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1. Phenylacetate
2. Phenylacetic Acid, Ammonium Salt
3. Phenylacetic Acid, Calcium Salt
4. Phenylacetic Acid, Cesium Salt
5. Phenylacetic Acid, Lithium Salt
6. Phenylacetic Acid, Mercury Salt
7. Phenylacetic Acid, Potassium Salt
8. Phenylacetic Acid, Rubidium Salt
9. Phenylacetic Acid, Sodium Salt
10. Phenylacetic Acid, Sodium Salt , Carboxy-(11)c-labeled Cpd
11. Sodium Phenylacetate
1. 2-phenylacetic Acid
2. Benzeneacetic Acid
3. 103-82-2
4. Phenylethanoic Acid
5. Alpha-toluic Acid
6. Acetic Acid, Phenyl-
7. Phenylacetate
8. Benzenacetic Acid
9. Benzylformic Acid
10. Phenyllacetic Acid
11. Benzylcarboxylic Acid
12. Phenyl Acetic Acid
13. Kyselina Fenyloctova
14. Phenylacetic Acid (natural)
15. .alpha.-toluic Acid
16. Kyselina Fenyloctova [czech]
17. Omega-phenylacetic Acid
18. Fema No. 2878
19. .omega.-phenylacetic Acid
20. Nsc 125718
21. Brn 1099647
22. Chebi:30745
23. Ai3-08920
24. Phenyl-acetic Acid
25. Chembl1044
26. Er5i1w795a
27. Benzeneacetate
28. Mfcd00004313
29. Nsc125718
30. Nsc-125718
31. Ncgc00159477-02
32. 51146-16-8
33. Dsstox_cid_1656
34. Dsstox_rid_76268
35. Dsstox_gsid_21656
36. 1173020-54-6
37. 17303-65-0
38. Cas-103-82-2
39. Hsdb 5010
40. Einecs 203-148-6
41. Unii-er5i1w795a
42. Phenylacetic
43. Phenylethanoate
44. Phenylessigsaure
45. W-phenylacetate
46. Alpha-toluate
47. Phenylactic Acid
48. A-toluate
49. A-toluic Acid
50. Benzeneacetiic Acid
51. Omega-phenylacetate
52. Organic White Solid
53. W-phenylacetic Acid
54. Phenylacetate, Xix
55. 2-phenyl-acetic Acid
56. Phenylacetic Acid, 99%
57. Bmse000220
58. Epitope Id:116202
59. Ec 203-148-6
60. Schembl1459
61. 4-09-00-01614 (beilstein Handbook Reference)
62. Phenyl-[13c6]-acetic Acid
63. Phenylacetic Acid [mi]
64. Phenylacetic Acid [fcc]
65. Dtxsid2021656
66. Phenylacetic Acid [fhfi]
67. Phenylacetic Acid [hsdb]
68. Bdbm16419
69. Zinc388462
70. Phenylacetic Acid_gurudeebansatyavani
71. Tox21_113042
72. Tox21_200533
73. Nsc139637
74. Phenylacetic Acid, Natural, >=99%
75. Stk297835
76. Phenylacetic Acid, Analytical Standard
77. Akos000291351
78. Tox21_113042_1
79. Db09269
80. Dl-0063
81. Nsc-139637
82. Phenylacetic Acid, >=99%, Fcc, Fg
83. Ncgc00159477-03
84. Ncgc00159477-05
85. Ncgc00258087-01
86. Bp-11383
87. Nci60_000596
88. Nci60_002571
89. Phenylacetic Acid, Natural, >=99%, Fg
90. Astugenal Component Phenylacetic Acid
91. Db-003759
92. Db-055176
93. Ft-0641197
94. Ft-0701063
95. Phenylacetic Acid, Plant Cell Culture Tested
96. Tropicamide Impurity D [ep Impurity]
97. C07086
98. Tropicamide Related Compound D [usp-rs]
99. Q410842
100. Tropicamide Related Compound D [usp Impurity]
101. Antineoplaston As 2-1 Component Phenylacetic Acid
102. Antineoplaston As2-1 Component Phenylacetic Acid
103. Benzylpenicillin Sodium Impurity B [ep Impurity]
104. Benzylpenicillin Potassium Impurity B [ep Impurity]
105. Procaine Benzylpenicillin Impurity E [ep Impurity]
106. 8727557e-aa75-49e9-8e5a-7a2412d71888
107. Tropicamide Related Compound D, United States Pharmacopeia (usp) Reference Standard
108. Tropicamide Impurity D (phenylacetic Acid - Drug Precursor), European Pharmacopoeia (ep) Reference Standard
Molecular Weight | 136.15 g/mol |
---|---|
Molecular Formula | C8H8O2 |
XLogP3 | 1.4 |
Hydrogen Bond Donor Count | 1 |
Hydrogen Bond Acceptor Count | 2 |
Rotatable Bond Count | 2 |
Exact Mass | 136.052429494 g/mol |
Monoisotopic Mass | 136.052429494 g/mol |
Topological Polar Surface Area | 37.3 Ų |
Heavy Atom Count | 10 |
Formal Charge | 0 |
Complexity | 114 |
Isotope Atom Count | 0 |
Defined Atom Stereocenter Count | 0 |
Undefined Atom Stereocenter Count | 0 |
Defined Bond Stereocenter Count | 0 |
Undefined Bond Stereocenter Count | 0 |
Covalently Bonded Unit Count | 1 |
For use as adjunctive therapy for the treatment of acute hyperammonemia and associated encephalopathy in patients with deficiencies in enzymes of the urea cycle.
Antimetabolites, Antineoplastic
Antimetabolites that are useful in cancer chemotherapy. (See all compounds classified as Antimetabolites, Antineoplastic.)
Volume of Distribution
19.2 3.3 L.
... Although exhaled volatile organic compound (VOC) patterns change in obstructive sleep apnea (OSA) patients, individual VOC profiles are not fully determined. The primary outcome was VOC characterizations; secondary outcomes included their relationships with sleep and clinical parameters in OSA patients. We prospectively examined 32 OSA patients with an apnea-hypopnea index (AHI) >/= 15 by full polysomnography, and 33 age- and sex-matched controls without obvious OSA symptoms. Nine severe OSA patients were examined before and after continuous positive airway pressure (CPAP) treatment. By applying a method which eliminates environmental VOC influences, exhaled VOCs were identified by gas chromatography (GC)-mass spectrometry, and their concentrations were determined by GC. Exhaled aromatic hydrocarbon concentrations (toluene, ethylbenzene, p-xylene, and phenylacetic acid) in the severe OSA groups (AHI >/= 30) and exhaled saturated hydrocarbon concentrations (hexane, heptane, octane, nonane, and decane) in the most severe OSA group (AHI >/= 60) were higher than those in the control group. Exhaled isoprene concentrations were increased in all OSA groups (AHI >/= 15); acetone concentration was increased in the most severe OSA group. Ethylbenzene, p-xylene, phenylacetic acid, and nonane concentrations were increased according to OSA severity, and correlated with AHI, arousal index, and duration of percutaneous oxygen saturation (SpO2) = 90%. Multiple regression analyses revealed these 4 VOC levels were associated with the duration of SpO2 = 90%. Isoprene and acetone decreased after CPAP treatment. OSA increased some toxic VOCs, and some correlated with OSA severity. CPAP treatment possibly ameliorates these productions.
PMID:28003437 Aoki T et al; Toxicol Sci 156 (2): 362-374 (2017)
The dose limiting toxicity and pharmacokinetics of phenylacetic acid (phenylacetate) were studied in 17 patients with advanced solid tumors who received single iv bolus doses followed by a 14 day continuous iv infusion of the drug in a phase I trial. Phenylacetic acid displayed nonlinear pharmacokinetics with evidence for induction of drug clearance. Ninety-nine percent of phenylacetic acid elimination was accounted for by conversion to phenylacetylglutamine which was excreted in the urine...
PMID:8137283 Thibault A et al; Cancer Res 54: 1690-94 (1994)
Phenylacetic acid... /is/ rapidly absorbed from human buccal tissues or membranes.
National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 754
Man excreted 93%...as glutamine conjugate... . New world monkeys excreted conjugates of glutamine, glycine and taurine, while old world species excreted large proportion of free acid and only glutamine and taurine conjugates. Non-primate species excreted only glycine connjugate.
The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 569
Distribution of conjugates in 24 hr urine samples showed marked species variation.
The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 569
Phenylacetate esterases found in the human liver cytosol. Human plasma esterase also hydrolyze phenylacetate. Phenylacetate hydrolysis involved arylesterase in plasma, both arylesterase and carboxylesterase in liver microsomes and carboxylesterase in liver cytosol. Plasma hydrolysis is less important and overall esterase activity is lower in humans than in the rat.
Although there has been increasing interest in the use of high protein diets, little is known about dietary protein related changes in the mammalian metabolome. We investigated the influence of protein intake on selected tryptophan and phenolic compounds, derived from both endogenous and colonic microbial metabolism. Furthermore, potential inter-species metabolic differences were studied. For this purpose, 29 healthy subjects were allocated to a high (n = 14) or low protein diet (n = 15) for 2 weeks. In addition, 20 wild-type FVB mice were randomized to a high protein or control diet for 21 days. Plasma and urine samples were analyzed with liquid chromatography-mass spectrometry for measurement of tryptophan and phenolic metabolites. In human subjects, we observed significant changes in plasma level and urinary excretion of indoxyl sulfate (P 0.004 and P 0.001), and in urinary excretion of indoxyl glucuronide (P 0.01), kynurenic acid (P 0.006) and quinolinic acid (P 0.02). In mice, significant differences were noted in plasma tryptophan (P 0.03), indole-3-acetic acid (P 0.02), p-cresyl glucuronide (P 0.03), phenyl sulfate (P 0.004) and phenylacetic acid (P 0.01). Thus, dietary protein intake affects plasma levels and generation of various mammalian metabolites, suggesting an influence on both endogenous and colonic microbial metabolism. Metabolite changes are dissimilar between human subjects and mice, pointing to inter-species metabolic differences with respect to protein intake.
PMID:26469515 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4607412 Poesen R et al; PLoS One 10 (10): e0140820 (2015)
Burkholderia heleia PAK1-2 is a potent biocontrol agent isolated from rice rhizosphere, as it prevents bacterial rice seedling blight disease caused by Burkholderia plantarii. Here, we isolated a non-antibacterial metabolite from the culture fluid of B. heleia PAK1-2 that was able to suppress B. plantarii virulence and subsequently identified as indole-3-acetic acid (IAA). IAA suppressed the production of tropolone in B. plantarii in a dose-dependent manner without any antibacterial and quorum quenching activity, suggesting that IAA inhibited steps of tropolone biosynthesis. Consistent with this, supplementing cultures of B. plantarii with either L-[ring-(2)H5]phenylalanine or [ring-(2)H2~5]phenylacetic acid revealed that phenylacetic acid (PAA), which is the dominant metabolite during the early growth stage, is a direct precursor of tropolone. Exposure of B. plantarii to IAA suppressed production of both PAA and tropolone. These data particularly showed that IAA produced by B. heleia PAK1-2 disrupts tropolone production during bioconversion of PAA to tropolone via the ring-rearrangement on the phenyl group of the precursor to attenuate the virulence of B. plantarii. B. heleia PAK1-2 is thus likely a microbial community coordinating bacterium in rhizosphere ecosystems, which never eliminates phytopathogens but only represses production of phytotoxins or bacteriocidal substances.
PMID:26935539 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776283 Wang M et al; Sci Rep 6: 22596 doi: 10.1038/srep22596 (2016)
2-phenylethylamine is an endogenous constituent of the human brain and is implicated in cerebral transmission. This bioactive amine is also present in certain foodstuffs such as chocolate, cheese and wine and may cause undesirable side effects in susceptible individuals. Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalyzed by monoamine oxidase B but the oxidation to its acid is usually ascribed to aldehyde dehydrogenase and the contribution of aldehyde oxidase and xanthine oxidase, if any, is ignored. The objective of this study was to elucidate the role of the molybdenum hydroxylases, aldehyde oxidase and xanthine oxidase, in the metabolism of phenylacetaldehyde derived from its parent biogenic amine. Treatments of 2-phenylethylamine with monoamine oxidase were carried out for the production of phenylacetaldehyde, as well as treatments of synthetic or enzymatic-generated phenylacetaldehyde with aldehyde oxidase, xanthine oxidase and aldehyde dehydrogenase. The results indicated that phenylacetaldehyde is metabolized mainly to phenylacetic acid with lower concentrations of 2-phenylethanol by all three oxidizing enzymes. Aldehyde dehydrogenase was the predominant enzyme involved in phenylacetaldehyde oxidation and thus it has a major role in 2-phenylethylamine metabolism with aldehyde oxidase playing a less prominent role. Xanthine oxidase does not contribute to the oxidation of phenylacetaldehyde due to low amounts being present in guinea pig. Thus aldehyde dehydrogenase is not the only enzyme oxidizing xenobiotic and endobiotic aldehydes and the role of aldehyde oxidase in such reactions should not be ignored.
Panoutsopoulos GI et al; Basic Clin Pharmacol Toxicol 95 (6): 273-9 (2004)
Phenylacetic acid, the major metabolite of phenylethylamine, has been identified and quantitated in rat brain regions by capillary column high-resolution gas chromatography mass spectrometry. Its distribution is heterogeneous and correlates with that of phenylethylamine. The values obtained were (ng/g +/- SEM): whole brain, 31.2 +/- 2.7; caudate nucleus, 64.6 +/- 6.5; hypothalamus, 60.1 +/- 7.4; cerebellum, 31.3 +/- 2.9; brainstem, 33.1 +/- 3.3, and the "rest," 27.6 +/- 3.0.
PMID:7077324 Durden DA, Boulton AA; J Neurochem 38 (6): 1532-6 (1982)
For more Metabolism/Metabolites (Complete) data for Phenylacetic acid (9 total), please visit the HSDB record page.
2-Phenylacetic acid is a known human metabolite of 3-hydroxyphenylacetic acid and 4-hydroxyphenylacetic acid.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560