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United States Pharmacopeia (USP) Reference Standard

4-Hydroxypyrazolo(3,4-d)pyrimidine, HPP, 1H-Pyrazolo(3,4-d)pyrimidin-4-ol, 4-Hydroxypyrazolo[3,4-d]pyrimidine
Empirical Formula (Hill Notation):
CAS Number:
Molecular Weight:
MDL number:
PubChem Substance ID:


pharmaceutical primary standard




>300 °C (lit.)


pharmaceutical (small molecule)



storage temp.


SMILES string




InChI key


Gene Information

human ... XDH(7498)

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General description

This product is provided as delivered and specified by the issuing Pharmacopoeia. All information provided in support of this product, including SDS and any product information leaflets have been developed and issued under the Authority of the issuing Pharmacopoeia.For further information and support please go to the website of the issuing Pharmacopoeia.

Biochem/physiol Actions

Inhibitor of xanthine oxidase and de novo pyrimidine biosynthesis. A classical agent in treatment of hyperuricemia and gout.

Analysis Note

These products are for test and assay use only. They are not meant for administration to humans or animals and cannot be used to diagnose, treat, or cure diseases of any kind.  ​

Other Notes

USP issued SDS can be found here.
Sales restrictions may apply.


Skull and crossbones

Signal Word


Hazard Statements

Hazard Classifications

Acute Tox. 3 Oral - Skin Sens. 1

Storage Class Code

6.1C - Combustible, acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects



Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificate of Analysis

Certificate of Origin

Dino Premilovac et al.
Diabetologia, 57(12), 2586-2595 (2014-09-13)
High sodium (HS) effects on hypertension are well established. Recent evidence implicates a relationship between HS intake and insulin resistance, even in the absence of hypertension. The aim of the current study was to determine whether loss of the vascular
Jennifer J DuPont et al.
American journal of physiology. Renal physiology, 306(12), F1499-F1506 (2014-04-25)
Oxidative stress promotes vascular dysfunction in chronic kidney disease (CKD). We utilized the cutaneous circulation to test the hypothesis that reactive oxygen species derived from NADPH oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation in CKD. Twenty subjects
Timothy Pearson et al.
PloS one, 9(5), e96378-e96378 (2014-05-31)
Skeletal muscle generation of reactive oxygen species (ROS) is increased following contractile activity and these species interact with multiple signaling pathways to mediate adaptations to contractions. The sources and time course of the increase in ROS during contractions remain undefined.
C C Wen et al.
Clinical pharmacology and therapeutics, 97(5), 518-525 (2015-02-14)
The first-line treatment of hyperuricemia, which causes gout, is allopurinol. The allopurinol response is highly variable, with many users failing to achieve target serum uric acid (SUA) levels. No genome-wide association study (GWAS) has examined the genetic factors affecting allopurinol
Lisa K Stamp et al.
Rheumatology (Oxford, England), 53(11), 1958-1965 (2014-06-06)
The aims of this study were to establish whether, in patients with gout, MPO is released from neutrophils and urate is oxidized to allantoin and if these effects are attenuated by allopurinol. MPO, urate, allantoin and oxypurinol were measured in

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