Absorption, Distribution and Excretion
SOME SMALL, WATER SOL, BUT NONIONIZABLE COMPD SUCH AS UREA READILY TRAVERSE MAMMALIAN MEMBRANES, PROBABLY ALONG WITH WATER, BY WAY OF THE PORES. THIS FILTRATION PROCESS IS PARTICULARLY RAPID BETWEEN CAPILLARIES & EXTRACELLULAR FLUID.
... UREA ... PENETRATES OTHER CELLS RAPIDLY, ENTERS THE BRAIN ONLY VERY SLOWLY ...
... DISTRIBUTED APPROX IN TOTAL BODY WATER ... HAVE BEEN USED FOR MEASUREMENT OF TOTAL BODY WATER.
EXCRETION OF UREA DURING SWEATING IN MAN: 1.84 SWEAT/PLASMA RATIO WITH PKA @ 13.8. /FROM TABLE/
For more Absorption, Distribution and Excretion (Complete) data for UREA (6 total), please visit the HSDB record page.

Interactions
A case of sudden collapse after the intra-amniotic injection of 5 mg dinoprostone (Prostaglandin E2) and 40 g urea for pregnancy termination in a 36 yr old woman after the diagnosis of fetal Down's syndrome is reported. Within one minute of injection of a test dose of one mg of dinoprostone, the patient collapsed. Intravenous injections of 100 mg hydrocortisone and 10 mg chlorpheniramine maleate were administered and the patient was given oxygen by a face mask. Within 10 minutes blood pressure had returned to 110/68 mm Hg, and after a further 15 minutes pulse rate was normal.
TREATMENT OF GUINEA PIGS WITH UREA INCR THE EFFECT OF THEIR SUBSEQUENT SENSITIZATION WITH EPOXY RESIN (EGK-19) OR K2CR207. UREA TREATMENT INCR PERCENTAGE OF ANIMALS SENSITIZED BY EPOXY RESINS FROM 50-87%. UREA ALONE DID NOT SENSITIZE SKIN.
The hemolytic action on human red blood cells (RBC) and the aggregations of human and rat red blood cells in the presence of sodium alginate were studied. Sodium alginate had no hemolytic action on human red blood cells. Human and rat red blood cells showed a marked aggregation by sodium alginate in a neutral medium. Sodium alginates having larger molecular weights showed more pronounced activities for aggregation of red blood cells as compared with those having smaller molecular weights, and the aggregation of red blood cells increased with an increase in the concentration of sodium alginate. The aggregation was inhibited by urea, suggesting the aggregation of red blood cells is caused by hydrogen bonding. When sodium alginate was added to human or rat blood rouleaux formation of red blood cells covered with fibrin net was observed in the coagulation cruor (blood clot).
Osmotic diuretics (mannitol, urea) decrease the effect on serum lithium level; significant increase in lithium excretion. /Lithium-drug interactions; from table/

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Non-Human Toxicity Values
LD100 Sheep 500 mg/l; mean survival time: 165 minutes
LD50 Sheep acute oral 28.5 g/100 kg
LD50 Rat oral 8471 mg/kg
LD50 Rat subcutaneous 8200 mg/kg
For more Non-Human Toxicity Values (Complete) data for UREA (7 total), please visit the HSDB record page.

[1]. The molecular basis for the chemical denaturation of proteins by urea. Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5142-7.

[2]. Urea: a comprehensive review of the clinical literature. Dermatol Online J. 2013 Nov 15;19(11):20392.

[3]. Urea. Subcell Biochem. 2014;73:7-29.

Urea appears as solid odorless white crystals or pellets. Density 1.335 g /cc. Noncombustible.
Urea is a carbonyl group with two C-bound amine groups. The commercially available fertilizer has an analysis of 46-0-0 (N-P2O5-K2O). It has a role as a flour treatment agent, a human metabolite, a Daphnia magna metabolite, a Saccharomyces cerevisiae metabolite, an Escherichia coli metabolite, a mouse metabolite and a fertilizer. It is a monocarboxylic acid amide and a one-carbon compound. It is functionally related to a carbonic acid. It is a tautomer of a carbamimidic acid.
A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.
Urea is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Urea has been reported in Ascochyta medicaginicola, Vicia faba, and other organisms with data available.
Urea is a nitrogenous compound containing a carbonyl group attached to two amine groups with osmotic diuretic activity. In vivo, urea is formed in the liver via the urea cycle from ammonia and is the final end product of protein metabolism. Administration of urea elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain, cerebrospinal fluid and eye, into interstitial fluid and plasma, thereby decreasing pressure in those tissues and increasing urine outflow.
Urea is a mineral with formula of CO(N3-H2)2 or CO(NH2)2. The corresponding IMA (International Mineralogical Association) number is IMA1972-031. The IMA symbol is Ur.
Urea is a metabolite found in or produced by Saccharomyces cerevisiae.
A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.
See also: Urea sulfate (active moiety of); Polynoxylin (monomer of); Hydrocortisone; urea (component of) ... View More ...

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Drug Indication
Urea is used topically for debridement and promotion of normal healing of hyperkeratotic surface lesions, particularly where healing is retarded by local infection, necrotic tissue, fibrinous or purulent debris or eschar. Urea is useful for the treatment of hyperkeratotic conditions such as dry, rough skin, dermatitis, psoriasis, xerosis, ichthyosis, eczema, keratosis, keratoderma, corns and calluses, as well as damaged, devitalized and ingrown nails.

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Mechanism of Action
... The primary mechanism of ammonia toxicosis appears to be inhibition of the citric acid cycle. There is an increase in anaerobic glycolysis, blood glucose, and blood lactate ... . Acidosis is manifested. The exact means by which ammonia blocks the citric acid cycle is not known. It is postulated that ammonia saturation of the glutamine-synthesizing system causes a backing-up in the citrate cycle, a decrease in its intermediates, and a decrease in energy production and cellular respiration, which leads to convulsions ... . The decrease of citrate cycle intermediates is postulated to result from reamination of pyruvic, ketoglutaric, and oxaloacetic acids.

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Therapeutic Uses
Dermatologic Agents; Diuretics, Osmotic
UREA IS /USED LESS COMMONLY THAN OTHER OSMOTIC AGENTS/ FOR THE SHORT-TERM REDUCTION OF INTRAOCULAR PRESSURE & VITREOUS VOL ... IN ANGLE-CLOSURE GLAUCOMA .. PRIOR TO SURGERY ... IN CHRONIC GLAUCOMA ... PRE- AND POSTOPERATIVE TREATMENT.
DOSE--USUAL, IV INFUSION, 100 MG TO 1 G/KG DAILY, AS 30% SOLN IN DEXTROSE INJECTION @ RATE NOT EXCEEDING 4 ML/MIN.
USED TOPICALLY IN THE TREATMENT OF PSORIASIS, ICHTHYOSIS, ATOPIC DERMATITIS, AND OTHER DRY, SCALY CONDITIONS.
For more Therapeutic Uses (Complete) data for UREA (14 total), please visit the HSDB record page.

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Drug Warnings
UREA SHOULD NOT BE USED IN PATIENTS WITH SEVERELY IMPAIRED RENAL FUNCTION.
UREA IS OFTEN RECONSTITUTED WITH INVERT SUGAR SOLN. INVERT SUGAR CONTAINS FRUCTOSE, WHICH CAN CAUSE SEVERE REACTION (HYPOGLYCEMIA, NAUSEA, VOMITING, TREMORS, COMA, & CONVULSIONS) IN PATIENTS WITH HEREDITARY FRUCTOSE INTOLERANCE (ALDOLASE DEFICIENCY).
In general osmotic diuretics are contraindicated in patients who are anuric due to severe renal disease or who are unresponsive to test doses of the drugs. Urea may cause thrombosis or pain if extravasation occurs, and it should not be admin to patients with impaired liver function because of the risk of elevation of blood ammonia levels. Both mannitol and urea are contraindicated in patients with active cranial bleeding.

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Pharmacodynamics
Urea is a keratolytic emollient that works to treat or prevent dry, rough, scaly, itchy skin.

CH4N2O

60.05

60.032

57-13-6

Urea-15N2;2067-80-3;Urea-d4;1433-11-0;Urea-13C,15N2;58069-83-3

1176

White to off-white solid powder

1.335

332.48°C

131-135 ºC

53.7±22.6 °C

<0.1 hPa (20 °C)

n20/D 1.40

-1.43

2

1

0

4

29

0

XSQUKJJJFZCRTK-UHFFFAOYSA-N

InChI=1S/CH4N2O/c2-1(3)4/h(H4,2,3,4)

urea

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~1665.00 mM)
H2O : ~100 mg/mL (~1665.00 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (41.63 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (41.63 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (41.63 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 100 mg/mL (1665.00 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)