Chloroacetic acid, solid is a colorless to light-brown crystalline material. It is soluble in water and sinks in water. Combustible. It is transported as a molten liquid and therefore can cause thermal burns. It is toxic by ingestion, skin absorption and inhalation of dust. It is corrosive to metals and tissue.
The metabolism of 14(C)-dichloroethyne was studied in rats by inhalation in a dynamic nose-only exposure system. ... Metabolites of dichloroethyne identified are: N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine, dichloroethanol, dichloroacetic acid, oxalic acid and chloroacetic acid in urine; N-acetyl-S-(1,2-dichlorovinyl-L-cysteine in feces...
The metabolism of MCA has been characterised in the mouse following MCA administration by intraperitoneal injection. Metabolites of MCA identified in the urine included S-carboxymethylcysteine (33%-43% free and 1%-6% conjugated), thiodiacetic acid (thiodiglycolic acid was found to be the major urinary metabolite of S-carboxymethylcysteine, and most of the glycolate was oxidized to carbon dioxide. The metabolism proceeds probably by enzymatic hydrolysis of the carbon-chlorine bond with the formation of glycolic acid . MCA also conjugates with GSH to form the S-carboxymethyl derivative of GSH, which is then converted to S-carboxymethyl cysteine. In Wistar rats given 50 mg/kg MCA by gavage, thiodiglycolic acid was identified as the major urinary metabolite, accounting for 60% of the administered dose. A greater percentage of administered MCA was excreted as thiodiglycolic acid in rats than in mice; in both species most of the remainder of the dose was excreted as S-carboxymethylcysteine. ... Preliminary pharmacokinetic studies with MCA in rats /showed/ that MCA was rapidly metabolized, and detoxication by conjugation with glutathione appeared to be a major metabolic pathway.
... A 17-year-old male ... ingested approximately 70 mL trichloroethene (TRI) in a suicide attempt. ... During /5 days/ ... blood and urine were collected and TRI and its metabolites were quantified. ... Trichloroethanol and trichloroacetic acid, metabolites of the cytochrome P450-mediated pathway, and N-acetyl-S-(1, 2-dichlorovinyl)-l-cysteine and N-acetyl-S-(2, 2-dichlorovinyl)-l-cysteine from the glutathione-dependent pathway of TRI were quantified in urine samples. Besides these known metabolites in humans, chloroacetic acid and dichloroacetic acid were identified ... in urine of a human exposed to TRI ...
In one human case the majority of MCA was excreted as nonmetabolized MCA. A minor part reacted with glutathione and was excreted in urine as the conjugate. A small amount was metabolized and excreted as carbon dioxide in exhaled air ... .
IDENTIFICATION AND USE: Chloroacetic acid (MCA) is a solid. Most of the chloroacetic acid produced is used to manufacture several hundred thousand tons annually of carboxymethyl cellulose. Another major application is the production of herbicides based on arylhydroxyacetic acids. HUMAN STUDIES: The anticipated acute and chronic human health hazards posed by MCA are effects on the cardiac system, the central nervous system, and kidneys. In addition, MCA is highly corrosive and irritating to the eyes, skin and respiratory tract. Acute dermal exposure of workers to MCA may result in death even after rapid and extensive washing of the skin area. The effects may be delayed. The biochemical mechanism of action resulting in death is not understood. Contributing factors apparently believed to be involved are: (i) the inhibition of the tricarboxylic acid cycle decreasing cellular energy supply and increasing acidosis with glycolic acid and oxalate production, and; (ii) effects on cellular components where sulfhydryl groups are critical for normal biological activity. Both of these effects may contribute to CNS, cardiovascular, renal and hepatic effects. In addition, the metabolites glycolic acid and oxalate may contribute to CNS and renal toxicity. A case of joint deformity reported after the use of a preparation containing MCA for topical wart treatment. MCA did not induce DNA strand breaks in human CCRF-CEM cells. ANIMAL STUDIES: Fatalities among rabbits are expected when only 3% of the skin is exposed. Thorough washing after 1 minute contact did not decrease mortalities. In rats after subcutaneous administration of MCA (108, 135 or 163 mg/kg) hypoglycemia and lung injury appear to cause death in response to MCA exposure. MCA caused front paw rigidity in 10% of mice surviving a single oral toxic dose (320-380 mg/kg). Male mice orally administered 300 mg/kg bw MCA showed tremors, respiratory depression, and occasionally tonic and clonic convulsions. Some survivors had a Straub tail, severe tremors, and front limb paralysis after 24 hours (after exposure). Pregnant rats were dosed MCA by oral intubation on gestation days 6 to 15 with 0, 17, 35, 70, or 140 mg/kg bw/day. The percentage of soft tissue malformations was increased, however not dose-related. No skeletal malformations were found. In the highest dose-group a statistically significant increase of malformations of the cardiovascular system, comprising predominantly levocardia, was found. MCA was not mutagenic in Salmonella typhimurium strains (TA98, TA100, TA102, TA104, TA1535, TA1537, and TA1538) and Escherichia coli strains (WP2uvrA and WP2uvrA/pKM101) with or without metabolic activation. ECOTOXICITY STUDIES: A large number of passerine birds, mainly greenfinches, were found dead or dying in a hedgerow close to a field of onions recently sprayed with sodium salt of MCA. Chemical analysis confirmed the exposure of the birds to the chemical. MCA had high regeneration toxicity with teratogenicity in Hydra digestive region.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A4：不能分类为人类致癌物。
A4: Not classifiable as a human carcinogen.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
暴露途径
这种物质可以通过吸入、皮肤接触和摄入被身体吸收。
The substance can be absorbed into the body by inhalation, through the skin and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
毒理性
吸入症状
喉咙痛。咳嗽。呼吸急促。胸骨后烧灼感。呼吸困难。症状可能有所延迟。更多信息请参阅“摄入”。
Sore throat. Cough. Shortness of breath. Burning sensation behind the breastbone. Laboured breathing. Symptoms may be delayed. Further see Ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
毒理性
皮肤症状
可能被吸收！发红。疼痛。皮肤烧伤。更多信息请见吞咽。
MAY BE ABSORBED! Redness. Pain. Skin burns. Further see Ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
Distribution, metabolism, and excretion of monochloroacetic acid (MCA) were examined in adult male rats at a subtoxic (10 mg/kg) and a toxic (75 mg/kg) dose. Rats were injected i.v. with 14(C)MCA and housed individually. Urine and feces were collected. ... Radioactivity in aliquots showed very rapid distribution of MCA to tissues. Concentrations of MCA in plasma, liver, heart, lungs, and brown fat paralleled each other, whereas those in brain and thymus did not. There was no dose proportionality in tissue concentrations. Elimination of MCA from plasma required modeling by two compartments. Most of the radioactivity found in plasma was parent MCA. Elimination rate constant (K(10)) and distribution rate constant (K(12)) were greatly reduced at the toxic dose. Elimination of the toxic dose was further retarded due to increased retention of MCA in the peripheral compartment as indicated by increased mean residence times in most tissues. A very large fraction of dose was found in the gastrointestinal tract, almost all of which was reabsorbed. Attempts to reduce toxicity by blocking the enterohepatic circulation with activated charcoal or cholestyramine failed. Radioactivity found in bile was associated with one metabolite more polar than the parent compound. A very large fraction of dose (73 and 59%) was found in urine, 55 to 68% of which was parent MCA. The rate-determining step in the toxicity of MCA was identified as its detoxification by the liver...
Rats were administered a single oral (10 (subtoxic) or 225 (toxic, LD20) mg/kg) or dermal (125 mg/kg, LD20) dose of (14)C-monochloroacetic acid (MCA) and the time-course (0.25, 0.75, 2, 4, 8, 16, and 32 hr postadministration) of radioactivity was determined in plasma, tissues, and excreta. At the subtoxic oral dose, concentration of (14)C-MCA peaked at 0.1% of dose by 2 hr. Most tissue profiles of MCA paralleled that of plasma with few exceptions. At the toxic oral dose, tissue concentrations remained initially below those seen after the subtoxic dose, because stomach retained most of the toxic dose for up to 8 hr. Peak plasma concentration was reached within 0.25 hr without an apparent subsequent uptake phase. Most of the dermal dose rapidly penetrated into the skin (>95% within 0.25 hr) and remained sequestered there and released slowly. Concentration in plasma peaked at 0.36% of dose by 0.75 hr and remained constant for up to 4 hr. Peak tissue concentrations were reached between 2 and 4 hr. Within 0.75 hr, 9% of the dermally absorbed dose was metabolized by liver and eliminated through bile, all of which was subsequently reabsorbed. Two percent of MCA appeared in colon by 0.75 hr, apparently as a result of direct transport through GI-wall in retrograde movement. About 70-80% of radioactivity recovered from the small intestine of orally dosed rats was parent compound. Fecal elimination was negligible (</=1%). Urinary excretion was 64-72% of the dose. At the toxic oral dose, urinary excretion was initially slow and accelerated after 8 hr. The plasma half-life was 2 hr for oral and 4 hr for dermal administration. Differential oral low and high dose kinetics was due to delayed stomach emptying and not to saturation of metabolic pathways. Dose-responses were steep, with no overt toxicity (coma/death) up to 200 (oral) and 100 (dermal) mg/kg, whereas 100% mortality occurred at 450 (LD50 > 400 and < 450) and 175 (LD50 145) mg/kg after oral and dermal exposure, respectively.
Distribution of monochloroacetic acid (CA) was studied in rats given a single oral dose of 0.1 mmole/kg body weight [1-(14)C]CA, by gavage. The animals were sacrificed at 4, 8, 12, 24 and 48 hr following the treatment. The distribution of (14)C-label, determined in different tissues, suggests that CA is rapidly absorbed and eliminated from the body. The elimination phase appears to be fast for intestine and kidney as compared to other tissues. Maximum radioactivity was detected in intestine and kidney at 4 and 8 hr following the treatment which was followed by liver, spleen, testes, lung, brain and heart in a decreasing order. A group of rats treated with a single oral dose of 1 mmole/kg (1-(14)C)CA, by gavage, was also sacrificed at 24 hr following the exposure to study the effect of a higher dose on distribution of (1-(14)C)CA. The distribution of (14)C-label at both dose levels indicates that toxicokinetic properties of CA are dose-dependent. Another group of rats administered 1 mmole/kg (1-(14)C) CA daily for three days was also sacrificed at 24 hr following the last dose to evaluate the bioaccumulating properties of CA and/or its metabolites in the tissues. As compared to the number of doses given, the accumulation of (14)C-label was not as large as expected. (14)C-Label determined in the dialyzed plasma, suggests an in vivo binding of (14)C-label to plasma proteins where albumin accounted for about 65% as determined by affinity chromatography...
... To understand the mechanism of monochloroacetic acid (MCA) toxicity, ... the tissue distribution of (1-(14)C)MCA in rats /was studied/ by a whole-body autoradiographic technique. Male Sprague-Dawley rats were given a tracer dose of (1-14C)MCA (6.8 ug/100 g (40 uCi) body weight) by tail vein and euthanized at different time intervals (5 min, 1, 4, 12, 24 and 48 hr). ... At 5 min, there was a rapid accumulation of (14)C-activity in the kidney cortex and stomach walls. The radioactivity was rapidly removed from the circulation. There was high accumulation of (14)C-activity in the myocardial tissues. The liver was also loaded with MCA and/or its metabolites. After 1 hr following administration of (14)MCA, radioactivity was extensively excreted into the small intestinal lumen. The accumulation of (14)C-activity in the brain, thymus, salivary glands and tongue was prominent at 1 hr. After 4 hr the liver and other tissues started to eliminate most of the radioactivity. Contrary to other tissues, however, the central nervous system, thymus and pancreas started to accumulate the radioactivity at later time periods. These observations suggest the accumulation of MCA and/or its metabolites into hydrophilic tissues at earlier time periods and into lipophilic tissues at later times.
peptide synthesis (SPPS). The robustness of the allenone-mediated peptide bond formation was showcased incisively by the synthesis of carfilzomib, which involved a rare racemization-/epimerization-free N to C peptide elongation strategy. Furthermore, the successful synthesis of the model difficult peptide ACP (65–74) on a solid support suggested that this method was compatible with SPPS. This method combines
Allenone 首次被鉴定为一种高效的肽偶联剂。肽键以α-羰基乙烯基酯为关键中间体形成，其形成和随后的氨解以无外消旋/差向异构化的方式自发进行。丙二烯酮偶联试剂不仅对简单酰胺和二肽的合成有效，而且还适用于肽片段缩合和固相肽合成 (SPPS)。卡非佐米的合成充分展示了丙二烯酮介导的肽键形成的稳健性，该合成涉及一种罕见的无消旋化/差向异构化的 N 到 C 肽延伸策略。此外，在固体支持物上成功合成模型困难肽 ACP (65-74) 表明该方法与 SPPS 兼容。该方法结合了传统活性酯和偶联剂的优点，同时克服了两种策略的缺点。因此，这种丙二烯酮介导的肽键形成策略代表了肽合成的颠覆性创新。
안트라센 유도체 화합물 및 이를 포함하는 유기전계발광소자
申请人：SFC CO., LTD. 에스에프씨 주식회사(120060087061) Corp. No ▼ 135511-0105889BRN ▼134-81-54429
公开号：KR102121583B1
公开（公告）日：2020-06-10
본 발명은 신규한 유기전계발광 화합물에 관한 것으로서, 하기 [화학식 1] 내지 [화학식 2]로 표시되는 화합물인 것을 특징으로 하고, 본 발명에 따른 유기전계발광 화합물은 높은 유리전이온도를 가져서 열적 안정성이 우수함과 동시에 이를 유기전계발광소자에 채용시 저전압 구동, 고휘도, 고색순도 및 장수명을 나타내는 유기전계발광소자의 구현이 가능하다. [화학식 1] [화학식 2]
Computer-aided moleculardesign (CAMD) is a well-known tool for the theoretical assessment of chemical structures before their experimental synthesis. In this study, we used this method to consider the important criteria for a chemical structure as an energetic plasticizer for an energetic azido binder. The number of new azido-ester structures were initially designed, and their physicochemical and
[EN] PROCESSES FOR THE PREPARATION OF FUNGICIDAL COMPOUNDS<br/>[FR] PROCÉDÉS DE PRÉPARATION DE COMPOSÉS FONGICIDES
申请人：GILEAD APOLLO LLC
公开号：WO2018161008A1
公开（公告）日：2018-09-07
Provided herein are processes for the preparation of stereomerically enriched compounds of Formulas I-014, I-020, I-064, I-074, I-082, I-089, I-090, I-095, I-171, I-181, I-184, I-186, I-189, I-191, I-192, I-193, I-205, I-206, I-208, I-211, I-212, I-213, I-220, I-229, I-231, I-233, I-234, I-246, I-251, I-258, I-259, I-262, I-263, I-285, I-323 and I-400. The compounds described herein exhibit activity as pesticides and are useful, for example, in methods for the control of fungal pathogens and diseases caused by fungal pathogens in plants. A preferred process is directed to preparing a stereomerically enriched compound of Formula V-1 or V-2-F by assymetrical reduction in the presence of a chiral organometallic catalyst.
