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1. Amistar
2. Azoxy-strobin
3. Icia 5504
4. Icia-5504
5. Icia5504
6. Methyl (2e)-2-(2-(6-(2-cyanophenoxy)pyrimidin-4-yloxy)phenyl)-3-methoxyacrylate
7. Quadris
1. 131860-33-8
2. Amistar
3. Bankit
4. Quadris
5. Heritage
6. Icia-5504
7. Azoxystrobin [iso]
8. Hsdb 7017
9. Tcmdc-125883
10. Ici-a 5504
11. Chebi:40909
12. Nyh7y08ipm
13. 215934-32-0
14. Benzeneacetic Acid, 2-((6-(2-cyanophenoxy)-4-pyrimidinyl)oxy)-alpha-(methoxymethylene)-, Methyl Ester, (e)-
15. Dndi1511705
16. Benzeneacetic Acid, 2-[[6-(2-cyanophenoxy)-4-pyrimidinyl]oxy]-alpha-(methoxymethylene)-, Methyl Ester, (alphae)-
17. Ncgc00163818-04
18. Methyl (2e)-2-(2-{[6-(2-cyanophenoxy)pyrimidin-4-yl]oxy}phenyl)-3-methoxyprop-2-enoate
19. Methyl (e)-2-[2-[6-(2-cyanophenoxy)pyrimidin-4-yl]oxyphenyl]-3-methoxyprop-2-enoate
20. Methyl (e)-2-[2-[6-(2-cyanophenoxy)pyrimidin-4-yloxy]phenyl]-3-methoxyacrylate
21. (alphae)-2-[[6-(2-cyanophenoxy)-4-pyrimidinyl]oxy]-alpha-(methoxymethylene) Benzeneacetic Acid Methyl Ester
22. Methyl (2z)-2-(2-{[6-(2-cyanophenoxy)pyrimidin-4-yl]oxy}phenyl)-3-methoxyacrylate
23. Unii-nyh7y08ipm
24. Azoxystrobine X
25. Einecs Annex I Index 607-256-00-x
26. 1sqb
27. Methyl (2e)-2-(2-{[6-(2-cyanophenoxy)pyrimidin-4-yl]oxy}phenyl)-3-methoxyacrylate
28. Methyl (e)-2-{2-[6-(2-cyanophenoxy)pyrimidin-4-yloxy]phenyl}-3-methoxyacrylate
29. Benzeneacetic Acid, 2-((6-(2-cyanophenoxy)-4-pyrimidinyl)oxy)-alpha-(methoxymethylene)-, Methyl Ester, (alphae)-
30. Azoxystrobin [mi]
31. Azoxystrobin [hsdb]
32. Dsstox_cid_12520
33. Dsstox_rid_78966
34. Methyl (e)-2-(2-(6-(2-cyanopheoxy)pyrimidin-4-yloxy)phenyl)-3-methoxypropenoate
35. Dsstox_gsid_32520
36. Schembl18823
37. Schembl55087
38. Chembl230001
39. Dtxsid0032520
40. Amy3587
41. Ici-a-5504
42. Hy-b0849
43. Tox21_400087
44. Bdbm50487147
45. Mfcd08277047
46. Zinc13827839
47. Akos015900562
48. Db07401
49. Ks-5365
50. Azoxystrobin 100 Microg/ml In Methanol
51. Methyl (2e)-2-(2-(6-(2-cyanophenoxy)pyrimidin-4-yloxy)phenyl)-3-methoxyacrylate
52. Azoxystrobin 1000 Microg/ml In Acetone
53. Azoxystrobin 1000 Microg/ml In Toluene
54. Ncgc00163818-01
55. Ncgc00163818-02
56. Ncgc00163818-03
57. Ncgc00163818-05
58. Ac-24498
59. Azoxystrobin 10 Microg/ml In Cyclohexane
60. Azoxystrobin 1000 Microg/ml In Methanol
61. Azoxystrobin 1000 Microg/ml In Acetonitrile
62. Cas-131860-33-8
63. Cs-0012863
64. C18558
65. F20623
66. Azoxystrobin, Pestanal(r), Analytical Standard
67. 860a338
68. A806322
69. J-006072
70. J-519625
71. Q2013860
72. Azoxystrobin, Certified Reference Material, Tracecert(r)
73. (e)-methyl 2-(2-(6-(2-cyanophenoxy)pyrimidin-4-yloxy)phenyl)-3-methoxyacrylate
74. (e)-methyl 2-[2-(6- (2-cyanophenoxy)pyrimidin-4-yloxy)phenyl]-3-methoxypropenoate
75. (e)-methyl 2-[2-(6-(2-cyanophenoxy)pyrimidin-4-yloxy)pheny]-3-methoxypropenoate
76. (e)-methyl 2-[2-(6-(2-cyanophenoxy)pyrimidin-4-yloxy)phenyl]-3-methoxypropenoate
77. Methyl (2e)-2-(2-{[6-(2-cyanophenoxy)-4-pyrimidinyl]oxy}phenyl)-3-methoxyacrylate
78. Methyl (e)-2-{2-[6-(2-cyano-phenoxy)pyrimidin-4-yloxy]phenyl}-3-methoxyacrylate
79. (.alpha.e)-2-((6-(2-cyanophenoxy)-4-pyrimidinyl)oxy)-.alpha.-(methoxymethylene)benzeneacetic Acid Methyl Ester
80. (e)-2-[2-[[6-(2-cyanophenoxy)-4-pyrimidinyl]oxy]phenyl]-3-methoxy-2-propenoic Acid Methyl Ester
81. Methyl (.alpha.e)-2-((6-(2-cyanophenoxy)-4-pyrimidinyl)oxy)-.alpha.-(methoxymethylene)benzeneacetate
| Molecular Weight | 403.4 g/mol |
|---|---|
| Molecular Formula | C22H17N3O5 |
| XLogP3 | 3.7 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 8 |
| Rotatable Bond Count | 8 |
| Exact Mass | 403.11682065 g/mol |
| Monoisotopic Mass | 403.11682065 g/mol |
| Topological Polar Surface Area | 104 Ų |
| Heavy Atom Count | 30 |
| Formal Charge | 0 |
| Complexity | 646 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 1 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Eight male and female rats were given 14 consecutive daily oral doses of unlabelled azoxystrobin at 1 mg/kg bw followed by a single oral dose of (14)C-pyrimidinyl-labelled azoxystrobin at 1 mg/kg bw. For the repeated doses, about 89.1% and 86.5% of the administered dose was excreted in the feces of the males and females rats within 7 days, respectively, and about 12.5% and 17.0% of the administered dose was excreted in the urine of the males and females rats within 7 days, respectively. In males and females, excretion of radioactivity was rapid, with > 96% being excreted during the first 48 hr. Approximately 0.62% and 0.39% of the administered dose was found in the carcass and tissues within 7 days after dosing in male and female rats, respectively. For the repeated dose, the highest concentrations of azoxystrobin-derived radioactivity were found in the kidneys (males and females, < 0.04 ug equivalents/g). The concentrations found in the liver were 0.02 and 0.01 ug equivalents/g for males and females, respectively. At termination, the total concentration of radioactivity in blood was 0.01 ug equivalents/g for males and females.
WHO/FAO; Joint Meeting on Pesticide Residues Evaluation for Azoxystrobin (131860-33-8) p.6 (2008). Available from, as of December 27, 2011: https://www.inchem.org/pages/jmpr.html
In toxicokinetic studies, groups of male and female Alpk:APfSD rats (five to eight per group, depending on experiment) were given azoxystrobin (purity, 99%) with or without pyrimidinyl label as a single dose at 1 or 100 mg/kg bw by gavage or as 14 repeated doses of 1 mg/kg bw per day. Biliary metabolites were assessed using rats with cannulated bile ducts given a single dose at 100 mg/kg bw by gavage. The vehicle was polyethylene glycol (PEG 600) at 4 mL/kg bw. Treated rats were housed in stainless steel metabolism cages for 7 days. Urine was collected at 6 hr, and urine and feces were collected separately at 12, 24, 36, 48 h and at 24 hr intervals until 7 days after dosing. At each collection, cages were rinsed with water and cage-washing collected together with the urine. At the end of the study, cages were thoroughly rinsed with ethanol/water (1:1 v/v) and retained for radiochemical analysis. Carbon dioxide and volatiles were trapped. After 7 days, various organs and tissues were removed and analyzed for radioactivity. ... For rats receiving a single lower dose (1 mg/kg bw), total excretion of radioactivity (urine, feces, and cage wash) was 93.75% and 91.44% for males and females, respectively over the 7 days. Most (> 85%) of the urinary and fecal excretion took place during the first 36 hr after dosing. In these rats, about 83.2% and 72.6% of the administered dose was excreted in the feces of males and females within 7 days, respectively, and about 10.2% and 17.9% of the administered dose was excreted in the urine of the males and females within 7 days, respectively. Approximately 0.34% and 0.31% of the administered dose was found in the carcass and tissues within 7 days after dosing in males and females, respectively. For rats at this dose (1 mg/kg bw), the highest concentrations of radiolabel were found in the liver (mean for males and females, 0.009 ug equivalents/g) and in the kidneys (males, 0.027 ug equivalents/g; and females, 0.023 ug equivalents/g). At termination, the total concentration of radioactivity in blood was 0.004 ug equivalents/g for males and females. Less than 0.6% of the administered dose was recovered in the expired. For rats receiving the single higher dose (100 mg/kg bw), total excretion of radioactivity (urine, feces, and cage wash) was 98.29% and 97.22% for males and females, respectively, over the 7 days. Most (> 82%) of the urinary and fecal excretion took place during the first 48 hr after dosing. At this dose, about 89.37% and 84.53% of the administered dose was excreted in the feces of the males and females within 7 days, respectively, and about 8.54% and 11.54% of the administered dose was excreted in the urine of the males and females within 7 days, respectively. Approximately 0.33% and 0.33% of the administered dose was found in the carcass and tissues within 7 days after dosing in males and females rats, respectively. At this higher dose, the highest concentrations of radiolabel were found in the kidneys (males, 1.373 ug equivalents/g; and females, 1.118 ug equivalents/g) and in the liver (males, 0.812 ug equivalents/g; and females, 0.714 ug equivalents/g). At termination, the total concentration of radioactivity in blood was 0.389 ug equivalents/g for males and 0.379 ug equivalents/g for females
WHO/FAO; Joint Meeting on Pesticide Residues Evaluation for Azoxystrobin (131860-33-8) p.5 (2008). Available from, as of December 27, 2011: https://www.inchem.org/pages/jmpr.html
The excretion and tissue distribution of radioactivity was investigated for 48 h in male and female rats given a single dose of azoxystrobin at 1 mg/kg bw by gavage. Treated rats were housed in metabolism cages to facilitate the collection of urine, feces, exhaled air and volatiles. One male and one female rat receiving azoxystrobin radiolabelled in each position were killed at 24 hr and 48 hr after dosing. Each carcass was frozen and sectioned in preparation for whole-body radiography. About 89% and 86% of the administered dose of (14)C-pyrimidinyl-labelled azoxystrobin was excreted within 48 hr in the urine and feces of male and female rats, respectively. Most of the radioactivity was excreted in the feces, with < 17% in the urine. The male and female rats treated with (14)C-phenylacrylate-labelled azoxystrobin excreted about 80% and 97% of the administered dose within 48 hr, respectively. Most of the radioactivity was excreted via the feces with < 21% in the urine. At 48 hr, males and females, excreted approximately 0.01% of the administered dose as carbon dioxide trap and approximately 0.01% as volatile metabolites. The male and female rats treated with (14)C-cyanophenyl- labelled azoxystrobin excreted about 95% and 98% of the administered dose within 48 hr, respectively. Most of the radioactivity was excreted via the feces, with < 16% in the urine. At 48 hr, males and females excreted small amounts of radioactivity as carbon dioxide (< 0.3%) and as volatile metabolites (0.01%). For all radiolabels, the distribution of radioactivity was similar in males and females, as shown by whole-body autoradiography. At 24 hr, most of the radiolabel was present in the alimentary canal, moderate amounts in the kidneys and small amounts in the liver. Forty-eight hours after dosing, the whole-body autoradiography results showed a marked reduction in radioactivity. The results of these studies indicated that there were no significant differences between the rates and routes of excretion or tissue distribution of azoxystrobin labelled in one of three positions. No sex-related difference in excretion profile was evident. Minor differences in excretion were primarily due to the small numbers of rats used in the study. No significant differences in the amount of radioactivity recovered in the exhaled air and as volatiles were observed between the three radiolabels or between sexes. On the basis of the results of this study, other studies of excretion and tissue retention were conducted using only pyrimidinyl-labelled azoxystrobin.
WHO/FAO; Joint Meeting on Pesticide Residues Evaluation for Azoxystrobin (131860-33-8) p.4 (2008). Available from, as of December 27, 2011: https://www.inchem.org/pages/jmpr.html
... (14)C-Cyanophenyl-labelled azoxystrobin was given to bile duct cannulated and non-cannulated rats at a dose of 100 mg/kg bw. Samples of urine, feces and bile were collected for up to 72 hr. The purpose of this study was to reevaluate certain plant and goat metabolites that were previously not identified in rats and further elucidate the metabolic pathway of azoxystrobin in rats. Three further metabolites, previously detected in either plants or goats, were identified. Compound 13 (2-hydroxybenzonitrile), resulting from cleavage of the diphenyl ether link, was detected in the bile and urine as the glucoronide conjugate at a concentration of up to 1.8% of the administered dose. Compound 20 ((2-(6-(2-cyanophenoxy) pyrimidin-4-yloxy) phenyl)acetic acid) was also detected in the bile and urine at a concentration of up to 1.3%. Compound 35 (2-(2-(6-(2-cyanophenoxy) pyrimidin-4-yloxy) phenyl)glycolic acid) was detected in the urine, feces and bile at a concentration of up to 0.6%. Compounds 24 (Methyl 2-(2(6-(2-cyanophenoxy)pyrimidin-4-yloxy) phenyl)-glycolate) and 30 (2-(6-(2-cyanophenoxy) pyrimidin-4-yloxy) benzoic acid) were not detected.
WHO/FAO; Joint Meeting on Pesticide Residues Evaluation for Azoxystrobin (131860-33-8) p.8 (2008). Available from, as of December 27, 2011: https://www.inchem.org/pages/jmpr.html
Bile-duct cannulated rats were given azoxystrobin radiolabelled in either the pyrimidinyl, cyanophenyl or phenylacrylate rings at 100 mg/kg bw by gavage. Comparison of the rates and routes of excretion and the profile of the metabolites showed (as previously) that there were no significant differences in the metabolism of the three differently labelled forms, thus indicating that there was minimal cleavage of the ether linkages between the aromatic rings. Experiments designed to identify metabolites were therefore conducted in bile-duct cannulated rats given (14)C-pyrimidinyl labelled azoxystrobin by gavage. In the bile-duct cannulated rats, excreta, bile, and cage wash were collected at 6, 12, 24, 36, and 48 hr and stored at -20 C. Samples of bile, feces and urine were collected between 0 hr and 48 hr and pooled. Samples for males and females were separated. Urine and feces were collected at up to 168 hr after dosing from rats given the single dose (higher or lower) and from rats receiving repeated doses for 14 days, and were used for quantification of metabolites. Some bile samples were enzymatically digested using cholylglycine hydrolase at 30 units/mL, pH 5.6 at 37 C overnight. Metabolites were identified using various analytical techniques, such as thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC), proton nuclear magnetic resonance spectroscopy (NMR) and mass spectrophotometry (MS). On the basis of biliary excretion data for rats given a single dose of either (14)C-pyrimidinyl-, (14)C-phenylacrylate-, or (14)C-cyanophenyl-labelled azoxystrobin at 100 mg/kg bw, 74.4% (males) and 80.7% (females) of the pyrimidinyl-derived radioactivity was excreted in the bile after 48 hr. For the cyanophenyl-derived radioactivity, 56.6% and 62.5% was excreted in the bile of males and females, respectively. For the phenylacrylate-derived radioactivity, 64.4% (males) and 63.6% (females) was excreted in the bile. Quantitatively, there were no significant differences in biliary excretion between males and females. Azoxystrobin was found to undergo extensive metabolism in rats. A total of 15 metabolites were detected in the excreta and subsequently identified. Seven additional metabolites were detected but not identified. None of the unidentified metabolites represented more than 4.9% of the administered dose. The quantitative data for the various metabolites in the faeces, urine and bile of rats receiving a single dose of azoxystrobin at 100 mg/kg bw ... . The mass balance for the study of metabolite identification indicated that a substantial percentage of the administered radiolabel (45.6-73.6%) was unaccounted for, although the studies of excretion showed total recovery of 91.75-103.99%, with 72.6-89.3% being in the feces. The percentage of unaccounted-for radiolabel was especially notable in the groups receiving a single lower dose and a repeated lower dose. The study authors indicated that the variable efficiency in recovery could be explained by the fact that, for metabolite identification, feces were extracted with acetonitrile which allowed partitioning of the parent compound when it was present in the faeces (i.e. rats receiving the higher dose). For the groups receiving a single lower dose or repeated lower dose (where quantities of the parent compound were minimal), most of the faecal radiolabel was associated with polar metabolites that would not be present in the acetonitrile extract. The resulting concentration of radiolabel in the extract would, therefore, be very low. For the group receiving the higher dose, greater amounts of parent compound were left unabsorbed, thereby resulting in greater amounts of parent compound available for partitioning into the acetonitrile extract. The glucuronide conjugate (metabolite V) was the most prevalent biliary metabolite in both males (29.3%) and females (27.4%). Metabolite I (parent compound) was not detected in the bile. Each of the other biliary metabolites accounted for between 0.9% and 9.0% of the administered dose. In the bile-duct cannulated rats, about 15.1% and 13.6% of the faecal radioactivity was metabolite I (parent compound) in male and female rats, respectively. No parent compound was detected in the urine of bile-duct cannulated male and female rats. The predominant metabolite in the urine of the bile-duct cannulated rats was unidentified metabolite 2, which accounted for about 1.8% and 2.0% of the administered dose in male and female rats, respectively. There was no evidence for a dose-influencing metabolism, but a sex-specific difference in biotransformation was observed, with females producing more metabolites than did males. Biotransformation was unaffected by dose. The study authors suggested that absorption was dose-dependent. The oral absorption at 1 mg/kg bw was nearly complete (100%) since no parent compound was detected. The oral absorption at the higher dose (100 mg/kg bw) was estimated to be approximately 74-81% since about 19-26% of the parent compound was detected. However, it is difficult to estimate the true oral absorption value owing to poor recoveries after extraction, especially at the lower dose. ... There were two principal metabolic pathway: hydrolysis to the methoxyacid, followed by glucuronide conjugation to give metabolite V; and glutathione conjugation of the cyanophenyl ring followed by further metabolism via a number of intermediates (VI, VII, and VIII) to the mercapturic acid metabolite IX. Azoxystrobin was also hydroxylated at the 8 and 10 positions on the cyanophenyl ring followed by glucuronide conjugation (metabolites II, III, IVa and IVb). There were several minor pathways involving the acrylate moiety, resulting in formation of the metabolite XIII and XIV. Three metabolites (X, XII, and XV) arising via the cleavage of the ether linkages were identified.
WHO/FAO; Joint Meeting on Pesticide Residues Evaluation for Azoxystrobin (131860-33-8) p.6 (2008). Available from, as of December 27, 2011: https://www.inchem.org/pages/jmpr.html
The metabolic fate of [(14)C]-methyl-(E)-2-[2-[6-(2-cyanophenoxy)pyrimidin-4-yloxy]phenyl]-3-methoxyacrylate (azoxystrobin) was determined in the male and female rat following a single oral dose of 1 and 100 mg x kg(-1) and in surgically prepared, bile duct-cannulated rats following a single oral dose of 100 mg x kg(-1). 2. Azoxystrobin was extensively metabolized with at least 15 metabolites. There was a sex difference, with females producing more metabolites than males. 3. The two principal metabolic pathways were hydrolysis of the methoxyacid followed by glucuronic acid conjugation and glutathione conjugation of the cyanophenyl ring followed by further metabolism leading to the mercapturic acid. There were also several other minor pathways.
PMID:12851042 Laird WJ et al; Xenobiotica 33 (6): 677-90 (2003)
Mode of action: fungicide with protectant, eradicant, translaminar & systemic properties. Powerfully inhibits spore germination &, in addition to its ability to inhibit mycelial growth, also shows antisporulant activity. Acts by inhibiting mitochondrial respiration by blocking electron transfer between cytochrome b & cytochrome c1. Controls pathogenic strains resistant to the 14 demethylase inhibitors, phenylamides, dicarboxamides or benzimidazoles.
Tomlin, C.D.S. (ed.). The Pesticide Manual - World Compendium. 10th ed. Surrey, UK: The British Crop Protection Council, 1994., p. 579
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PharmaCompass offers a list of Azoxystrobin API manufacturers, exporters & distributors, which can be sorted by GMP, USDMF, JDMF, KDMF, CEP (COS), WC, Price,and more, enabling you to easily find the right Azoxystrobin manufacturer or Azoxystrobin supplier for your needs.
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A AZOXYSTROBIN [MI] manufacturer is defined as any person or entity involved in the manufacture, preparation, processing, compounding or propagation of AZOXYSTROBIN [MI], including repackagers and relabelers. The FDA regulates AZOXYSTROBIN [MI] manufacturers to ensure that their products comply with relevant laws and regulations and are safe and effective to use. AZOXYSTROBIN [MI] API Manufacturers are required to adhere to Good Manufacturing Practices (GMP) to ensure that their products are consistently manufactured to meet established quality criteria.
A AZOXYSTROBIN [MI] supplier is an individual or a company that provides AZOXYSTROBIN [MI] active pharmaceutical ingredient (API) or AZOXYSTROBIN [MI] finished formulations upon request. The AZOXYSTROBIN [MI] suppliers may include AZOXYSTROBIN [MI] API manufacturers, exporters, distributors and traders.
AZOXYSTROBIN [MI] Active pharmaceutical ingredient (API) is produced in GMP-certified manufacturing facility.
GMP stands for Good Manufacturing Practices, which is a system used in the pharmaceutical industry to make sure that goods are regularly produced and monitored in accordance with quality standards. The FDA’s current Good Manufacturing Practices requirements are referred to as cGMP or current GMP which indicates that the company follows the most recent GMP specifications. The World Health Organization (WHO) has its own set of GMP guidelines, called the WHO GMP. Different countries can also set their own guidelines for GMP like China (Chinese GMP) or the EU (EU GMP).
PharmaCompass offers a list of AZOXYSTROBIN [MI] GMP manufacturers, exporters & distributors, which can be sorted by USDMF, JDMF, KDMF, CEP (COS), WC, API price, and more, enabling you to easily find the right AZOXYSTROBIN [MI] GMP manufacturer or AZOXYSTROBIN [MI] GMP API supplier for your needs.
A AZOXYSTROBIN [MI] CoA (Certificate of Analysis) is a formal document that attests to AZOXYSTROBIN [MI]'s compliance with AZOXYSTROBIN [MI] specifications and serves as a tool for batch-level quality control.
AZOXYSTROBIN [MI] CoA mostly includes findings from lab analyses of a specific batch. For each AZOXYSTROBIN [MI] CoA document that a company creates, the USFDA specifies specific requirements, such as supplier information, material identification, transportation data, evidence of conformity and signature data.
AZOXYSTROBIN [MI] may be tested according to a variety of international standards, such as European Pharmacopoeia (AZOXYSTROBIN [MI] EP), AZOXYSTROBIN [MI] JP (Japanese Pharmacopeia) and the US Pharmacopoeia (AZOXYSTROBIN [MI] USP).
