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Fig. 1 · Structure
Cat. No.
A10055
CAS No.
315-30-0
Formula
C5H4N4O
Mol. Weight
136.11

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Allopurinol

Cat. No. A10055 CAS 315-30-0
Allopurinol is a purine analog; it is a structural isomer of hypoxanthine (a naturally occurring purine in the body) and is an inhibitor of the enzyme xanthine oxidase.

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Biological Activity

Bioactivity / Mechanism

Allopurinol produces time-dependent inhibition of purified bovine xanthine oxidoreductase. Matched enzyme experiments distinguish its effects from those of directly added oxypurinol, particularly during hypoxanthine oxidation. These responses depend on substrate and assay conditions and do not define a universal IC50. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
xanthine oxidase

In Vitro Studies

In human fibroblasts, allopurinol reduced an early purine-synthesis endpoint despite undetectable xanthine oxidase activity in tested extracts. Lower-concentration inhibition depended on normal PRT activity; PRT-deficient strains responded differently. The proposed nucleotide-mediated explanation was not directly established. [2]

Substrate-dependent inhibition of purified bovine xanthine oxidoreductase

Biochemical assay · Purified bovine milk XO and XDH; xanthine or hypoxanthine substrates. [1]

Matched parent/metabolite comparisons show time-dependent inhibition by allopurinol and a stronger effect on hypoxanthine oxidation than directly added oxypurinol. No universal IC50 is assigned.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Urate generation from xanthinequalitative time course Allopurinol progressively inhibited urate production; at matched inhibitor concentrations inhibition developed more rapidly than with oxypurinol.[1]
Hypoxanthine depletion and xanthine/urate productionauthor-reported time course For XO, the authors describe inhibition of hypoxanthine-to-xanthine conversion at 10 μM allopurinol within about 5 min and immediate inhibition at 50 μM; xanthine accumulation remained evident even with 500 μM oxypurinol. XDH showed a similar qualitative distinction.[1]

Literature-Reported Treatment Conditions

Treatment concentration
Xanthine series: 2–50 μM allopurinol or oxypurinol. Hypoxanthine HPLC series: 2–50 μM allopurinol versus 2–500 μM oxypurinol.
Exposure duration
Selected Figure 3A–D panels span 10–60 min; Figure 4A spans 10 min and 4B spans 30 min.
Method
Figure 3A–D: 2.38 nM XO, 50 μM xanthine, 0.1 M pyrophosphate/acetic acid pH 8.5, 0.2 mM EDTA, 25 °C; urate absorbance at 295 nm. Figure 4A: 5 nM XO, 2–2.5 μM hypoxanthine, 0.1 M potassium phosphate pH 7.4, 0.2 mM EDTA, 25 °C; HPLC. Figure 4B: 3 nM XDH, 3–3.5 μM hypoxanthine at pH 8.5; shared XDH assay includes 500 μM β-NAD+.
Co-treatment
No therapeutic combination; oxypurinol is a separately added comparator.
Reported limits
Inhibitor stock solvent, compound vendor/lot and replicate counts for these time courses were not specified in the reviewed assay methods/captions. No IC50 extracted.
Methods and source locations

Compound reported in the paper: Allopurinol; Compound label in the paper: Allopurinol

Evidence concerns the reported experimental material and model; it does not establish Adooq lot performance or a clinical regimen.

Figures 3A–D and 4A–B; Table 1; Experimental procedures: Purification and enzyme assays of XOR; HPLC conditions

Urate generation from xanthine: 295-nm absorbance time courses with no-inhibitor control. Exact stop times not adopted because text and Table 1 differ for some conditions. — Figure 3A–D and caption; Results: Comparison of the inhibitory effects; Table 1

Hypoxanthine depletion and xanthine/urate production: HPLC substrate/product time courses with no-inhibitor and separate oxypurinol controls. Approximate timing is author-reported, not digitized. — Figure 4A–B and caption; Results: Inhibition of allopurinol and oxypurinol on the oxidation of hypoxanthine to xanthine

Purine synthesis in human fibroblasts with differing PRT activity

Cell-based study · Four human fibroblast strains with normal hypoxanthine-guanine phosphoribosyltransferase (PRT+) and three genetically deficient strains (PRT−). [2]

Allopurinol inhibited the early purine-synthesis endpoint in PRT+ cells at lower concentrations than in PRT− cells. XO activity was undetectable in the tested extracts. This supports a cellular effect beyond the demonstrated XO assay, while the responsible metabolite/mechanism remained unresolved.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
FGAR synthesis relative to control activityconcentration-dependent response PRT+ strains were inhibited at concentrations as low as 2 × 10−4 mole/liter. PRT− strains showed a modest increase at that concentration and inhibition at 6 × 10−4 mole/liter and above.[2]
Control evidence and limits on cellular mechanismqualitative control/limitation XO activity was not detected spectrophotometrically or by a more sensitive radioisotopic assay. Allopurinol ribonucleoside/ribonucleotide derivatives could not be demonstrated; the authors emphasize poor detection sensitivity.[2]

Literature-Reported Treatment Conditions

Treatment concentration
Allopurinol Figure 3: 2 × 10−4 to 8 × 10−4 mole/liter.
Method
Radiolabeled formate incorporation into N-formylglycinamide ribonucleotide (FGAR) in fibroblast suspensions in the presence of 0.3 mM azaserine; FGAR separated by electrophoresis and quantified by scintillation counting. Responses expressed relative to control activity.
Co-treatment
Azaserine is an assay reagent used to accumulate FGAR; it is not a therapeutic combination.
Reported limits
FGAR incubation duration, allopurinol stock solvent and Figure 3 error-bar definition are not specified in the reviewed methods/caption. Four normal and three deficient strains are model counts, not an inferred replicate n.
Methods and source locations

Compound reported in the paper: Allopurinol; Compound label in the paper: Allopurinol

Evidence concerns the reported experimental material and model; it does not establish Adooq lot performance or a clinical regimen.

Figure 3; Table I and III; Methods pp602–603; Results pp604–605; Discussion pp607–608

FGAR synthesis relative to control activity: Radiolabeled formate-to-FGAR assay. Exact percentages are not estimated from the plotted curves. — Figure 3 and Results, printed p605; Table III p604; Methods pp602–603

Control evidence and limits on cellular mechanism: Extract assays included boiled-extract controls in Table I. Failure to detect derivatives does not establish their absence. — Table I and Results, printed p604; XO assay Methods p603; Discussion pp607–608

In Vivo Studies

In male rats, oral allopurinol given before and during intermittent hypoxia preserved acetylcholine-induced dilation measured in isolated resistance arteries. Nitroprusside responses, systemic oxidative-stress markers and vessel morphometry showed no significant group differences. Direct XO inhibition and reduced local oxidative stress were not demonstrated by these measurements. [3]

Vascular responses after allopurinol in rats exposed to intermittent hypoxia

Animal study · Adult male Sprague-Dawley rats; normoxia-vehicle n = 12, normoxia-allopurinol n = 9, hypoxia-vehicle n = 11, hypoxia-allopurinol n = 9. [3]

Allopurinol pretreatment preserved acetylcholine-induced dilation in gracilis arteries assessed ex vivo after intermittent hypoxia. Nitroprusside responses and systemic oxidative-stress markers did not differ significantly. XO activity was not directly measured.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Change in vessel diameter after 10−6 M acetylcholinemean ± SEM diameter change Hypoxia-vehicle +4 ± 4 μm versus normoxia-vehicle +21 ± 6 μm (p = 0.01); hypoxia-allopurinol +26 ± 6 μm versus normoxia-allopurinol +34 ± 9 μm (p = 0.55). Hypoxia-allopurinol versus hypoxia-vehicle p = 0.001. Values are means ± SEM. Group n: NV 12, NA 9, HV 11, HA 9.[3]
Endothelium-independent dilation to 10−4 M sodium nitroprussidenegative control No significant difference among the four groups (p = 0.43).[3]
Systemic oxidative stress and vascular structurelimiting results No significant group difference in urinary malondialdehyde/creatinine (p = 0.95), plasma HNE-His adducts (p = 0.55), wall:lumen ratio (p = 0.43) or intima-media thickness (p = 0.52).[3]
Urinary uric acid normalized to creatinineindirect target engagement Lower in pooled allopurinol-treated versus vehicle-treated rats (p = 0.02), an indirect indication of XO inhibition.[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Treatment course
3 weeks total: starting 1 week before and continuing during 2 weeks of exposure.
Vehicle
1% (w/v) methylcellulose
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Hypoxia + allopurinol
65 mg/kg/day		Hypoxia + methylcellulose vehicle, n = 11; normoxia vehicle and normoxia allopurinol groups.Greater acetylcholine-induced dilation than hypoxia-vehicle; no demonstrated systemic oxidative-stress benefit.[3]
Normoxia + allopurinol
65 mg/kg/day		Normoxia + methylcellulose vehicle, n = 12.Acetylcholine-induced dilation did not differ significantly from normoxia-vehicle or hypoxia-allopurinol.[3]
Hypoxia + allopurinol
Model: Male Sprague-Dawley rats exposed to intermittent hypoxia for 14 days; n = 9.
Reported limits: Supplier/lot and salt characterization of allopurinol are not specified in the reviewed dosing section.
Normoxia + allopurinol
Model: Male Sprague-Dawley rats exposed to normoxia; n = 9.
Reported limits: Supplier/lot and salt characterization of allopurinol are not specified in the reviewed dosing section.
Methods and source locations

Compound reported in the paper: Allopurinol; Compound label in the paper: Allopurinol

Evidence concerns the reported experimental material and model; it does not establish Adooq lot performance or a clinical regimen.

Figure 1A–B and caption; Table 1; Methods: Allopurinol Dosing, Vessel Reactivity Studies, Data Analysis; Results and Methodological Considerations

Change in vessel diameter after 10−6 M acetylcholine: Isolated pressurized gracilis arteries, no flow, 80 mm Hg; diameter change at maximal response. Rank-transformed ANOVA and Fisher protected pairwise comparisons. — Abstract; Figure 1A and caption; Results: Response of Resistance Arteries; Table 1

Endothelium-independent dilation to 10−4 M sodium nitroprusside: Ex vivo vessel diameter response; same study controls. — Figure 1B and caption; Results: Response of Resistance Arteries

Systemic oxidative stress and vascular structure: Systemic assays and histological morphometry; these negative findings do not prove absence of local oxidative stress. — Results: Biomarkers of Oxidative Stress, Vessel Morphometry Analysis; Methodological Considerations

Urinary uric acid normalized to creatinine: Urinary enzymatic colorimetry normalized to creatinine; Wilcoxon rank-sum test. XO activity was not directly measured. — Results: Characteristics of Study Animals; Data Analysis; Methodological Considerations

Hypoxia + allopurinol · Figure 1A–B and caption; Table 1; Methods: Allopurinol Dosing, Vessel Reactivity Studies, Data Analysis; Results and Methodological Considerations

Normoxia + allopurinol · Figure 1A–B and caption; Table 1; Methods: Allopurinol Dosing, Vessel Reactivity Studies, Data Analysis; Results and Methodological Considerations

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 315-30-0
Formula C5H4N4O
Molecular Weight 136.11
SMILES
C1=C2C(=NC=NC2=O)NN1

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 23 mg/mL (168.97 mM)
Water 3 mg/mL (22.04 mM)
Ethanol 3 mg/mL (22.04 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Mai Sekine, Ken Okamoto, Emil F. Pai, et al. Allopurinol and oxypurinol differ in their strength and mechanisms of inhibition of xanthine oxidoreductase Journal of Biological Chemistry (2023). PMID: 37625592 DOI: 10.1016/j.jbc.2023.105189 Source material
  2. [2] William N. Kelley, James B. Wyngaarden. Effects of allopurinol and oxipurinol on purine synthesis in cultured human cells Journal of Clinical Investigation (1970). PMID: 5415686 DOI: 10.1172/JCI106271 Source material
  3. [3] John M. Dopp, Nathan R. Philippi, Noah J. Marcus, et al. Xanthine Oxidase Inhibition Attenuates Endothelial Dysfunction Caused by Chronic Intermittent Hypoxia in Rats Respiration (2011). PMID: 21846958 DOI: 10.1159/000329341 Source material

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