过氧乙酸 | 79-21-0

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 中文名称: 过氧乙酸
• 中文别名: 过醋酸；过乙酸
• 英文名称: peracetic acid
• 英文别名: Peroxyacetic acid；PAA；ethaneperoxoic acid
• CAS: 79-21-0
• 化学式: C₂H₄O₃
• 分子量: 76.052
• InChiKey: KFSLWBXXFJQRDL-UHFFFAOYSA-N

物化性质

• 稳定性/保质期：
  1. 具有弱酸性，易挥发，具有强烈的刺激性气味和明显的乙酸味。它对纸、木塞、橡胶和皮肤等材料具有腐蚀作用。过氧乙酸是爆炸性物质，但在有机溶剂中浓度小于55%时，室温下操作相对安全。该试剂应在通风橱内使用，并准备一个安全护罩。 2. 稳定性：不稳定 3. 禁配物：强还原剂、强碱和金属盐类 4. 应避免接触的条件：受热、光照或震动 5. 聚合危害：不发生聚合 6. 分解产物：氧气

计算性质

• 辛醇/水分配系数(LogP)：
  -0.4
• 重原子数：
  5
• 可旋转键数：
  1
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  46.5
• 氢给体数：
  1
• 氢受体数：
  3

ADMET

代谢

在动力学研究中尚未识别出降解产物。然而，根据物质的分子结构，预计会产生以下降解产物：醋酸、氧气、过氧化氢和水。过氧化氢也被认为会迅速降解成氧气和水。

Degradation products have not been identified during kinetic studies. However, based on the structure of the substance the following degradation products are expected: acetic acid, oxygen, hydrogen peroxide and water. Hydrogen peroxide is also presumed to be rapidly degraded into oxygen and water.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 毒性总结

过醋酸（PAA）作为一种平衡的水溶液商业化，其中过醋酸与过氧化氢、醋酸和水处于平衡状态。在某些平衡溶液中，过醋酸、过氧化氢和醋酸的浓度分别可达到约40%、30%和40%。几乎所有关于过醋酸对人类健康和环境影响的研究都是使用平衡溶液进行的。PAA还作为一种主要含过醋酸和水的蒸馏产品商业化。在常温条件下，蒸馏PAA溶液不稳定，会重新达到与过氧化氢和醋酸的平衡。通过冷却到0°C以下，可以减缓水解反应。这些水溶液中过醋酸的量大约在0.15%到40%之间。 人体健康： 在37°C下进行的体外皮肤渗透试验中，使用了0.8%的PAA（非腐蚀性），表明猪完整皮肤对过醋酸的皮肤吸收很低。当大鼠的皮肤暴露于腐蚀性浓度的（14）C标记PAA时，发现（14）C的摄取量相当大，但不知道（14）C是以过醋酸、醋酸还是CO2的形式存在。预计腐蚀性浓度的PAA会破坏皮肤的正常屏障功能。 两项可靠的体外研究使用不同的分析方法表明，在大鼠血液中过醋酸迅速降解。当大鼠血液稀释1000倍时，过醋酸的半衰期小于5分钟。在未稀释血液中，预计半衰期将更短，只有几秒钟或更少。因此，过醋酸的分布可能非常有限，在接触过醋酸溶液后，不太可能系统性可用。在动力学研究中尚未识别出降解产物。然而，基于物质的 结构，预计的降解产物包括醋酸、氧气、过氧化氢和水。还假设过氧化氢会迅速降解为氧气和水。 急性毒性测试的结果以过醋酸这一成分为基础表达，这是根据用于急性测试的产品的组成计算得出的。使用气溶胶和蒸气的急性吸入研究显示，4小时-LC50在76至>241 mg/m³之间。在大鼠和家兔中对PAA溶液的急性皮肤毒性进行了测试。当大鼠暴露于0.15-15%的溶液中时，没有观察到皮肤毒性的迹象，而家兔的LD50值为56.1和228.8 mg PAA/kg bw，对应的PAA浓度分别为4.9%和11.7%。皮肤毒性与不同PAA溶液造成的皮肤损伤程度有关，因为PAA溶液的腐蚀性可能会破坏皮肤的完整性。在口服毒性研究中，LD50值在9.0至202.8 mg/kg bw之间，基于过醋酸这一成分。偶尔与稀释溶液接触食道可能导致组织腐蚀而死亡，这可以解释LD50值的变异性。 在所有研究中，病理和症状相似，表明与测试材料接触的组织出现刺激和腐蚀。当将10%及以上的PAA溶液应用于家兔皮肤时，应考虑其具有腐蚀性（在3分钟内）。在接触时间为45分钟或更长时间时，5%的PAA浓度对家兔皮肤通常是腐蚀性的。小于0.34%的PAA浓度仅是轻微刺激物或非刺激物，这取决于皮肤暴露的持续时间。当在兔眼测试中，0.34%及以上的PAA浓度是腐蚀性的。在0.15%或更低的PAA浓度下，眼睛轻微或没有刺激。偶然的人类皮肤和眼睛刺激发现支持动物研究。 过醋酸在小鼠的Alarie试验中呈阳性反应，RD50值（产生呼吸速率下降50%的浓度）为12和17 mg/m³（来自配方和仅过醋酸的蒸气混合物）。人类数据支持过醋酸的感官刺激性。 在三次Buhler试验中，不同配方的PAA未观察到皮肤致敏。在测试期间，过醋酸的暴露浓度在0.15%至1.2%之间。此外，长期的生产和使用经验表明，PAA没有致敏潜力。 为了研究重复剂量毒性，对大鼠进行了符合GLP指南的研究，通过灌胃连续13周暴露于5%的PAA，稀释到不同浓度（过醋酸成分的0.018%至0.55%）。在0.75 mg/kg/天时，观察到两只雌性出现短暂的或间歇性的大声呼吸，但该效应不被认为是不良反应。根据这一研究的结果，NOAEL为0.75 mg/kg bw/天（过醋酸成分）。观察到的唯一效果是与浓度相关的局部效果。因此，定义一个无观察到不良反应的浓度而不是经典的NOAEL是合理的。基于过醋酸成分，局部效果的NOAEC为0.055%。 在细菌基因突变试验中，无论是否进行代谢激活，结果均为阴性。在人类胎儿肺细胞进行的两项DNA修复试验未表明PAA具有遗传毒性。在体外染色体畸变试验中，仅在细胞毒性浓度下获得了阳性结果。

Peracetic acid (PAA) is commercialized as an equilibrium aqueous solution in which peracetic acid is in equilibrium with hydrogen peroxide, acetic acid and water. The concentration of peracetic acid, hydrogen peroxide and acetic acid can reach levels of about 40, 30 and 40 %, respectively, in certain equilibrium solutions. Nearly all toxicity studies, related with human health and environment, were done with equilibrium solutions. PAA is also commercialized as a distilled product containing primarily peracetic acid and water. Distilled PAA solutions are unstable under ambient conditions and re-equilibrate under formation of hydrogen peroxide and acetic acid. By cooling below 0 °C the hydrolysis reaction is slowed down. The amount of peracetic acid in these aqueous solutions ranges from about 0.15 to 40 %. ... Human Health: An in vitro dermal penetration assay at 37 °C using 0.8 % PAA (non corrosive) indicated a low dermal uptake of peracetic acid through the intact skin of pigs. When the skin of rats was exposed to a corrosive concentration of (14)C-labelled PAA a considerable uptake of (14)C was found but it is unknown if the (14)C was present as peracetic acid, acetic acid or CO2. It is expected that corrosive concentrations of PAA would compromise the normal barrier function of the skin. Two reliable in vitro studies, using different analytical methods, showed a rapid degradation of peracetic acid in rat blood. When rat blood was diluted 1000 times, the half-life of peracetic acid was < 5 minutes. In undiluted blood the half-life is expected to be several seconds or less. For this reason the distribution of peracetic acid is probably very limited and it is not expected to be systemically available after exposure to peracetic acid solutions. Degradation products have not been identified during the kinetic studies. However, based on the structure of the substance the following degradation products are expected: acetic acid, oxygen, hydrogen peroxide and water. Hydrogen peroxide is also presumed to be rapidly degraded into oxygen and water. The results of acute toxicity tests are expressed on the component peracetic acid, which was calculated based on the composition of the product used for the acute tests. The available acute inhalation studies with aerosols and vapour revealed an 4 hr-LC50 ranging from 76 to >241 mg/cu m. The acute dermal toxicity of PAA solutions was tested in rats and rabbits. No sign of dermal toxicity was observed when rats were exposed to solutions of 0.15-15%, while LD50 values of 56.1 and 228.8 mg PAA/kg bw were reported for rabbits for concentrations of 4.9 and 11.7 % PAA, respectively. The dermal toxicity depends on the degree of skin damage caused by the different PAA solutions, since the corrosive properties of PAA solutions may compromise the integrity of the skin. In oral toxicity studies LD50 values ranged between 9.0 and 202.8 mg/kg bw based on the component peracetic acid. sporadic contact with even dilute solutions with the oesophagus could lead to deaths due to corrosion of the tissue and could explain the variability in the LD50. The pathology and symptoms were similar across all studies, indicating irritation and corrosion of tissues in contact with the test material. PAA solutions should be considered as corrosive (within 3 minutes) at concentrations of 10 % and higher when applied to the skin of rabbits. PAA was generally corrosive to rabbit skin at a concentration of 5 % if contact lasted 45 minutes or longer. Concentrations of less than 0.34 % PAA were only slight irritants or non-irritants, depending on the exposure duration of the skin. PAA was corrosive at concentrations of 0.34 % and higher when tested in the rabbit eye. Slight or no eye irritation was found at concentrations of 0.15 % or less PAA. Incidental human findings on skin and eye irritation are supporting the animal studies. Peracetic acid gave a positive response in Alarie assay in the mouse, with an RD50 value (concentration producing a 50 % decrease in the respiratory rate) of 12 and 17 mg/m3 (peracetic acid in vapour mixture from the formulation and peracetic acid only). Human data support the sensory irritating properties of peracetic acid. No skin sensitisation was observed in three Buhler tests in guinea pigs with different formulations of PAA. The exposure concentration of peracetic acid ranged from 0.15 to 1.2 % during the tests. Additionally, long term experience with production and use of PAA has shown that PAA has no sensitisation potential. To investigate the repeated dose toxicity, a GLP guideline study was done with rats, which were exposed by gavage for 13 weeks to 5 % PAA diluted to various concentrations (0.018 % to 0.55 % of the component peracetic acid). At 0.75 mg/kg/day transient or intermittent loud breathing was observed in two females but the effect was not considered adverse. Based on the results of this study the NOAEL was 0.75 mg/kg bw/day (component peracetic acid). The only observed effects were local effects that are concentration related. It is therefore reasonable to define a No Observed Adverse Effect Concentration rather than a classical NOAEL. Based on the component peracetic acid, the NOAEC for local effects was 0.055 %. Gene mutation assays in bacteria tests, with and without metabolic activation, showed negative results. Two DNA repair tests in human foetal lung cells did not indicate a genotoxic potential of PAA. In the in vitro chromosome aberration test, positive findings were obtained only at cytotoxic concentrations. Under in vivo conditions, PAA (4.5 and 5.17% product) did not produce micronuclei in two mouse micronucleus tests after oral administration. In two in vivo/ex vivo assays of unscheduled DNA synthesis in rats after oral administration, PAA did not show significant genotoxicity potential. Overall these data do not raise concern with regard to the mutagenic and genotoxic potential of PAA However, peracetic acid is not systemically available and this could explain the lack of in vivo mutagenicity, but site of contact effects cannot be excluded completely. No valid carcinogenicity study with PAA is available. No valid data on fertility are available. However, in a well documented GLP and guideline study aqueous dilutions of 5 % PAA were administered daily by gavage to Sprague-Dawley rats for 13 weeks. No effects of peracetic acid on the reproductive organs of both sexes following macroscopic post mortem examinations and microscopic examinations (histopathology) were notable during the study. Because peracetic acid is rapidly degraded in blood, distribution to reproductive organs is not anticipated, and therefore it is unlikely to be a reproductive toxicant. In addition, the degradation product hydrogen peroxide did not indicate any effect in the reproductive organs during a 90-day drinking water study and furthermore, a rapid degradation was presumed resulting in a lack of systemic availability In a well documented GLP and guideline developmental toxicity study performed with 32-38 % PAA, pregnant Wistar rats were administered dose levels of 100, 300 or 700 mg peracetic acid/l (corresponding to 12.5, 30.4 and 48.1 mg peracetic acid/kg bw/day) via the drinking water from day 5 to 20 of gestation. No teratogenic effect was evident up to and including the high dose level of 700 mg peracetic acid/l (48.1 mg peracetic acid/kg bw/day). Dose and treatment-related maternal toxicity was observed, considering water and food consumption, above 100 mg/L (12.5 mg PAA/kg bw). At 700 mg peracetic acid/L (48.1 mg/kg bw) this resulted in severe reductions in drinking water and food consumption and in absolute body weight as well as by a drastic reduction in overall body weight gain and in body weight gain corrected for uterine weight. At the high dose level, fetal weight was statistically significantly reduced (5 %) but litter size at this dose level was about 13 % higher than in controls. However, it is doubtful if the reduction of 5% is biologically relevant The overall NOAEL for foetal toxicity is therefore 300 mg/L (30.4 mg PAA/kg bw) based on a statistically significantly lower body weight and an increased incidence of poor and/or hypertrophic ossification (bone formation) in the presence of severe maternal effects (maternal NOAEL = 100 mg/L or 12.5 mg PAA/kg bw/day). Environment Peracetic acid is an organic substance which is completely miscible with water (water solubility of 1000 g/l at 20 °C) and which displays oxidising properties. Pure peracetic acid is not available because it is explosive. For this reason it is technically not possible to perform an experimental study according to the guidelines to determine the melting point, boiling point and vapor pressure of pure peracetic acid. Based on modelling, the melting point, boiling point and vapour pressure were estimated to be -42 °C, about 105 °C and 32 hPa (at 25 °C), respectively. The log Pow was reported to be -0.52 (measured value) and the Henry Law's constant is 0.22 Pa cu m/mol. The pKa of peracetic acid is 8.2 at 20 °C and therefore the substance is mainly present in the environment as peracetic acid at a neutral pH (pH = 7), while peracetate would mainly be present if the pH is significantly higher than 8.2. Based on the high water solubility, low vapour pressure and low octanol-water partition coefficient, peracetic acid is expected to partition almost exclusively to the aquatic compartment (99.95 %). In air the half-life of peracetic acid is 22 minutes. The abiotic degradation of peracetic acid increases with temperature and pH. At a temperature of 25 °C and at pH of 4, 7 and 9, the degradation half-life value were 48, 48 and < 3.6 hours respectively. Peracetic acid was readily biodegradable during a biodegradation test when an inhibition of the micro-organisms (biocidal effect) was prevented. Peracetic acid will be degraded in a sewage treatment plant if the influent concentration is not extremely high (eg > 100 ppm). If effluents generated during the production or use of PAA are treated by a waste water treatment plant, no emission of peracetic acid to the aquatic environment is expected. Several studies on acute toxicity to aquatic species are available for all trophic levels. The pH of the test solutions was not adapted during the studies because a decrease of the pH was not found. In most cases the endpoints of the aquatic toxicity tests were based on nominal concentrations. The 96-hr LC50 values for fish ranged between 0.9 and 3.3 mg/l in most freshwater species. The 48-hr EC50 for D. magna ranged between 0.5 and 1.0 mg/L. Based on the representative standard toxicity tests, the lowest 72-hr NOEC of 0.084 mg/L was found for Pseudokirchneriella subcapitata (formerly known as Selenastrum capricornutum). The lowest EC50 value of 0.18 mg/L was found during a 120-hr growth inhibition test with P. subcapitata. . To determine the toxicity for microorganisms, two respiration inhibition tests with activated sludge of predominantly domestic sewage treatment plants were conducted. The EC50 after 3 hours was 5.1 and 38.6 mg peracetic acid/l (based on nominal concentrations), respectively. In general, the aquatic tests with fish, invertebrates and algae were reproducible if concentrations were expressed as peracetic acid irrespective of the concentrations of hydrogen peroxide and acetic acid. Thus, the peracetic acid concentration alone may explain the toxicity of PAA formulations. Exposure The global number of production sites is estimated to be 40-100 and the majority of the production sites are located in Europe. The equilibrium peracetic acid consumption (as such) in 2004 was estimated to be: - 40,000 - 80,000 tonnes in Europe - less than 20,000 tonnes in the USA and - less than 10,000 tonnes in the rest of the world. The quantities of equilibrium peracetic acid, given above, are mainly used for disinfection. Neither use of peracetic acid for chemical synthesis nor in situ generation of peracetic acid is included. Major uses of peracetic acid are in chemical synthesis, disinfection and bleaching. Low concentrations (1-15 %) are used as sanitisers, disinfectants and sterilants in agriculture, food, beverage and medical industries. High-strength equilibrium (> 15 %) and distilled peracetic acid products are in general employed as oxidising agents in the manufacture of organic chemicals and pharmaceuticals. Distilled peracetic acid is also used as bleaching agent in TCF cellulose pulp production processes replacing chlorine dioxide. Peracetic acid seems to be used in certain European countries in consumer products, which are used for example for hard surface disinfection. Peracetic acid is also generated in situ when products, containing an activator (eg tetra-acetyl ethylenediamine, TAED) and a persalt (sodium perborate or sodium percarbonate), are dissolved in water. These products could be laundry detergents but they could also be used for surface disinfection (eg hospitals, farms). World-wide consumption in chemical synthesis including captive use (internal use by a company) and in situ generation has been estimated at 45,000-50,000 tonnes peracetic acid (100 %) in 1998. During use of peracetic acid the substance may be released to the aquatic environment Also in situ formation may result in an exposure of the aquatic environment. However, if the effluents are treated by wastewater treatment plants no emission of peracetic acid to the aquatic environment is expected.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 暴露途径

所有暴露途径都会产生严重的局部影响。

Serious local effects by all routes of exposure.

来源:ILO-WHO International Chemical Safety Cards (ICSCs)

毒理性

• 吸入症状

灼热感。咳嗽。呼吸困难。气短。喉咙痛。症状可能延迟出现。

Burning sensation. Cough. Laboured breathing. Shortness of breath. Sore throat. Symptoms may be delayed.

来源:ILO-WHO International Chemical Safety Cards (ICSCs)

毒理性

• 皮肤症状

可能被吸收！红斑。疼痛。水泡。皮肤烧伤。

MAY BE ABSORBED! Redness. Pain. Blisters. Skin burns.

来源:ILO-WHO International Chemical Safety Cards (ICSCs)

毒理性

• 眼睛症状

红斑。疼痛。严重深度烧伤。

Redness. Pain. Severe deep burns.

来源:ILO-WHO International Chemical Safety Cards (ICSCs)

吸收、分配和排泄

在37°C下使用0.8% PAA（非腐蚀性）进行的体外皮肤渗透试验表明，过氧乙酸通过完整猪皮的皮肤摄取量很低。当大鼠皮肤暴露于腐蚀性浓度的(14)C标记PAA时，发现(14)C的摄取量相当大，但尚不清楚(14)C是以过氧乙酸、醋酸还是CO2的形式存在。预计腐蚀性浓度的PAA会破坏皮肤的正常屏障功能。

An in vitro dermal penetration assay at 37 °C using 0.8 % PAA (non-corrosive) indicated a low dermal uptake of peracetic acid through the intact skin of pigs. When the skin of rats was exposed to a corrosive concentration of (14)C-labelled PAA, a considerable uptake of (14)C was found but it is unknown if the (14)C was present as peracetic acid, acetic acid, or CO2. It is expected that corrosive concentrations of PAA would compromise the normal barrier function of the skin.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

两项使用不同分析方法的可靠体外研究表明，过氧乙酸在大鼠血液中迅速降解。当大鼠血液稀释1000倍时，过氧乙酸的半衰期小于5分钟。在未稀释的血液中，预计半衰期将只有几秒钟甚至更短。因此，过氧乙酸的分布可能非常有限，并且预期在接触过氧乙酸溶液后不会在全身范围内可用。

Two reliable in vitro studies, using different analytical methods, showed a rapid degradation of peracetic acid in rat blood. When rat blood was diluted 1000 times, the half-life of peracetic acid was < 5 minutes. In undiluted blood the half-life is expected to be several seconds or less. For this reason the distribution of peracetic acid is probably very limited and it is not expected to be systemically available after exposure to peracetic acid solutions.

来源:Hazardous Substances Data Bank (HSDB)

制备方法与用途

过氧乙酸作为一种多功能试剂，在有机合成中具有广泛的应用。以下是其一些主要应用：

1. 脂肪酸环氧化：

   • 通过在合适的催化剂存在下，使用过氧乙酸对烯烃进行环氧化反应，可以高效地生成环氧化合物。
   • 常用的催化剂包括三价铁离子螯合物和二价锰离子配合物。

2. 特定结构的环氧化物制备：

   • 可以通过特殊方法从多烯化合物如1,3-环戊二烯、1,3-庚二烯和1,3-辛二烯等制备易分解的丙烯基环氧化物。

3. 选择性反应特点：

   • 环氧化反应通常具有区域选择性和立体选择性，倾向于在电子云密度较大的双键上发生。

4. 其他功能化应用：

   • 可以用于将硫醚转化为亚砜或烷基亚磺酰基。
   • 氧化氮杂环化合物（如吡啶）形成N-氧化物。
   • 过氧乙酸还具有作为漂白剂、催化剂、消毒剂和杀菌剂的应用价值。

5. 特定类型的化学转化：

   • 对芳香族化合物，过氧乙酸能够催化产生相应的醌类化合物。
   • 可以对共轭双烯、烯丙基叠氮化物以及α,β-不饱和酯进行氧化反应。

总的来说，过氧乙酸因其高反应活性和选择性，在有机合成领域中有着广泛的应用前景。通过不同的催化剂和反应条件的选择，可以实现多种复杂的化学转化。

反应信息

• 作为反应物：
  描述：

  过氧乙酸 在 溶剂黄146 、 sodium bromide 作用下， 生成 溴甲烷
  参考文献：
  名称：

  Erlenmeyer, Helvetica Chimica Acta, 1925, vol. 8, p. 795

  摘要：

  DOI：
• 作为产物：
  描述：

  乙酸丁酯 在 硫酸 、 双氧水 作用下， 以 1,4-二氧六环 、 硝基苯 为溶剂， 反应 9.0h， 生成 过氧乙酸
  参考文献：
  名称：

  Chalabiev, Ch. A.; Guseinov, M. M.; Akhverdiev, I. R., Russian Journal of Physical Chemistry, 1980, vol. 54, # 8, p. 1195 - 1197

  摘要：

  DOI：
• 作为试剂：
  描述：

  5-甲氧基嘧啶 在 过氧乙酸 、 硫酸 作用下， 以 水 、 溶剂黄146 为溶剂， 反应 1.0h， 以42%的产率得到4-羟基-5-甲氧基嘧啶
  参考文献：
  名称：

  Chemistry of pyrimidine. II. Synthesis of pyrimidine N-oxides and 4-pyrimidinones by reaction of 5-substituted pyrimidines with peracids. Evidence for covalent hydrates as reaction intermediates

  摘要：

  DOI：

  10.1021/jo00217a012

文献信息

• EPR, ¹H and ²H NMR, and Reactivity Studies of the Iron–Oxygen Intermediates in Bioinspired Catalyst Systems
  作者：Oleg Y. Lyakin、Konstantin P. Bryliakov、Evgenii P. Talsi

  DOI：10.1021/ic200088e

  日期：2011.6.20

  following intermediates have been observed: [(L)FeIII(OOR)(S)]2+, [(L)FeIV═O(S)]2+ (L = BPMEN or TPA, R = H or tBu, S = CH3CN or H2O), and the iron–oxygen species 1c (L = BPMEN) and 2c (L = TPA). It has been shown that 1c and 2c directly react with cyclohexene to yield cyclohexene oxide, whereas [(L)FeIV═O(S)]2+ react with cyclohexene to yield mainly products of allylic oxidation. [(L)FeIII(OOR)(S)]2+

  配合物[（BPMEN）Fe II（CH 3 CN）2 ]（ClO 4）2（1，BPMEN = N，N'-二甲基-N，N'-双（2-吡啶基甲基）-1,2-二氨基乙烷）和[（TPA）Fe II（CH 3 CN）2 ]（ClO 4）2（2，TPA =三（2-吡啶基甲基）胺）是用于烃类生物启发性氧化的最佳非血红素铁基催化剂。使用EPR以及1 H和2 H NMR光谱，在催化剂体系中形成的铁-氧中间体1，2 / H 2 ö 2 ; 1，2 / H 2 ö 2 / CH 3 COOH; 1，2 / CH 3 CO 3 H; 1，2 /米-CPBA; 1，2 / PhIO; 1，2 /吨BuOOH; 和1，2 /吨BuOOH / CH 3 COOH进行了研究（米-CPBA是米-氯过苯甲酸）。以下中间体已经观察到：[（L）的Fe III（OOR）（S）] 2 +，[（L）的Fe IV = O（S）] 2+（L
• Intramolecular Hydrogen-Bond Interactions Tune Reactivity in Biomimetic Bis(μ-hydroxo)dicobalt Complexes
  作者：Alyssa A. DeLucia、Kimberly A. Kelly、Kevin A. Herrera、Danielle L. Gray、Lisa Olshansky

  DOI：10.1021/acs.inorgchem.1c02210

  日期：2021.10.18

  R becomes increasingly electron-withdrawing, the intramolecular H-bond interaction between bridging μ–OH and κ1-acetate ligands results in increasingly “oxo-like” μ–OH bridges. Deprotonation of the bridging μ–OH results in the quantitative conversion to corresponding cubane complexes: [Co4(μ-O)4(μ3-OAc)4(pyR)4] (2R), which represent the thermodynamic sink of self-assembly. These reactions are unusually

  活性位点氢键（H-键）网络是金属酶控制高价过渡金属氧中间体形成和部署的关键组成部分。我们报道了一系列双核钴配合物，它们可作为非血红素二铁酶家族的结构模型，并具有通过分子内氢键相互作用稳定的Co 2 (μ–OH) 2金刚石核心。我们定义了这些复合物的动力学控制合成所需的条件：[Co 2 (μ–OH) 2 (μ-OAc)(κ 1 -OAc) 2 (py R ) 4 ][PF 6 ] ( 1 R ),其中 OAc = 乙酸盐和 py R=带有对位取代基R的吡啶，我们描述了1个R的同源系列，其中吡啶上的对位R取代基被调节。1 R的固态 X 射线衍射 (XRD) 结构在整个系列中相似，但在溶液中，它们的1 H NMR 光谱揭示了线性自由能关系 (LFER)，其中，随着 R 的吸电子性增加，分子内桥接 μ-OH 和 κ 1 -乙酸酯配体之间的氢键相互作用导致越来越“类似氧代”的 μ-OH 桥。桥接 μ-OH
• Iron-Catalyzed Olefin Epoxidation in the Presence of Acetic Acid:  Insights into the Nature of the Metal-Based Oxidant
  作者：Rubén Mas-Ballesté、Lawrence Que

  DOI：10.1021/ja075115i

  日期：2007.12.1

  [BPMEN = N,N'-bis-(2-pyridylmethyl)-N,N'-dimethyl-1,2-ethylenediamine; TPA = tris-(2-pyridylmethyl)amine] catalyze the oxidation of olefins by H2O2 to yield epoxides and cis-diols. The addition of acetic acid inhibits olefin cis-dihydroxylation and enhances epoxidation for both 1 and 2. Reactions carried out at 0 degrees C with 0.5 mol % catalyst and a 1:1.5 olefin/H2O2 ratio in a 1:2 CH3CN/CH3COOH

  铁配合物 [(BPMEN)Fe(OTf)2] (1) 和 [(TPA)Fe(OTf)2] (2) [BPMEN = N,N'-bis-(2-pyridylmethyl)-N,N' -二甲基-1,2-乙二胺；TPA = tris-(2-pyridylmethyl)amine] 通过 H2O2 催化烯烃氧化，生成环氧化物和顺式二醇。乙酸的加入抑制了烯烃的顺式二羟基化并增强了 1 和 2 的环氧化。在 0 摄氏度下，使用 0.5 mol% 催化剂和 1:1.5 烯烃/H2O2 比率在 1:2 CH3CN/CH3COOH 溶剂混合物中进行反应导致环辛烯在 1 分钟内几乎定量转化为环氧化物。已在低温下探测了在乙酸存在下形成的活性物质的性质。对于 2，在没有底物的情况下，可以观察到 [(TPA)FeIII(OOH)(CH3COOH)]2+ 和 [(TPA)FeIVO(NCCH3)]2+ 中间体。然而，
• Triflic Acid Catalyzed Oxidative Lactonization and Diacetoxylation of Alkenes Using Peroxyacids as Oxidants
  作者：Yan-Biao Kang、Lutz H. Gade

  DOI：10.1021/jo202491y

  日期：2012.2.3

  A clean and efficient diacetoxylation reaction of alkenes catalyzed by triflic acid using commercially available peroxyacids as the oxidants has been developed. This method was also applied in oxidative lactonizations of unsaturated carboxylic acids in good to high yields.

  已经开发了使用可商购的过氧酸作为氧化剂的三氟甲磺酸催化的烯烃的清洁且有效的二乙酰氧基化反应。该方法还以高产率到高产率用于不饱和羧酸的氧化内酯化。
• Discovery of the Human Immunodeficiency Virus Type 1 (HIV-1) Attachment Inhibitor Temsavir and Its Phosphonooxymethyl Prodrug Fostemsavir
  作者：Tao Wang、Yasu Ueda、Zhongxing Zhang、Zhiwei Yin、John Matiskella、Bradley C. Pearce、Zheng Yang、Ming Zheng、Dawn D. Parker、Gregory A. Yamanaka、Yi-Fei Gong、Hsu-Tso Ho、Richard J. Colonno、David R. Langley、Pin-Fang Lin、Nicholas A. Meanwell、John F. Kadow

  DOI：10.1021/acs.jmedchem.8b00759

  日期：2018.7.26

  leading to the identification of 3 with characteristics that provided for targeted exposure and PK properties in three preclinical species. However, the physical properties of 3 limited plasma exposure at higher doses, both in preclinical studies and in clinical trials as the result of dissolution- and/or solubility-limited absorption, a deficiency addressed by the preparation of the phosphonooxymethyl prodrug

  描述了从1开始递送替米沙韦（3，BMS-626529）的HIV-1附着抑制剂（AIs）的4-甲氧基-6-氮杂吲哚系列的优化。通过将N-连接的，sp 2-杂化的杂芳基环并入杂环核的7位，可获得最有效的药效和药代动力学（PK）性能提高。遵守共面性模型的化合物可提供靶向的抗病毒效力，从而鉴定出3种具有为三种临床前物种提供靶向暴露和PK特性的特征。但是3的物理性质在临床前研究和临床试验中，由于溶解和/或溶解度受限的吸收而限制了较高剂量的血浆暴露，这是膦酰氧甲基前药4（BMS-663068，fostemsavir）的制备所解决的缺陷。4的缓释制剂目前正处于III期临床试验中，已显示出有望在高度治疗经验丰富的HIV-1感染患者中作为药物联合疗法的一部分。