes – every one editable in MolDraw.

## Sources

- [Nelson & Cox, Lehninger Principles of Biochemistry, 8th ed., 2021, ch. 22](https://openlibrary.org/isbn/9781319228002) Textbook
- [Berg, Tymoczko, Gatto & Stryer, Biochemistry, 9th ed., 2019](https://openlibrary.org/isbn/9781319114657) Textbook
- [Voet & Voet, Biochemistry, 4th ed., Wiley 2011](https://openlibrary.org/isbn/9780470570951) Textbook
- [Elion, Kovensky & Hitchings, Biochem. Pharmacol. 1966, 15, 863](https://doi.org/10.1016/0006-2952(66)90163-8) Original paper

## How to use this template

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## Frequently asked questions

### Is the Purine breakdown to uric acid template free?

You can preview the Purine breakdown to uric acid template here and open and edit it in MolDraw for free. Downloading or exporting it is part of MolDraw Pro, together with the other premium templates.

### Can I edit the Purine breakdown to uric acid template?

Yes. It opens as an ordinary MolDraw drawing, so every structure, arrow, label and colour can be changed, and you can add your own content around it.

### Is the chemistry checked?

Every structure is checked with RDKit and every curly arrow passes MolDraw’s electron-flow audit. The sources used are listed on this page.

### Are the biochemical pathways drawn with structures?

Yes. Pathway templates show the intermediates as structures, with enzymes and cofactors (NAD⁺, FAD, ATP) on the arrows.

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