Allopurinol 2.5mg/5ml oral suspension
Prescription only
Requires a prescription from a doctor or prescriber
Oral suspension
2.5mg/5ml
Oral
Gout is a disease that occurs by the deposition of monosodium urate crystals (MSU) in body tissues, especially around joints [A175942].
Active ingredients:
Allopurinol
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
Oral TDLO (rat): 10 mg/kg; Oral LD50 (mouse): 78 mg/kg; Oral TDLO (mouse): 100 mg/kg F3985
Use in pregnancy
Reproductive studies have been completed using rats and rabbit models at doses up to twenty times the normal human dose ( about 5 mg/kg per day), and it was concluded that fertility was not impaired and there was no fetal harm.
Use in pregnancy
Reproductive studies have been completed using rats and rabbit models at doses up to twenty times the normal human dose ( about 5 mg/kg per day), and it was concluded that fertility was not impaired and there was no fetal harm.
There is a published report of a study in pregnant mice administered 50 or 100 mg/kg allopurinol intraperitoneally on gestation days 10 or 13.
There were increased numbers of dead fetuses in dams administered 100 mg/kg allopurinol, however, death did not occur in those given 50 mg/kg.
There were higher numbers of external malformations in fetuses at both doses of allopurinol on gestation day 10 and higher numbers of skeletal malformations in fetuses at both doses on gestation day 13.
Despite the above findings, there are no adequate or well-controlled studies in pregnant women.
Breastfeeding
Use in nursing
Both allopurinol and the metabolite oxipurinol have been found in the milk of a mother who was receiving allopurinol.
Both allopurinol and the metabolite oxipurinol have been found in the milk of a mother who was receiving allopurinol.
Since the effect of allopurinol on the nursing infant is unknown, it is advisable to exercise caution when allopurinol is taken by a nursing woman [FDA label].
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Allopurinol
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Allopurinol
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
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WHO defined daily dose (DDD)
400 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Allopurinol
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(2)
Gout: diagnosis and management (NG219)
NG219
NICE guideline
Updated Jun 2022Renal and ureteric stones: assessment and management (NG118)
NG118
NICE guideline
Updated Jan 2019Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
1-2 hours
Mechanism
Allopurinol is a structural analog of the natural purine base, hypoxanthine.
Food interactions
3 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
This drug is about 90% absorbed from the gastrointestinal tract.…
Half-life
1-2 hours
The plasma half-life of allopurinol is 1-2 hours, due to its rapid renal clearance [FDA label].
Protein binding
Allopurinol and oxypurinol are only negligibly bound to plasma proteins .
[A175954][A175948]
[A175954][A175948]
Volume of distribution
Allopurinol and oxypurinol are both substrates for the enzyme xanthine oxidase, which is present in the cytoplasm of endothelial cells of capillaries,…
Metabolism
Allopurinol is rapidly metabolized to the corresponding xanthine analog, oxipurinol (alloxanthine), which is also an inhibitor of xanthine oxidase enzyme [FDA label].…
Elimination
80%
Approximately 80% of orally ingested allopurinol is found excreted in the urine as various metabolites .
[A175948]…
[A175948]…
Clearance
10 to 20 mL/min
Since allopurinol and its metabolites are mainly eliminated by the kidney, accumulation of this drug can occur in patients with renal dysfunction…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Gout is a disease that occurs by the deposition of monosodium urate crystals (MSU) in body tissues, especially around joints [A175942]. This disease has been well-documented in historical medical records and appears in the biographies of several prominent, historically recognized individuals [A175942].
Allopurinol is a xanthine oxidase enzyme inhibitor that is considered to be one of the most effective drugs used to decrease urate levels and is frequently used in the treatment of chronic gout [A36705]. It was initially approved by the FDA in 1966 [L5674] and is now formulated by several manufacturers [L5677].
Allopurinol is a xanthine oxidase enzyme inhibitor that is considered to be one of the most effective drugs used to decrease urate levels and is frequently used in the treatment of chronic gout [A36705]. It was initially approved by the FDA in 1966 [L5674] and is now formulated by several manufacturers [L5677].
Properties:
View FDA drug labelsolid
Avg. mass: 136.11 Da
DrugBank indication
Allopurinol is indicated in [FDA label]:
1) the management of patients with signs and symptoms of primary or secondary gout (acute attacks, tophi, joint destruction, uric acid lithiasis, and/or nephropathy).
2) the management of patients with leukemia, lymphoma and malignancies who are receiving cancer therapy which causes elevations of serum and urinary uric acid levels. Treatment with allopurinol should be discontinued when the potential for overproduction of uric acid is no longer present.
3) the management of patients with recurrent calcium oxalate calculi whose daily uric acid excretion exceeds 800 mg/day in male patients and 750 mg/day in female patients. Therapy in such patients should be carefully assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks.
1) the management of patients with signs and symptoms of primary or secondary gout (acute attacks, tophi, joint destruction, uric acid lithiasis, and/or nephropathy).
2) the management of patients with leukemia, lymphoma and malignancies who are receiving cancer therapy which causes elevations of serum and urinary uric acid levels. Treatment with allopurinol should be discontinued when the potential for overproduction of uric acid is no longer present.
3) the management of patients with recurrent calcium oxalate calculi whose daily uric acid excretion exceeds 800 mg/day in male patients and 750 mg/day in female patients. Therapy in such patients should be carefully assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks.
Also known as(50)
1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidin-4-one
1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidine-4-one
1H-Pyrazolo(3,4-d)pyrimidin-4-ol
4-HPP
4-Hydroxy-1H-pyrazolo(3,4-d)pyrimidine
4-Hydroxy-3,4-pyrazolopyrimidine
4-Hydroxypyrazolo(3,4-d)pyrimidine
4-Hydroxypyrazolopyrimidine
Dosage forms(27)
Tablet (Oral) — 300 mg
Tablet (Oral)
Tablet (Oral) — 100 mg
Injection, powder, lyophilized, for solution (Intravenous) — 500 mg/25mL
Tablet (Oral) — 100.00 mg
Tablet (Oral) — 200 mg
Tablet, effervescent (Oral) — 100 MG
Tablet, effervescent (Oral) — 300 MG
Molecular properties(19)
Drug interactions(1126)
Known interactions with other medications. Always consult a healthcare professional.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Ramipril.
Fosinopril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Fosinopril.
Trandolapril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Trandolapril.
Benazepril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Benazepril.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Enalapril.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Moexipril.
Lisinopril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Lisinopril.
Perindopril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Perindopril.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Quinapril.
Omapatrilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Omapatrilat.
Rescinnamine
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Rescinnamine.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Captopril.
Cilazapril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Cilazapril.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Spirapril.
Temocapril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Temocapril.
Enalaprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Enalaprilat.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Imidapril.
Zofenopril
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Zofenopril.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Delapril.
Benazeprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Benazeprilat.
Fosinoprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Fosinoprilat.
Ramiprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Ramiprilat.
Trandolaprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Trandolaprilat.
Moexiprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Moexiprilat.
Perindoprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Perindoprilat.
Quinaprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Quinaprilat.
Cilazaprilat
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Cilazaprilat.
Torasemide
Unknown severity
The risk or severity of adverse effects can be increased when Torasemide is combined with Allopurinol.
Furosemide
Unknown severity
The risk or severity of adverse effects can be increased when Furosemide is combined with Allopurinol.
Bumetanide
Unknown severity
The risk or severity of adverse effects can be increased when Bumetanide is combined with Allopurinol.
Etacrynic acid
Unknown severity
The risk or severity of adverse effects can be increased when Etacrynic acid is combined with Allopurinol.
Piretanide
Unknown severity
The risk or severity of adverse effects can be increased when Piretanide is combined with Allopurinol.
The risk or severity of adverse effects can be increased when Azosemide is combined with Allopurinol.
The risk or severity of adverse effects can be increased when Tripamide is combined with Allopurinol.
Methyclothiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Methyclothiazide.
Chlorthalidone
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Chlorthalidone.
Bendroflumethiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Bendroflumethiazide.
Metolazone
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Metolazone.
Benzthiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Benzthiazide.
Hydroflumethiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Hydroflumethiazide.
Indapamide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Indapamide.
Chlorothiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Chlorothiazide.
Hydrochlorothiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Hydrochlorothiazide.
Trichlormethiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Trichlormethiazide.
Polythiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Polythiazide.
Quinethazone
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Quinethazone.
Cyclopenthiazide
Moderate
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Cyclopenthiazide.
The risk of a hypersensitivity reaction to Allopurinol is increased when it is combined with Epitizide.
The serum concentration of Caffeine can be increased when it is combined with Allopurinol.
Theophylline
Unknown severity
The serum concentration of Theophylline can be increased when it is combined with Allopurinol.
Showing 50 of 1126 interactions
Food & lifestyle interactions
Avoid Alcohol
Avoid alcohol.
Advice
Take with a full glass of water.
Take With Food
Take with food.
Toxicity & overdose
Oral TDLO (rat): 10 mg/kg; Oral LD50 (mouse): 78 mg/kg; Oral TDLO (mouse): 100 mg/kg F3985
Use in pregnancy
Reproductive studies have been completed using rats and rabbit models at doses up to twenty times the normal human dose ( about 5 mg/kg per day), and it was concluded that fertility was not impaired and there was no fetal harm. There is a published report of a study in pregnant mice administered 50 or 100 mg/kg allopurinol intraperitoneally on gestation days 10 or 13. There were increased numbers of dead fetuses in dams administered 100 mg/kg allopurinol, however, death did not occur in those given 50 mg/kg.
There were higher numbers of external malformations in fetuses at both doses of allopurinol on gestation day 10 and higher numbers of skeletal malformations in fetuses at both doses on gestation day 13. Despite the above findings, there are no adequate or well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if it is absolutely required [FDA label].
Use in nursing
Both allopurinol and the metabolite oxipurinol have been found in the milk of a mother who was receiving allopurinol.
Since the effect of allopurinol on the nursing infant is unknown, it is advisable to exercise caution when allopurinol is taken by a nursing woman [FDA label].
Mutagenicity and carcinogenicity
Cytogenic studies demonstrate that allopurinol does not induce chromosomal abnormalities in human blood cells in vitro at concentrations up to 100 g/mL and in vivo at doses up to 60 mg/day for an average duration of 40 months. Allopurinol does not form nitroso compounds (which may be carcinogenic) or affect lymphocyte transformation in vitro. Evidence suggests that allopurinol does not have deleterious effects on DNA at any stage of the cell cycle and was not found to be mutagenic.
No evidence of carcinogenicity has been observed in mice treated with allopurinol for up to a 2 year period F3988.
Use in pregnancy
Reproductive studies have been completed using rats and rabbit models at doses up to twenty times the normal human dose ( about 5 mg/kg per day), and it was concluded that fertility was not impaired and there was no fetal harm. There is a published report of a study in pregnant mice administered 50 or 100 mg/kg allopurinol intraperitoneally on gestation days 10 or 13. There were increased numbers of dead fetuses in dams administered 100 mg/kg allopurinol, however, death did not occur in those given 50 mg/kg.
There were higher numbers of external malformations in fetuses at both doses of allopurinol on gestation day 10 and higher numbers of skeletal malformations in fetuses at both doses on gestation day 13. Despite the above findings, there are no adequate or well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if it is absolutely required [FDA label].
Use in nursing
Both allopurinol and the metabolite oxipurinol have been found in the milk of a mother who was receiving allopurinol.
Since the effect of allopurinol on the nursing infant is unknown, it is advisable to exercise caution when allopurinol is taken by a nursing woman [FDA label].
Mutagenicity and carcinogenicity
Cytogenic studies demonstrate that allopurinol does not induce chromosomal abnormalities in human blood cells in vitro at concentrations up to 100 g/mL and in vivo at doses up to 60 mg/day for an average duration of 40 months. Allopurinol does not form nitroso compounds (which may be carcinogenic) or affect lymphocyte transformation in vitro. Evidence suggests that allopurinol does not have deleterious effects on DNA at any stage of the cell cycle and was not found to be mutagenic.
No evidence of carcinogenicity has been observed in mice treated with allopurinol for up to a 2 year period F3988.
How it works
Mechanism of action
Allopurinol is a structural analog of the natural purine base, hypoxanthine. After ingestion, allopurinol is metabolized to its active metabolite, oxypurinol (alloxanthine) in the liver T508, which acts as an inhibitor of xanthine oxidase enzyme [FDA label].
Allopurinol and its active metabolite inhibit xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Inhibition of this enzyme is responsible for the effects of allopurinol. This drug increases the reutilization of hypoxanthine and xanthine for nucleotide and nucleic acid synthesis by a process that involves the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase). This process results in an increased nucleotide concentration, which causes feedback inhibition of de novo purine synthesis. The end result is decreased urine and serum uric acid concentrations F3988, which decreases the incidence of gout symptoms.
Accompanying the reduction of serum uric acid by allopurinol is an increase in the serum and urine concentrations of hypoxanthine and xanthine (due to inhibition of xanthine oxidase). In the absence of allopurinol, regular urinary excretion of oxypurines almost entirely occurs in the form of uric acid. After the ingestion of allopurinol, the contents of excreted urine are hypoxanthine, xanthine, and uric acid. Because each substance has its own individual solubility, the concentration of uric acid in plasma is decreased without exposing the renal tissues to a high load of uric acid, thereby decreasing the risk of crystalluria. By lowering the uric acid concentration in the plasma below its limits of solubility, allopurinol encourages the dissolution of gout tophi. Although the levels of hypoxanthine and xanthine are found to be increased after allopurinol ingestion, the risk of deposition in renal tissues is less than that of uric acid, as they become more soluble and are rapidly excreted by the kidney F3988.
Allopurinol and its active metabolite inhibit xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Inhibition of this enzyme is responsible for the effects of allopurinol. This drug increases the reutilization of hypoxanthine and xanthine for nucleotide and nucleic acid synthesis by a process that involves the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase). This process results in an increased nucleotide concentration, which causes feedback inhibition of de novo purine synthesis. The end result is decreased urine and serum uric acid concentrations F3988, which decreases the incidence of gout symptoms.
Accompanying the reduction of serum uric acid by allopurinol is an increase in the serum and urine concentrations of hypoxanthine and xanthine (due to inhibition of xanthine oxidase). In the absence of allopurinol, regular urinary excretion of oxypurines almost entirely occurs in the form of uric acid. After the ingestion of allopurinol, the contents of excreted urine are hypoxanthine, xanthine, and uric acid. Because each substance has its own individual solubility, the concentration of uric acid in plasma is decreased without exposing the renal tissues to a high load of uric acid, thereby decreasing the risk of crystalluria. By lowering the uric acid concentration in the plasma below its limits of solubility, allopurinol encourages the dissolution of gout tophi. Although the levels of hypoxanthine and xanthine are found to be increased after allopurinol ingestion, the risk of deposition in renal tissues is less than that of uric acid, as they become more soluble and are rapidly excreted by the kidney F3988.
Pharmacodynamics
Allopurinol decreases the production of uric acid by stopping the biochemical reactions that precede its formation [FDA label]. This process decreases urate and relieves the symptoms of gout, which may include painful tophi, joint pain, inflammation, redness, decreased range of motion, and swelling [A665].
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
This drug is about 90% absorbed from the gastrointestinal tract. Peak plasma levels normally occur at 1.5 hours and 4.5 hours post-dose for allopurinol and oxipurinol respectively. Following one oral dose of 300 mg of allopurinol, maximum plasma levels of about 3 mcg/mL of allopurinol and 6.5 mcg/mL of oxipurinol were measured [FDA label].
Half-life
The plasma half-life of allopurinol is 1-2 hours, due to its rapid renal clearance [FDA label].
Protein binding
Allopurinol and oxypurinol are only negligibly bound to plasma proteins .
[A175954][A175948]
[A175954][A175948]
Volume of distribution
Allopurinol and oxypurinol are both substrates for the enzyme xanthine oxidase, which is present in the cytoplasm of endothelial cells of capillaries, including sinusoids, with the highest activity demonstrated in the liver and intestinal lining. Tissue concentrations of allopurinol have not yet been reported in humans, however, it is probable that allopurinol and the metabolite oxypurinol would be measured in the highest concentrations in the abovementioned tissues. In animals, allopurinol concentrations are found to reach the highest levels in the blood, liver, intestine and heart, and lowest in the brain and lung tissues .
[A175948]
[A175948]
Metabolism
Allopurinol is rapidly metabolized to the corresponding xanthine analog, oxipurinol (alloxanthine), which is also an inhibitor of xanthine oxidase enzyme [FDA label].
Both allopurinol and oxypurinol inhibit the action of this enzyme. Allopurinol and oxypurinol are also converted by the purine salvage pathway to their respective ribonucleotides. The effect of these ribonucleotides related to the hypouricemic action of allopurinol in humans is not fully elucidated to this date.
These metabolites may act to inhibit de novo purine biosynthesis by inhibiting the enzyme, amidophosphoribosyltransferase. The ribonucleotides have not been found to be incorporated in DNA .
[A175945]
Both allopurinol and oxypurinol inhibit the action of this enzyme. Allopurinol and oxypurinol are also converted by the purine salvage pathway to their respective ribonucleotides. The effect of these ribonucleotides related to the hypouricemic action of allopurinol in humans is not fully elucidated to this date.
These metabolites may act to inhibit de novo purine biosynthesis by inhibiting the enzyme, amidophosphoribosyltransferase. The ribonucleotides have not been found to be incorporated in DNA .
[A175945]
Route of elimination
Approximately 80% of orally ingested allopurinol is found excreted in the urine as various metabolites .
[A175948]
About 20% of ingested allopurinol is excreted in the feces [FDA label].
[A175948]
About 20% of ingested allopurinol is excreted in the feces [FDA label].
Clearance
Since allopurinol and its metabolites are mainly eliminated by the kidney, accumulation of this drug can occur in patients with renal dysfunction or failure, and the dose of allopurinol should, therefore, be reduced. With a creatinine clearance of 10 to 20 mL/min, a daily dosage of 200 mg of allopurinol is suitable. When the creatinine clearance is less than 10 mL/min, the daily dosage should not be higher than 100 mg.
With severe renal impairment (creatinine clearance measured at less than 3 mL/min) a longer interval between doses may be required [FDA label].
With severe renal impairment (creatinine clearance measured at less than 3 mL/min) a longer interval between doses may be required [FDA label].
Drug targets(1)
Proteins and enzymes this drug interacts with in the body
Xanthine dehydrogenase/oxidase
XDH
inhibitor
Specific function2 iron, 2 sulfur cluster binding
Cellular location
Cytoplasm
General function & pharmacology
Key enzyme in purine degradation. Catalyzes the oxidation of hypoxanthine to xanthine. Catalyzes the oxidation of xanthine to uric acid.
Contributes to the generation of reactive oxygen species. Has also low oxidase activity towards aldehydes (in vitro)
Contributes to the generation of reactive oxygen species. Has also low oxidase activity towards aldehydes (in vitro)
Metabolizing enzymes(3)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
AOX1Aldehyde oxidase
substrate
XDHXanthine dehydrogenase/oxidase
inhibitor
CYP1A2Cytochrome P450 1A2
inhibitor
Transporters(4)
Proteins that transport this drug across cell membranes
Organic anion transporter 3
SLC22A8
substrate
Specific functionorganic anion transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Functions as an organic anion/dicarboxylate exchanger that couples organic anion uptake indirectly to the sodium gradient .
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
Solute carrier family 22 member 7
SLC22A7
substrate
Specific functionalpha-ketoglutarate transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Functions as a Na(+)-independent bidirectional multispecific transporter .
PMID:11327718 PMID:18216183 PMID:21446918 PMID:28945155
Contributes to the renal and hepatic elimination of endogenous organic compounds from the systemic circulation into the urine and bile, respectively .
PMID:11327718 PMID:25904762
Capable of transporting a wide range of purine and pyrimidine nucleobases, nucleosides and nucleotides, with cGMP, 2'deoxyguanosine and GMP being the preferred substrates .
PMID:11327718 PMID:18216183 PMID:26377792 PMID:28945155
Functions as a pH- and chloride-independent cGMP bidirectional facilitative transporter that can regulate both intracellular and extracellular levels of cGMP and may be involved in cGMP signaling pathways .
PMID:18216183 PMID:26377792
Mediates orotate/glutamate bidirectional exchange and most likely display a physiological role in hepatic release of glutamate into the blood .
PMID:21446918
Involved in renal secretion and possible reabsorption of creatinine .
PMID:25904762 PMID:28945155
Able to uptake prostaglandin E2 (PGE2) and may contribute to PGE2 renal excretion (Probable). Also transports alpha-ketoglutarate and urate .
PMID:11327718 PMID:26377792
Apart from the orotate/glutamate exchange, the counterions for the uptake of other SLC22A7/OAT2 substrates remain to be identified PMID:26377792
PMID:11327718 PMID:18216183 PMID:21446918 PMID:28945155
Contributes to the renal and hepatic elimination of endogenous organic compounds from the systemic circulation into the urine and bile, respectively .
PMID:11327718 PMID:25904762
Capable of transporting a wide range of purine and pyrimidine nucleobases, nucleosides and nucleotides, with cGMP, 2'deoxyguanosine and GMP being the preferred substrates .
PMID:11327718 PMID:18216183 PMID:26377792 PMID:28945155
Functions as a pH- and chloride-independent cGMP bidirectional facilitative transporter that can regulate both intracellular and extracellular levels of cGMP and may be involved in cGMP signaling pathways .
PMID:18216183 PMID:26377792
Mediates orotate/glutamate bidirectional exchange and most likely display a physiological role in hepatic release of glutamate into the blood .
PMID:21446918
Involved in renal secretion and possible reabsorption of creatinine .
PMID:25904762 PMID:28945155
Able to uptake prostaglandin E2 (PGE2) and may contribute to PGE2 renal excretion (Probable). Also transports alpha-ketoglutarate and urate .
PMID:11327718 PMID:26377792
Apart from the orotate/glutamate exchange, the counterions for the uptake of other SLC22A7/OAT2 substrates remain to be identified PMID:26377792
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Solute carrier family 22 member 2
SLC22A2
Specific functionacetylcholine transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics .
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
Scientific references(10)
Pacher P., Nivorozhkin A., Szabo C.
Therapeutic Effects of Xanthine Oxidase Inhibitors: Renaissance Half a Century after the Discovery of Allopurinol.
Pharmacological Reviews
200658(1):87-114. doi: 10.1124/pr.58.1.6
Schlesinger N.
Diagnosing and treating gout: a review to aid primary care physicians.
Postgrad Medicine
2010 Mar122(2):157-61. doi: 10.3810/pgm.2010.03.2133
Suzuki I., Yamauchi T., Onuma M., Nozaki S.
Allopurinol, an inhibitor of uric acid synthesis--can it be used for the treatment of metabolic syndrome and related disorders? Drugs Today (Barc). 2009 May;45(5):363-78. doi: 10.1358/dot.2009.45.
5
1370460
Terkeltaub R.
Update on gout: new therapeutic strategies and options.
Nature Review Rheumatol
2010 Jan6(1):30-8. doi: 10.1038/nrrheum.2009.236
George J., Struthers A.D.
Role of urate, xanthine oxidase and the effects of allopurinol in vascular oxidative stress. Vascular Health and Risk Management. 2009;:265. doi: 10.
2147/vhrm
s4265
Seth R., Kydd A.S., Buchbinder R., Bombardier C., Edwards C.J.
Allopurinol for chronic gout.
Cochrane Database of Systematic Reviews
2014 Oct 14(10):CD006077. doi: 10.1002/14651858.CD006077.pub3
Ragab G., Elshahaly M., Bardin T.
Gout: An old disease in new perspective - A review.
Journal Advanced Research
2017 Sep8(5):495-511. doi: 10.1016/j.jare.2017.04.008. Epub 2017 May 10
Murrell G.A., Rapeport W.G.
Clinical pharmacokinetics of allopurinol.
Clinical Pharmacokinetics
1986 Sep-Oct11(5):343-53. doi: 10.2165/00003088-198611050-00001
Reiter S., Simmonds H.A., Webster D.R., Watson A.R.
On the metabolism of allopurinol.
Biochemical Pharmacology
198332(14):2167-2174. doi: 10.1016/0006-2952(83)90222-8
Turnheim K., Krivanek P., Oberbauer R.
Pharmacokinetics and pharmacodynamics of allopurinol in elderly and young subjects.
British Journal of Clinical Pharmacology
199948(4):501-509. doi: 10.1046/j.1365-2125.1999.00041.x
ATC classification(2 codes)
ATC M04AA01
ATC M04AA51
Affected organisms(1)
Humans and other mammals
International brands(8)
Salt forms(1)
Allopurinol sodium(DBSALT000350)
Experimental properties(6)
Protein Data Bank entries(1)
Commercial products(387)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Allopurinol
Additional database identifiers
Drugs Product Database (DPD)
9388
ChemSpider
2010
BindingDB
50140241
PDB
A1BD4
ZINC
ZINC000013298313
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12805
GenAtlas
XDH
GeneCards
XDH
GenBank Gene Database
D11456
GenBank Protein Database
10336525
Guide to Pharmacology
2646
UniProt Accession
XDH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:553
GeneCards
AOX1
GenBank Gene Database
L11005
GenBank Protein Database
438656
Guide to Pharmacology
3186
UniProt Accession
AOXA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12805
GenAtlas
XDH
GeneCards
XDH
GenBank Gene Database
D11456
GenBank Protein Database
10336525
Guide to Pharmacology
2646
UniProt Accession
XDH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10971
GeneCards
SLC22A7
GenBank Gene Database
AF097518
GenBank Protein Database
5001689
UniProt Accession
S22A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10966
GeneCards
SLC22A2
GenBank Gene Database
X98333
GenBank Protein Database
2281942
Guide to Pharmacology
1020
UniProt Accession
S22A2_HUMAN
International reference pricing
14 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $0.04/ml
To $612.30/vial
Suspendol-s liquid
$0.04/ml
Apo-Allopurinol 100 mg Tablet
$0.08/tablet
Novo-Purol 100 mg Tablet
$0.08/tablet
Apo-Allopurinol 200 mg Tablet
$0.14/tablet
Novo-Purol 200 mg Tablet
$0.14/tablet
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
8 active patents, 1 expired
8546436
United States
Approved 1 Oct 2013 · Expires 29 Feb 2032
5y 11m
9956205
United States
Approved 1 May 2018 · Expires 28 Dec 2031
5y 9m
9216179
United States
Approved 22 Dec 2015 · Expires 2 Aug 2030
4y 4m
8084483
United States
Approved 27 Dec 2011 · Expires 17 Aug 2029
3y 4m
8546437
United States
Approved 1 Oct 2013 · Expires 29 Apr 2029
3 years
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)