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Uric acid

Alias: uric acid; 69-93-2; urate; Lithic acid; 2,6,8-trioxypurine;
Cat No.:V29578 Purity: ≥98%
Uric acid is an oxygen radical scavenger and a very important antioxidant that helps maintain blood pressure stability and resist oxidative stress.
Uric acid
Uric acid Chemical Structure CAS No.: 69-93-2
Product category: New1
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
1g
Other Sizes

Other Forms of Uric acid:

  • Uric acid sodium (monosodium urate)
  • Uric acid-13C,15N3 (uric acid 13C, 15N3)
  • Uric acid-15N2 (uric acid-15N2)
  • Uric acid-13C3
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Top Publications Citing lnvivochem Products
Product Description
Uric acid is an oxygen radical scavenger and a very important antioxidant that helps maintain blood pressure stability and resist oxidative stress. Uric acid can scavenge reactive oxygen species (ROS), like singlet oxygen and peroxynitrite, and inhibit lipid peroxidation.
Uric acid (CAS 69-93-2) is a heterocyclic purine derivative and the final oxidation product of purine metabolism in humans. With a molecular formula of C₅H₄N₄O₃ and a molecular weight of 168.11 g/mol, it is a white to off-white crystalline powder. Uric acid is an endogenous antioxidant that scavenges reactive oxygen species (ROS), including singlet oxygen, oxygen radicals, and peroxynitrite. It is sparingly soluble in water and insoluble in alcohol. Elevated levels of uric acid in the blood (hyperuricemia) can lead to the formation of urate crystals in joints, causing gout, and in the urinary tract, causing kidney stones.
Biological Activity I Assay Protocols (From Reference)
Targets
Antioxidant
Uric acid does not have a specific therapeutic target but acts as an endogenous antioxidant. It is the end product of purine metabolism in humans and is excreted by the kidneys. Its primary role is as a waste product, but it also has beneficial antioxidant properties. It is a scavenger of reactive oxygen species, helping to protect cells from oxidative damage. However, at high concentrations, it can be pro-inflammatory and contribute to the development of gout and kidney stones.
ln Vitro
Uric acid (400 μM; 48 hours) protects Caco-2 cells from indomethacin-induced lipid peroxidation [2]. Co-treatment of cells with indomethacin and uric acid (200 μM IND plus 400 μM UA; 24 hours) significantly lowered ROS levels compared to cells treated with indomethacin alone. Cell viability in Caco-2 cells treated with both indomethacin and uric acid (200 μM IND plus 400 μM UA; 24 h) was higher than that in cells treated with indomethacin alone. Uric acid has a protective effect against indomethacin-induced alterations in intestinal cells through its antioxidant activity [2].
In vitro, Uric acid is used as a standard in clinical diagnostics to measure serum and urine uric acid levels for the assessment of gout and renal function. It is also used as a reference compound in biochemical research to study purine metabolism and oxidative stress. Its antioxidant activity can be measured in cell-free assays, such as the ABTS or DPPH assays.
ln Vivo
In vivo, Uric acid is an important biomarker for various diseases. Elevated levels are associated with gout, kidney stones, and cardiovascular disease. It is also a risk factor for metabolic syndrome and hypertension. The compound is not used as a therapeutic agent, but drugs that lower uric acid levels (e.g., allopurinol, febuxostat) are used to treat gout.
Enzyme Assay
In vitro non-cell enzyme assays for Uric acid are not typical, as it is a metabolite. Its antioxidant activity can be measured using cell-free assays such as the ABTS or DPPH radical scavenging assays. Its concentration can be quantified using enzymatic methods, such as the uricase-peroxidase method, which is used in clinical diagnostics.
Cell Assay
In vitro cell-based assays for Uric acid are used to study its effects on cellular function, particularly its role in oxidative stress and inflammation. Cells are treated with uric acid, and parameters such as cell viability, ROS production, and inflammatory cytokine production are measured. These studies help to elucidate the dual role of uric acid as an antioxidant and a pro-inflammatory factor.
Animal Protocol
Animal/Disease Models: 8weeks old male C57BL/6J mice [2]
Doses: 250 mg/kg body weight
Route of Administration: Po
Experimental Results: When mice are given indomethacin at the same time, uric acid can be used for animal modeling to construct a hypertension model. . After oral administration of uric acid, the ulcer area was Dramatically diminished in a uric acid dose-dependent manner.
In vivo animal studies for Uric acid are typically conducted to study the pathophysiology of hyperuricemia and gout. Animal models of hyperuricemia are used to test the efficacy of urate-lowering drugs. The effects of uric acid on renal function, cardiovascular health, and metabolic syndrome are also studied in these models.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Uric acid is primarily excreted through the kidneys. Metabolism/Metabolites In higher primates and humans, uricase is absent, so uric acid cannot be further metabolized and is directly excreted. In all other mammals, uric acid is metabolized by uricase into allantoin, which is then excreted.
Uric acid has a molecular weight of 168.11 g/mol and a molecular formula of C₅H₄N₄O₃. It is a white to off-white crystalline powder. One gram dissolves in about 15,000 parts cold water and about 2000 parts boiling water. It is soluble in glycerol and solutions of alkali hydroxides, but insoluble in alcohol. It has a melting point of >300 °C.
Toxicity/Toxicokinetics
Uric acid is generally considered safe at normal physiological levels. However, high levels can lead to gout and kidney stones. The compound is not intended for therapeutic use. Standard laboratory safety precautions should be followed when handling the compound.
References

[1]. Recent Progress on Uric Acid Detection: A Review. Crit Rev Anal Chem. 2020;50(4):359-375.

[2]. Uric acid ameliorates indomethacin-induced enteropathy in mice through its antioxidant activity. J Gastroenterol Hepatol. 2017 Nov;32(11):1839-1845.

Additional Infomation
7,9-Dihydro-1H-purine-2,6,8(3H)-trione is an oxopurine in which the purine ring is substituted with oxo groups at positions 2, 6, and 8. It is found in humans, E. coli, and mice as a metabolite. It is a tautomer of 2,6-dihydroxy-7,9-dihydro-8H-purine-8-one, 9H-purine-2,6,8-triol, 7H-purine-2,6,8-triol, 1H-purine-2,6,8-triol, and 5,7-dihydro-1H-purine-2,6,8(9H)-trione. Uric acid is the final product of purine metabolism in the human body. Uric acid production is catalyzed by xanthine oxidase, an enzyme that oxidizes oxopurines. Normally, a small amount of uric acid exists in the human body, but when the uric acid content in the blood is too high (called hyperuricemia), it can lead to gout and kidney stones. As a therapeutic agent, uric acid is known to increase during oxidative stress, thus possessing antioxidant properties. As of August 2013, there are no approved uric acid preparations or indications. In Spain, uric acid is an investigational drug undergoing a Phase III clinical trial to investigate its efficacy as an adjunct to alteplase in the treatment of acute ischemic stroke. Uric acid is a metabolic product of Escherichia coli (K12 strain, MG1655 strain). It has also been reported to be present in fruit flies, pomegranates, and other organisms with relevant data. Uric acid is a white, tasteless, odorless crystalline protein metabolic product found in blood and urine, and in trace amounts in various organs of the human body. In various disease states, uric acid can accumulate and form stones or crystals. Uric acid is a metabolic product of Saccharomyces cerevisiae, and is also a product of the oxidation of xanthine and hypoxanthine, among other oxypurines, by xanthine oxidase. Uric acid is the final oxidation product of purine metabolism in humans and primates, while in most other mammals, uricase further oxidizes it to allantoin. See also: ... See more ...
Drug Indications
Currently (August 2013), there are no approved indications for uric acid. A potential therapeutic use for uric acid is as adjunctive therapy for acute ischemic stroke.
Mechanism of Action
The exact mechanism of the antioxidant effect of uric acid has not been elucidated.
Uric acid is the final oxidation product of purine metabolism in humans and an endogenous antioxidant. It is a biomarker for gout and renal function. It is not approved as a drug but is used as a diagnostic marker and in research.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C5H4N4O3
Molecular Weight
168.1103
Exact Mass
168.028
CAS #
69-93-2
Related CAS #
Uric acid sodium;1198-77-2;Uric acid-13C,15N3;2421217-23-2;Uric acid-15N2;62948-75-8;Uric acid-13C3;2832998-22-6
PubChem CID
1175
Appearance
White to off-white solid powder
Density
1.9±0.1 g/cm3
Boiling Point
863ºC at 760 mmHg
Melting Point
>300 °C(lit.)
Flash Point
475.7ºC
Index of Refraction
1.721
LogP
-1.08
Hydrogen Bond Donor Count
4
Hydrogen Bond Acceptor Count
3
Rotatable Bond Count
0
Heavy Atom Count
12
Complexity
332
Defined Atom Stereocenter Count
0
SMILES
C12=C(NC(=O)N1)NC(=O)NC2=O
InChi Key
LEHOTFFKMJEONL-UHFFFAOYSA-N
InChi Code
InChI=1S/C5H4N4O3/c10-3-1-2(7-4(11)6-1)8-5(12)9-3/h(H4,6,7,8,9,10,11,12)
Chemical Name
7,9-dihydro-3H-purine-2,6,8-trione
Synonyms
uric acid; 69-93-2; urate; Lithic acid; 2,6,8-trioxypurine;
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
1M NaOH : 8.33 mg/mL (~49.55 mM)
H2O : ~6.25 mg/mL (~37.18 mM)
DMSO :< 1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: 10 mg/mL (59.48 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 5.9485 mL 29.7424 mL 59.4849 mL
5 mM 1.1897 mL 5.9485 mL 11.8970 mL
10 mM 0.5948 mL 2.9742 mL 5.9485 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

Calculator

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g/mol

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Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
Efficacy Study of Combined Treatment With Uric Acid and rtPA in Acute Ischemic Stroke
CTID: NCT00860366
Phase: Phase 2/Phase 3
Status: Completed
Date: 2015-03-10
A clinical study comparing the renal effects of dotinurad and febuxostat in patients with chronic kidney disease and hyperuricemia
CTID: UMIN000059852
Status: Pending
Date: 2025-11-30
Study on renal protective effect of serum urate lowering therapy
CTID: UMIN000059065
Phase: Not applicable
Status: Recruiting
Date: 2025-09-12
Investigation of the relationship between ameloblastoma and salivary uric acid levels and microRNAs
CTID: UMIN000057717
Status: Recruiting
Date: 2025-04-25
Beneficial effect by Xanthine oxidase inhibitor on endothelial function beyond Uric Acid trial
CTID: UMIN000031096
Status: Complete: follow-up complete
Date: 2018-02-01
Topiroxostat PMS
CTID: jRCT1080223727
Status: completed
Date: 2017-11-22
Suggestion Of Using topiroxostat for a Group of Hyperuricemic CHF patients with preserved ejection fraction for better Treatment outcomes study (SOUGHT study)
CTID: UMIN000024981
Status: Complete: follow-up complete
Date: 2016-11-24
Therapeutic Strategy for Efficient Reduction of Serum Uric Acid Levels with Allopurinol versus Benzbromarone in Hyperuricemic Patients with Essential Hypertension-A Randomized Crossover Study (TERAO study)
CTID: UMIN000023905
Phase: Not applicable
Status: Complete: follow-up complete
Date: 2016-09-02
The Effect of Xanthine Oxidase Inhibitor in ChronIc heart failure patients complicaTED with hyper-UricemiA : A (Prospective) Randomized Controlled Clinical Trial of Topiroxostat and Alloprinol
CTID: UMIN000020939
Status: Complete: follow-up complete
Date: 2016-02-09
Influence of XOI, Febuxostat, on Vascular Function in Patients with Hyperuricemia and Cardiovascular Risk Factors
CTID: UMIN000019530
Status: Complete: follow-up complete
Date: 2015-10-28
A randomized trial Comparing the Effects of Febuxostat and Allopurinol on renal function and left ventricular hypertrophy for chronic heart failure patient with hyperuricemia complicated by chronic kidney disease stage G3-G4.
CTID: UMIN000014309
Phase: Not applicable
Status: Pending
Date: 2014-06-19
Examination of the effect of a combination of benzbromarone and febuxostat in patients with hyperuricemia complicating diabetic nephropathy
CTID: UMIN000012628
Status: Recruiting
Date: 2013-12-19
A multicenter, randomized, comparative trial on the effect of febuxostat in preventing cerebral and cardiorenovascular events in patients with hyperuricemia
CTID: UMIN000012134
Phase: Not applicable
Status: Complete: follow-up complete
Date: 2013-10-28
Influence of febuxostat and allopurinol on renal function for hyperuricemia
CTID: UMIN000005964
Status: Complete: follow-up complete
Date: 2011-07-11
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