Oxamyl is a white, crystalline solid, with slight sulfurous odor. Used as an insecticide, nematicide and acaricide on many field crops, vegetables, fruits, and ornamentals. (EPA, 1998)
颜色/状态：
White crystalline solid
气味：
Slight sulfurous odor
沸点：
Decomposes on distillation
熔点：
100-102 °C, changes to a different crystalline form, mp 108-110 °C
The metabolism of oxamyl ... has not been much studied in humans. Oxime production would be expected to occur again ... with subsequent ketone formation as for methomyl. The dimethylacetyl group may hydrolyze to form N,N-dimethylformamide, excreted as N-methylformamide and formamide in urine ... or N,N-dimethyl carbamic acid.
All three of the oxime carbamates, aldicarb, methomyl, and oxamyl, will produce the N-methylformamide ... and N-methylamino formic acid ... as a result of R1 cleavage. The former is a urinary biological monitoring marker for N,N-dimethylformamide ... .
(14)C-oxamyl was degraded by two major pathways in rats that received 1 mg each (2.5 to 4.6 mg/kg) after having received nonradioactive oxamyl for 18 days or more at a dietary level of 50 to 150 ppm (about 2.5 to 7.4 mg/kg/day). Oxamyl was hydrolyzed to an oximino metabolite (methyl N-hydroxy-N',N'-dimethyl-1-thioxamimidate) or converted enzymatically via N,N-dimethyl-1-cyanoformide (DMCF) to N,N-dimethyloxamic acid. Conjugates of the oximino cmpd, the acid, and their monomethyl derivatives constituted over 70% of the metabolites excreted in the urine and feces. Less than 0.3% of the oxamyl was exhaled as carbon dioxide, but incorporation of (14)C-CO2 accounted for more than 50% of the radioactivity remaining in the tissues ... .
The major component present in the urine was glucuronide of oxime (31 - 37% of the dose), metabolite oxime (13 - 18% of the dose) and the parent oxamyl (7 - 11% of the dose).
来源:Hazardous Substances Data Bank (HSDB)
代谢
甲酰胺通过肝脏酶促水解；降解产物由肾脏和肝脏排出。
The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (L793)
Oxamyl is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
癌症分类：人类非致癌性证据E组
Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
对人类无致癌性（未列入国际癌症研究机构IARC清单）。
No indication of carcinogenicity to humans (not listed by IARC).
Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).
When (14)C-oxamyl was administered to lactating goats, most of the dose was rapidly eliminated via urine and feces. Some (14)CO2 also formed. No intact oxamyl or related metabolites were detected in milk, blood, urine or tissues; however, (14)C was incorporated into lactose, casein, triglyceride fats, and amino acids of protein in blood and tissues.
Following ip injection of (14)C oxamyl, mice excreted 75.5% of the activity within 6 hours. By 96 hours, 88.7% had been excreted in the urine and 7.7% in the feces. At 6 and 72 hours after injection, organosoluble radioactive material constituted 24.7 and 6.5%, respectively, of the total radioactivity in the urine. The organosoluble cmpds identified included oxamyl and methyl N'-methyl-N-(methyl(carbomyl)oxy)-1-thiooxamimidate ...
Little information is available on the distribution of carbamates in the various organs and tissues in mammals following exposure by inhalation or the oral route. The organs in which residues have been reported are the liver, kidneys, brain, fat, and muscle. The half-life in the rat is of the order of 3-8 hr. It seems that the excretion of carbamates via urine is also rapid in man, and that the metabolic pathways in man are the same as those in the rat. /Carbamate pesticides/
In a rat metabolism study, SD rats (5 animals/sex/group) received a single oral dose of 14C-oxamyl (1 mg/kg) by gavage. Approximately 80% of the administered radioactivity was eliminated in the urine after 24 hours of dosing, and approximately 91% of the dose was eliminated in the urine by 168 hours. Less than 3% of the dose was found in the feces, and approximately 1% of the dose was found in the carcass. Except for muscle and skin, less than 1% of the dose was found in any tissue examined. The data indicated that oxamyl was readily absorbed with oral administration and rapidly metabolized and eliminated in the urine. There was no sex difference m the pattern of elimination, and there was essentially no sequestration of oxamyl or its metabolites in any tissue examined.
The metabolic fate of (1-14C)oxamyl in a lactating goat was investigated. The test animal was administered five consecutive daily doses orally at 31 ppm oxamyl dietary burden. Most of the radioactivity was eliminated via urine (45.3%) and feces (7.2%). (14C)Oxamyl equivalents in edible tissues (liver, kidney, muscle, and fat) and in milk accounted for 6.7 and 10.2% of the dose, respectively. A small percentage (1.9%) of the dose was exhaled as volatile metabolites (primarily 14CO2). No oxamyl nor any closely related metabolites were detected in tissues, milk, or urine. Extensive degradation/metabolism of (1-14C)oxamyl was observed. Radioactive thiocyanate was the major metabolite identified in the milk as well as in the methanol/water extracts for all tissue samples.
Phloem mobility of xenobiotics VI. A phloem-mobile pro-nematicide based on oxamyl exhibiting root-specific activation in transgenic tobacco
摘要：
AbstractPhloem mobility is a desirable attribute for pesticides in many applications, and the physicochemical properties necessary for phloem mobility are now well understood. However, attempts to derivatize pesticides to make them phloem mobile are often frustrated by a concomitant loss of activity. This study describes a phloem‐mobile pro‐nematicide, a hydroxymethyloxamyl glucuronide (JR522) coupled with an in‐situ activation mechanism in transgenic tobacco expressing Escherichia coli β‐glucuronidase in its root tips. When applied foliarly to the transgenic tobacco, JR522 and its methyl ester (JM775) showed greater nematicidal activity than oxamyl against root‐knot nematodes. This example of combining pro‐pesticide chemistry with crop genetic engineering for site‐specific activation provides a model system for demonstrating how to circumvent the often mutual exclusivity of phloem mobility and pesticidal activity. Additional advantages of this scheme include the potential mammalian safety of the propesticide, as exhibited by JR522 in this study, and a high degree of site‐specific release of xenobiotics in plants.
N-Phosphinoaminosulfinylcarbamate esters and their use as insecticides
申请人：Regents of the University of California
公开号：US04410518A1
公开（公告）日：1983-10-18
A novel class of chemical compounds useful as pesticides consists of N-phosphinoaminosulfinylcarbamate esters. The preparation of these compounds and their formulation to control insects are exemplified.
[EN] A NOVEL CRYSTALLINE FORM OF OXAMYL, A PROCESS FOR ITS PREPARATION AND USE OF THE SAME<br/>[FR] NOUVELLE FORME CRISTALLINE D'OXAMYLE, SON PROCÉDÉ DE PRÉPARATION ET SON UTILISATION
申请人：JIANGSU ROTAM CHEMISTRY CO LTD
公开号：WO2018099203A1
公开（公告）日：2018-06-07
The present invention describes a crystalline form of oxamyl of formula (I), a crystal preparation process, the analyses of the crystal through various analytical methods and using the crystalline form to prepare a stable agrochemical formulation. The invention also describes the use of various solvents towards the crystalline form preparation conditions.
Reduction of the Carbamate Pesticides Oxamyl and Methomyl by Dissolved Fe<sup>II</sup> and Cu<sup>I</sup>
作者：Timothy J. Strathmann、Alan T. Stone
DOI：10.1021/es001824j
日期：2001.6.1
carbamates undergo a net two-electron reduction that is coupled to the sequential one-electron oxidation of two Fe(II) ions. The observed products are a substituted nitrile, methanethiol, and methylamine. A radical intermediate is inferred by polymerization of the radical scavenger acrylonitrile. Redox kinetics (i) vary with carbamate identity, (ii) exhibit first-order dependence on both Fe(II) and carbamate
Difluoromethyltriazolone compounds, use of the same and intermediates for the production thereof
申请人：——
公开号：US20030119670A1
公开（公告）日：2003-06-26
A triazolone compound of the formula [I]:
1
wherein;
R
1
represents optionally substituted phenyl or the like, T represents m-phenylene optionally substituted by methyl or the like;
and a fungicidal composition containing it as an active ingredient.
The present invention provides novel amidine compounds and novel pesticides containing these amidine compounds as active ingredients. The amidine compounds are expressed by formula I:
1
wherein X and Y are the same or different and are independently halogen, nitro, cyano, or C
1
-C
6
alkyl; Z is C
1
-C
6
haloalkyl or C
1
-C
6
haloalkoxy; R
1
is hydrogen, halogen, C
1
-C
6
alkyl, C
1
-C
6
haloalkyl, C
1
-C
6
alkoxy, C
1
-C
6
haloalkoxy, or a group of formula: S(O)
n
—R
5
(wherein R
5
is C
1
-C
6
alkyl or C
1
-C
6
haloalkyl; and n is 0, 1, or 2); R
2
and R
3
are the same or different and are independently halogen or C
1
-C
6
haloalkyl; and R
4
is a group of formula: NR
6
R
7
or N═CR
8
R
9
(wherein R
6
is hydrogen, C
1
-C
6
alkyl, (C
1
-C
6
alkoxy)-carbonyl, (C
1
-C
6
alkoxy) C
1
-C
6
alkyl, or C
2
-C
6
acyl; R
7
is hydrogen, C
1
-C
6
alkyl, (C
1
-C
6
alkoxy)carbonyl, or C
2
-C
6
acyl; R
8
is C
1
-C
6
alkyl or hydrogen; and R
9
is C
1
-C
6
alkoxy, C
1
-C
6
alkyl, or di(C
1
-C
6
alkyl)amino).
