Henry's Law constant = 6.00X10-8 atm-cu m/mol at 25 °C
大气OH速率常数:
7.70e-12 cm3/molecule*sec
自燃温度:
748 °F (398 °C)
分解:
When heated to decomposition it emits acrid smoke and irritating fumes.
粘度:
/p>PEG 400: 105 to 130 mPa.s at 20 °C; PEG 3000: 75 to 100 mPa.s at 20 °C; PEG 3350: 83 to 120 mPa.s at 20 °C; PEG 4000: 110 to 170 mPa.s at 20 °C; PEG 6000: 200 to 270 mPa.s at 20 °C; PEG 8000: 260 to 510 mPa.s at 20 °C; For polyethylene glycols having a average molecular weight greater than 400, the viscosity is determined on a 50 per cent m/m solution of the candidate substance in water
燃烧热:
1189.2 kJ/mol
汽化热:
50.5 kJ/mol
表面张力:
47.99 mN/m at 25 °C; 45.76 mN/m at 50 °C; 43.54 mN/m at 75 °C; 41.31 mN/m at 100 °C
Multiple metabolites contribute to the toxic effects. Glycolaldehyde and glyoxylate are more toxic than glycolate, although the latter is the only metabolite that accumulates in appreciable amounts, owing to the rate-limiting effect of lactate dehydrogenase or glycolate oxidase. Glyoxylate can be converted to numerous metabolites, the most toxic of which is oxalic acid (oxalate). Oxalate complexes with calcium to form calcium oxalate crystals, which are deposited in various tissues.
Although oxalate normally is a minor metabolic product of ethylene glycol metabolism, urinary oxalate crystals are a common, but not invariable, feature of ethylene glycol intoxication. There are two forms of urinary calcium oxalate crystals: the octahedral or tent-shaped form of the dihydrate crystals, and the prism or dumbell-shaped monohydrate. The latter form is stable under normal physiologic conditions; the dihydrate form appears only during high urinary calcium and oxalate concentrations, as seen in ethylene glycol poisoning. The dihydrate form can transform into the monohydrate form.
In oxidative metabolism of ethylene glycol in mammals, species variations occur which explain... differences in toxicity. Glycol is oxidized by major pathway into carbon dioxide, and by minor pathway to ... oxalic acid. Extent of formation of oxalic acid is dependent on dose level, but has ... been shown to vary with species ...
Rabbits and rats were given doses of 0.1-2.0 g/kg /of (14)C-ethylene glycol/. Rabbits received the doses orally or by subcutaneous injection, rats were given subcutaneous injections. In rabbits and rats, approximately 20% to 30% of the (14)C label from ethylene glycol (14)C was eliminated in the urine. Metabolites found in the 24-hr urine incl unchanged ethylene glycol (6.0 to 15.1%) and a trace of oxalic acid (0.1%
The main steps in degradation of ethylene glycol are as follows: ethylene glycol--> glycoaldehyde--> glycolic and glyoxylic acid. Glyoxylic acid is then metabolized into a number of chemicals that have been identified in expired air, urine, or blood. The metabolism of ethylene glycol to glycoaldehyde is mediated by alcohol dehydrogenase. Glycoaldehyde is metabolized to glycolic acid by aldehyde oxidase or to a lesser extent to glyoxal. Glyoxal is changed both to glycolic acid in the presence of lactic dehydrogenase, aldehyde oxidase, or possibly both enzymes, and to glyoxylic acid via some oxidative mechanism. The main path of the degradation of glycolic acid is to glyoxylic acid. This reaction is mediated by lactic dehydrogenase or glycolic acid oxidase. Once glyoxylic acid is formed, it is apparently degraded very rapidly to a variety of products, a few of which have been observed. Its breakdown to 2-hydroxy-3-oxoadipate it is thought, is mediated by thiamine pyrophosphate in the presence of magnesium ions. The formation of glycine involves pyridoxal phosphate and glyoxylate transaminase, whereas the formation of carbon dioxide and water via formic acid apparently involves coenzyme A (CoA) and flavin mononucleotides. Oxalic acid formation from glyoxylic acid, has been considered to be the results from the action of lactic dehydrogenase or glycolic acid oxidase. (T29)
IDENTIFICATION: Ethylene glycol is a colorless, odorless, sweet tasting, relatively non-volatile liquid and is completely soluble in water. This chemical has numerous uses, in manufacturing of polyethylene terephthalate, in natural gas processing, and as an antifreeze agent. HUMAN EXPOSURE: In humans ethylene glycol has induced only minimal dermal irritation, Nasal and or throat irritation were reported in a small number of subjects inhaling ethylene glycol, while higher concentrations caused eye irritation. Available data from acute poisoning cases indicate that the kidney is the critical organ for the toxicity of ethylene glycol. Available data are inadequate to assess the potential adverse neurological or immunological effects associated with long term exposure to ethylene glycol, although neurobehavioral and neurological disorders have been reported in cases of acute ethylene glycol poisonings in humans. In the limited number of investigations examined, neurological effects have not been observed at doses below those that have induced renal toxicity. ANIMAL STUDIES: Ethylene glycol has low acute toxicity in experimental animals following oral, inhalation and dermal exposure. Ethylene glycol exhibited no evidence of carcinogenicity based on a two year bioassay with rats and mice. Ethylene glycol induces developmental effects in rats and mice by all routes of exposure, although at doses greater than those associated with renal effects in male rats. Ethylene glycol is teratogenic, inducing primarily skeletal and external malformations, sometimes at doses less than those that are maternally toxic, with mice being more sensitive than rats. Reproductive studies with ethylene glycol show that in repeated dose toxicity studies, no evidence of an adverse impact on reproductive organs was observed. In special studies, including a three generation study in rats and continuous breeding protocols in mice, evidence of reproductive effects have been restricted to mice (but not rabbits or rats) exposed to doses considerably higher than those associated with developmental effects in this species or renal effects in rats. Consistent treatment related effects on the immune system related parameters have not be observed in repeated dose toxicity studies, in which several species have been exposed to ethylene glycol either orally or by inhalation.
Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids. Ethylene glycol produces central nervous system depression. The glycol probably causes the initial CNS depression; oxalate and the other intermediates seem to be responsible for nephrotoxicity. Glycoaldehyde and glyoxylate may be the principal metabolites responsible for EG nephrotoxicity and do so by causing ATP depletion and phospholipid and enzyme destruction. Glycine and acidosis, by-products of EG metabolism, can attenuate glyoxylate-mediated injury. This suggests that naturally occurring but incomplete protective pathways may be operative during the evolution of EG cytotoxicity. (A612, A613, A310)
During 4 hr following iv dose of (14)C-ethylene glycol, urinary excretion of (14)C was more rapid from rats (38%) than from rhesus monkeys (10%), but excretion in expired air was similar (about 5%). Some (14)C entered body carbon pool. Oral dose was also more rapidly excreted by rats.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
肾清除乙二醇的研究表明,肾小球滤过和被动重吸收是乙二醇在肾脏排泄中的主要机制。
Study of renal clearance of ethylene glycol suggests that glomerular filtration and passive reabsorption are main mechanisms involved in renal excretion of ethylene glycol.
The proportion of administered (14)C (as ethylene glycol) excreted in urine of rats varied with dosage, being 21% at dose of 0.1 g/kg and 78% at dose of 7.5 g/kg. Distribution of radioactivity 24 hr after administration ...to rats was highest in bones (2-10%); highest in muscle of rabbits (3.4%), although liver contained 1.4 and bone 1.7% of dose.
A dose-dependent change was observed in disposition of (14)C-labeled ethylene glycol after iv administration of 20, 200, 1000, and 2000 mg/kg to Fischer 344 rats. Part of the dose was expired as carbon dioxide and decreased from 39% at 20 and 200 mg/kg to 26% at 1000 and 2000 mg/kg, while urinary excretion of radiocarbon increased from 35 to 56%. As dose increased from 20 to 2,000 mg/kg increases in urinary (14)C was almost entirely attributable to (14)C-glycolate, which comprised 20% of dose in 24 hrs at two higher dose levels and only 2% at lower doses. Blood clearance of (14)C occurred in initial rapid phase (half-life, 3-5 hr), when plasma comprised predominantly of ethylene glycol, that persisted for 12 hrs at 20 mg/kg and 30 hr at 2000 mg/kg administered iv to Fischer 344 rats.
1.周国泰,化学危险品安全技术全书,化学工业出版社,1997 2.国家环保局有毒化学品管理办公室、北京化工研究院合编,化学品毒性法规环境数据手册,中国环境科学出版社.1992 3.Canadian Centre for Occupational Health and Safety,CHEMINFO Database.1998 4.Canadian Centre for Occupational Health and Safety, RTECS Database, 1989
[EN] PROCESS FOR REMOVING FORMALDEHYDE FROM A COMPOSITION COMPRISING GLYCOLALDHEDYDE [FR] PROCÉDÉ POUR ÉLIMINER LE FORMALDÉHYDE D'UNE COMPOSITION COMPRENANT DU GLYCOLALDÉHYDE
[EN] ACC INHIBITORS AND USES THEREOF<br/>[FR] INHIBITEURS DE L'ACC ET UTILISATIONS ASSOCIÉES
申请人:GILEAD APOLLO LLC
公开号:WO2017075056A1
公开(公告)日:2017-05-04
The present invention provides compounds I and II useful as inhibitors of Acetyl CoA Carboxylase (ACC), compositions thereof, and methods of using the same.
Solid-phase synthesis of C-terminal peptide aldehydes from amino acetals anchored to a backbone amide linker (BAL) handle
作者:Fanny Guillaumie、Joseph C Kappel、Nicholas M Kelly、George Barany、Knud J Jensen
DOI:10.1016/s0040-4039(00)00950-3
日期:2000.8
Peptide aldehydes were synthesized, starting from amino acetals, by a solid-phasebackboneamidelinker (BAL) strategy.
通过固相主链酰胺接头(BAL)策略从氨基缩醛开始合成肽醛。
Compositions for Treatment of Cystic Fibrosis and Other Chronic Diseases
申请人:Vertex Pharmaceuticals Incorporated
公开号:US20150231142A1
公开(公告)日:2015-08-20
The present invention relates to pharmaceutical compositions comprising an inhibitor of epithelial sodium channel activity in combination with at least one ABC Transporter modulator compound of Formula A, Formula B, Formula C, or Formula D. The invention also relates to pharmaceutical formulations thereof, and to methods of using such compositions in the treatment of CFTR mediated diseases, particularly cystic fibrosis using the pharmaceutical combination compositions.
[EN] THIOPHENE DERIVATIVES FOR THE TREATMENT OF DISORDERS CAUSED BY IGE<br/>[FR] DÉRIVÉS DE THIOPHÈNE POUR LE TRAITEMENT DE TROUBLES PROVOQUÉS PAR IGE
申请人:UCB BIOPHARMA SRL
公开号:WO2019243550A1
公开(公告)日:2019-12-26
Thiophene derivatives of formula (I) and a pharmaceutically acceptable salt thereof are provided. These compounds have utility for the treatment or prevention of disorders caused by IgE, such as allergy, type 1 hypersensitivity or familiar sinus inflammation.
[EN] CATHEPSIN CYSTEINE PROTEASE INHIBITORS<br/>[FR] INHIBITEURS DE PROTÉASES À CYSTÉINE DE TYPE CATHEPSINES
申请人:MERCK SHARP & DOHME
公开号:WO2015054038A1
公开(公告)日:2015-04-16
This invention relates to a novel class of compounds which are cysteine protease inhibitors, including but not limited to, inhibitors of cathepsins K, L, S and B. These compounds are useful for treating diseases in which inhibition of bone resorption is indicated, such as osteoporosis.