When heated to decomposition it emits toxic vapors of /hydrogen chlorid, hydrogen fluoride, and nitrogen oxides/.
碰撞截面：
190.4 Ų [M+HCOO]-
保留指数：
2218.3
稳定性/保质期：
如果按照规定使用和储存，则不会发生分解，并且没有已知的危险反应。
计算性质
辛醇/水分配系数(LogP)：
4.5
重原子数：
23
可旋转键数：
4
环数：
2.0
sp3杂化的碳原子比例：
0.266
拓扑面积：
38
氢给体数：
0
氢受体数：
5
ADMET
代谢
氯fenapyr几乎不具有解偶联活性，但通过微粒体氧化去除N-乙氧基甲基团，释放出相应的自由吡咯（AC 303,268），这是一种具有很强解偶联活性的疏水性弱酸... AC 302,268在脊椎动物和昆虫中的急性毒性高于氯fenapyr（例如，大鼠口服LD50为29毫克/千克）。当注射到昆虫体内时，它几乎立即并大量刺激呼吸，而母体氯fenapyr只有在显著延迟后才会这样做。所有这些观察结果支持氯fenapyr是一种前杀虫剂的观点，并且需要代谢转化为活性解偶联剂AC 303,268，才能发挥毒性作用。
Chlorfenapyr shows virtually no uncoupling activity but removal of the N-ethoxymethyl group through microsomal oxidation releases the corresponding free pyrrole (AC 303,268) which is a lipophilic weak acid with very strong uncoupling activity ... AC 302,268 has an acute toxicity higher than that of chlorfenapyr in both vertebrates and insects (eg, the acute oral LD50 for the rat is 29 mg/kg). Upon injection into insects it cause an almost immediate and massive stimulation of respiration whereas the parent chlorfenapyr does so only after a significant delay. All these observations support the idea that chlorfenapyr is a proinsecticide and requires metabolic conversion to the active uncoupler, AC 303,268, before it exert a toxic action.
[2-Pyrrole-14C]CL 303,630 or [Phenyl-(U)-14C]CL 303,630 (radiochemical,purity: 99-100%, S.A. 134.7 uCi/mg and 411.4 uCi/mg, respectively) and nonlabeled CL 303,630 (...98.8% purity) were suspended in 0.5% (w/w) CMC solution and administered via gavage to 5 rats/sex as single doses of 20.7 or 206.7 mg/kg and as multiple oral doses: pretreat 5 rats/sex daily with nonlabeled CL 303,630 for 14 days prior to pulsing with 20.5 mg/kg [2-Pyrrole-14C]CL 303,630 or [Phenyl-(U)-14C]CL 303,630. Regardless of treatment regimen, 14C CL 303,630 was eliminated mainly by the fecal route. By 48 hours, 70.4-91.4% and 3.9-9.7% of the administered radioactivity was detected in feces and urine, respectively. Blood and tissue concentrations were higher in females than in males indicating that there are substantial sex-related differences. The excreted fecal residue was mainly unchanged parent compound plus minor N-dealkylated, debrominated, and hydroxylated oxidation products. Absorbed CL 303,630 was extensively metabolized in tissues and urine by N-dealkylation, debromination, ring hydroxylation, and conjugation.
来源:Hazardous Substances Data Bank (HSDB)
代谢
AC 303,268 及其进一步降解产物是氯虫苯甲酰胺在脊椎动物研究中常见的代谢物...口服给药大鼠的尿代谢物包括 N-烷氧基侧链氧化和消除产物（例如，AC 303,268）以及环羟基化产物及其共轭物。在山羊和母鸡中也获得了类似的结果。在鱼和土壤中，观察到脱溴作为额外的代谢途径。
AC 303,268, and its further degradation products, is a common metabolites of chlorfenapyr found in studies with vertebrates ... Urinary metabolites /from an oral dose admin in rats/ included products of N-alkoxy side chain oxidation and removal (eg, AC 303,268) and ring hydroxylation products and their conjugates. Similar results were obtained with goats and hens. In fish and soil, debromination is observed as an additional metabolic route.
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
癌症分类：有致癌性的提示性证据，但不足以评估对人类致癌的可能性
Cancer Classification: Suggestive Evidence of Carcinogenicity, but Not Sufficient to Assess Human Carcinogenic Potential
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
口服（L96）；吸入（L96）；皮肤给药（L96）
Oral (L96) ; inhalation (L96) ; dermal (L96)
来源:Toxin and Toxin Target Database (T3DB)
吸收、分配和排泄
氯fenapyr口服给药在大鼠中吸收不良，超过80%在粪便中排出...
An oral dose of chlorfenapyr was poorly absorbed in rats and over 80% was eliminated in the feces ...
Radioactive chlorfenapyr was administered to rats by oral gavage at dose levels of 20 mg/kg/day as a single dose or following a 14-day pre-treatment with non-radioactive chlorfenapyr, or at 200 mg/kg as a single dose. Based on the metabolites identified, the major deposition route of orally administered chlorfenapyr is fecal excretion of unaltered parent compound. The two rings of the molecule are not cleaved. Metabolites are excreted primarily in urine; accumulation in tissues is minimal.
[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.
[EN] BICYCLYL-SUBSTITUTED ISOTHIAZOLINE COMPOUNDS<br/>[FR] COMPOSÉS ISOTHIAZOLINE SUBSTITUÉS PAR UN BICYCLYLE
申请人：BASF SE
公开号：WO2014206910A1
公开（公告）日：2014-12-31
The present invention relates to bicyclyl-substituted isothiazoline compounds of formula (I) wherein the variables are as defined in the claims and description. The compounds are useful for combating or controlling invertebrate pests, in particular arthropod pests and nematodes. The invention also relates to a method for controlling invertebrate pests by using these compounds and to plant propagation material and to an agricultural and a veterinary composition comprising said compounds.
The present invention relates to azoline compounds of formula (I) wherein A, B1, B2, B3, G1, G2, X1, R1, R3a, R3b, Rg1 and Rg2 are as defined in the claims and the description. The compounds are useful for combating or controlling invertebrate pests, in particular arthropod pests and nematodes. The invention also relates to a method for controlling invertebrate pests by using these compounds and to plant propagation material and to an agricultural and a veterinary composition comprising said compounds.
