Urethane (Carbamic acid ethyl ester)
(Synonyms: 氨基甲酸乙酯; Ethyl carbamate; Carbamic acid ethyl ester; Ethylurethane) 目录号 : GC33902
Urethane (Carbamic acid ethyl ester, Ethyl carbamate, Ethylurethane) is a kind of antineoplastic agent that is also used as a veterinary anesthetic. It is a intermediate in organic synthesis.
Cas No.:51-79-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Urethane (Carbamic acid ethyl ester, Ethyl carbamate, Ethylurethane) is a kind of antineoplastic agent that is also used as a veterinary anesthetic. It is a intermediate in organic synthesis.
urethane has a spectrum of action on ion channels, which is distinct from other anesthetics. It significantly potentiates the current responses of both GABAA and glycine receptors in a reversible and concentration-dependent manner. Conversely, urethane (10–300 mM) inhibits the responses of NMDA and AMPA receptors. Also, urethane potentiates the function of an nACh receptor and neuronal nicotinic acetylcholine, γ-aminobutyric acid A, and glycine receptors[3].
Urethane, a carcinogenic substance, is favored for acute in vivo electrophysiological experiments because it induces long-lasting steady level of anesthesia with muscle relaxation and minimally affects the autonomic and cardiovascular systems[2]. Urethane affects both inhibitory and excitatory systems but the magnitude of the alterations is less than that produced by other more selective anesthetics[3]. But also, Urethane anesthesia is usually restricted to terminal (acute) experiments due to its potential long-term toxicity[1].
[1] Barth AM, et al. J Neurosci. 31(3):851-860. [2] Maggi CA, et al. Experientia. 1986, 42(2):109-114. [3] Hara K, et al. Anesth Analg. 2002, 94(2):313–318.
| Cas No. | 51-79-6 | SDF | |
| 别名 | 氨基甲酸乙酯; Ethyl carbamate; Carbamic acid ethyl ester; Ethylurethane | ||
| Canonical SMILES | NC(OCC)=O | ||
| 分子式 | C3H7NO2 | 分子量 | 89.09 |
| 溶解度 | DMSO : ≥ 125 mg/mL (1403.08 mM); H2O: ≥20mg/mL | 储存条件 | Store at RT |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 11.2246 mL | 56.123 mL | 112.246 mL |
| 5 mM | 2.2449 mL | 11.2246 mL | 22.4492 mL |
| 10 mM | 1.1225 mL | 5.6123 mL | 11.2246 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Hazards of Urethane (ethyl carbamate): a review of the literature
Lab Anim 1988 Jul;22(3):255-62.PMID:3050270DOI:10.1258/002367788780746331.
Urethane (ethyl carbamate) is used alone or in combination with other drugs to produce anaesthesia in laboratory animals. Although originally studied as a potential phytocide, Urethane demonstrated antineoplastic properties when administered to rats with the Walker rat carcinoma 256. Subsequent trials in humans led to its use as a chemotherapeutic agent for various leukaemias. Mice develop pulmonary adenomas earlier in life and at a higher incidence following Urethane administration. Urethane's carcinogenic influence is greater in neonatal mice; it also has a transplacental influence in mice. In rats, Urethane increases the incidence of pulmonary adenomas, Zymbal Gland tumours, and a variety of other neoplasms. Urethane is absorbed sufficiently from the skin of laboratory animals to produce a transient narcosis. The carcinogenic effect appears to be due to an undefined oncogenic intermediate formed in the blood. Considering the properties Urethane demonstrates in animals, the safety of its use by laboratory personnel is in question. However, if appropriate guidelines are followed, Urethane should continue to be a useful anaesthetic agent for laboratory animals.
Mutagenicity, metabolism, and DNA interactions of Urethane
Toxicol Ind Health 1990 Jan;6(1):71-108.PMID:2190358DOI:10.1177/074823379000600106.
Urethane, a known animal carcinogen, has been the subject of intensive research efforts spanning 40 years. Recent concerns have focused on the presence of Urethane in a variety of fermented foods and alcoholic beverages, although no epidemiological studies or human case reports have been published. Much information is available about the mutagenesis, metabolism, and DNA interactions of Urethane in experimental systems. Urethane is generally not mutagenic in bacteria although in some instances it acts as a weak mutagen. Urethane is not mutagenic in Nuerospora but is weakly mutagenic in Saccharomyces. Drosophila appear to be the only organisms that consistently give positive mutagenic results with Urethane, but its mutagenicity is weak and in many cases shows no clear dose dependence. Urethane is a good clastogen in mammalian somatic cells in vivo, but it shows variable results with cells in vitro. It efficiently induces sister chromatid exchanges in a variety of cells. Mammalian spermatogenic cells are insensitive to the induction of specific locus and dominant lethal mutations by Urethane. Mutational synergism has been reported to occur between ethyl methanesulfonate and Urethane when administered two generations apart, and some investigators have suggested possible synergism for cancer-causing mutations in mice exposed to X-rays and Urethane one generation apart. These studies are controversial and have not been confirmed. Studies on the induction of cancer-causing dominant mutations by Urethane are at variance with results from extensive studies with the specific locus test in mice. Urethane studies with the unscheduled DNA synthesis assay in mouse spermatogenic cells and with the sperm abnormality test have given negative results. Urethane is rapidly and evenly distributed in the body. The rate of elimination of Urethane from plasma is a saturable process and varies according to the strain and age of the animal. Recent studies have concentrations similar to those in wine, ethanol inhibits the tissue distribution of Urethane in mice. These results are important because they suggest a lower carcinogenic/mutagenic risk than expected from exposure to Urethane in alcoholic beverages. Although research on the metabolic activation of Urethane has been extensive, no conclusive results have been obtained about its active metabolite, at one time thought to be N-hydroxyurethane. More recently, it has been postulated that Urethane is activated to vinyl carbamate and that this metabolite is capable of reacting with DNA.(ABSTRACT TRUNCATED AT 400 WORDS)
Inhibition of the metabolism of Urethane by ethanol
Drug Metab Dispos 1988 May-Jun;16(3):355-8.PMID:2900725doi
Ethanol has been shown to inhibit the localization of [ethyl-1-14C] Urethane in the male mouse, but the effect of ethanol on the metabolism of Urethane has not been clarified. Consequently, the concentration of unchanged Urethane was determined in the blood of male mice up to 11 hr after oral administration of Urethane with or without ethanol. A high and constant blood level of Urethane persisted for 8 hr after the administration of an ethanolic solution of [ethyl-1-14C] Urethane (125 mumol/kg, 10 muCi/20 g of mouse, 5 g of ethanol per kg, po); the blood level of ethanol was at or above 150 mg/dl during these 8 hr. In contrast, rapid clearance of radioactivity was observed in mice treated with [ethyl-1-14C]Urethane dissolved in water. Coadministration of ethanol with Urethane decreased the rate of 14CO2 expiration; furthermore, covalent binding with liver protein was delayed about 8 hr and was less than that in the group treated with Urethane in water. The metabolism of Urethane and production of 14CO2 from [carbonyl-14C]Urethane by mouse liver homogenate in vitro were inhibited by the presence of ethanol (greater than 10 mM); these concentrations of ethanol in vitro are about the same as those that are inhibitory in vivo, but the extent of inhibition suggests that the liver is not the only site of metabolism of Urethane. These results indicate that ethanol can inhibit the initial metabolism of Urethane, prevent the formation of active metabolites, and allow Urethane to persist in blood.
Carcinogenesis of Urethane: simulation versus experiment
Chem Res Toxicol 2015 Apr 20;28(4):691-701.PMID:25642734DOI:10.1021/tx500459t.
The carcinogenesis of Urethane (ethyl carbamate), a byproduct of fermentation that is consistently found in various food products, was investigated with a combination of kinetic experiments and quantum chemical calculations. The main objective of the study was to find ΔG(⧧), the activation free energy for the rate-limiting step of the SN2 reaction among the ultimate carcinogen of Urethane, vinyl carbamate epoxide (VCE), and different nucleobases of the DNA. In the experimental part, the second-order reaction rate constants for the formation of the main 7-(2-oxoethyl)guanine adduct in aqueous solutions of deoxyguanosine and in DNA were determined. A series of ab initio, density functional theory (DFT), and semiempirical molecular orbital (MO) calculations was then performed to determine the activation barriers for the reaction between VCE and nucleobases methylguanine, methyladenine, and methylcytosine. Effects of hydration were incorporated with the use of the solvent reaction field method of Tomasi and co-workers and the Langevine dipoles model of Florian and Warshel. The computational results for the main adduct were found to be in good agreement with the experiment, thus presenting strong evidence for the validity of the proposed SN2 mechanism. This allowed us to predict the activation barriers of reactions leading to side products for which kinetic experiments have not yet been performed. Our calculations have shown that the main 7-(2-oxoethyl)deoxyguanosine adduct indeed forms preferentially because the emergence of other adducts either proceeds across a significantly higher activation barrier or the geometry of the reaction requires the Watson-Crick pairs of the DNA to be broken. The computational study also considered the questions of stereoselectivity, the ease of the elimination of the leaving group, and the relative contributions of the two possible reaction paths for the formation of the 1,N(2)-ethenodeoxyguanosine adduct.
The kinetics of Urethane elimination in the mouse
Toxicol Appl Pharmacol 1983 May;68(3):354-8.PMID:6857669DOI:10.1016/0041-008x(83)90278-8.
Data from several investigators suggest that the prevalence of urethane-induced lung adenomas in the mouse is more nearly linearly related to the square of the Urethane dose than to the dose itself. However, the relationship between Urethane dose and integrated internal exposure to Urethane has not been established. Outbred male Swiss mice between 41 and 45 days old were injected ip with one of seven doses of Urethane ranging from 0.4 to 1.8 mg/g. The rate of elimination of Urethane from the blood was followed by assaying the ethanol liberated from Urethane by alkaline hydrolysis. The results indicated that Urethane elimination is saturable, and saturated at all doses used, with a Vmax of 0.087 mg/ml/hr. Thus, internal exposure to Urethane, measured as the area under the blood concentration, time curve, is not linearly related to Urethane dose. In the range of doses used in this study, the area under the curve is C0(2)/2Vmax or (D/VD)2 (1/2Vmax), where C0 is the initial concentration; D, the dose; and VD, the volume of distribution. This relationship can be used to predict internal exposure to Urethane as a function of dose.