Phenyl acetate targets tumor cells and induces differentiation, growth inhibition, and apoptosis. It is an aromatic fatty acid metabolite of phenylalanine. Its mechanism of action involves the induction of cellular differentiation and the inhibition of tumor cell proliferation. It is also used as adjunctive therapy for the prevention and treatment of hyperammonemia in patients with urea cycle enzymopathy.

In vitro, phenyl acetate induces differentiation, growth inhibition, and apoptosis in tumor cells. It has demonstrated potential antineoplastic activity in various cancer cell lines. Its activity is measured by assessing cell viability, proliferation, differentiation markers, and apoptosis in cultured tumor cells. It is used in cancer research to study the mechanisms of tumor cell differentiation and death.

In vivo, phenyl acetate is naturally occurring in mammals and has potential antineoplastic activity. It is used as adjunctive therapy for the prevention and treatment of hyperammonemia in the chronic management of patients with urea cycle enzymopathy. Its therapeutic effects are being investigated in the treatment of cancer.

In vitro enzyme assays with phenyl acetate typically involve studying its metabolism or its effects on cellular enzymes. As a metabolite of phenylalanine, it may be involved in pathways related to amino acid metabolism. Standard assays involve incubating the compound with enzyme preparations and analyzing products by chromatographic methods to characterize its metabolic fate and biological activity.

In vitro cell culture experiments with phenyl acetate involve treating tumor cell lines with the compound to study its antineoplastic effects. Cells are treated with various concentrations, and endpoints include assessment of cell viability (MTT assay), proliferation, apoptosis (Annexin V staining, caspase activity), and differentiation markers. These experiments characterize the compound's mechanism of action in cancer cells.

In vivo animal experiments with phenyl acetate typically involve using animal models of cancer or hyperammonemia. The compound is administered via oral gavage or injection, and key endpoints include tumor growth inhibition, survival rates, blood ammonia levels, and histopathological examination of tissues. These studies evaluate the therapeutic potential of phenyl acetate in cancer and metabolic disorders.

Metabolism / Metabolites
Phenylacetyl acetate is metabolized to phenol in humans, pigs, rabbits, and peas. This study used ion chromatography to quantify the hydrolysis rate and investigated the substrate specificity of carboxylesterases (CEs) in different respiratory tissues of F344/N rats, New Zealand white rabbits, and Syrian hamsters. Thirteen esters were tested: valeric acid, phenylacetic acid, and β-butyrolactone for interspecies comparisons. The rat liver S9 enzyme showed the highest catalytic activity, while the activity of the rabbit and hamster tracheal and nasal S9 enzymes was comparable to or higher than that of the liver. Except for valeric acid, the activity of all other tested substrates was higher than that of the liver. The esterase activity of the lung S9 enzyme was lower than that of other tissues. Straight-chain alcohol esters were hydrolyzed the fastest, while tertiary esters were hydrolyzed the slowest. … The substrate specificity of phosphotriester hydrolases and serine esterases for carboxyl esters was determined. Serum was collected from 452 subjects (including healthy individuals and patients with hyperlipidemia). The correlation between enzyme activity, reversible EDTA inhibition, and progressive inhibition by organophosphorus compounds and carbamates was investigated. Hydrolysis of paraoxonium (POX), phenylacetic acid (PA), and β-naphthylacetic acid (BNA) was studied. Results showed that two paraoxonases hydrolyze POX, one EDTA-sensitive and the other EDTA-insensitive. The EDTA-sensitive paraoxonase also hydrolyzes β-naphthylacetic acid. Hydrolysis of EDTA-insensitive β-naphthylacetic acid and phenylacetic acid was identified as serine esterase-catalyzed. EDTA-sensitive hydrolysis of phenylacetic acid may be catalyzed by multiple enzymes, including aryl esterases and carboxyl esterases. Esterases in human liver microsomes hydrolyze phenylacetic acid (Vmax 57 ± 8 μmol/min/g tissue), while esterases in human hepatocyte solutes hydrolyze phenylacetic acid (Vmax 37 ± 2.9 μmol/min/g tissue). …Human plasma esterases hydrolyze phenylacetic acid (Vmax 250 ± 17 μmol/min/mL). ...The hydrolysis of phenylacetic acid involves aryl esterases in plasma, aryl esterases and carboxylesterases in liver microsomes, and carboxylesterases in hepatocyte solutes. ...
For more complete metabolite/metabolite data on phenylacetic acid (6 metabolites in total), please visit the HSDB record page.

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The pharmacokinetic (PK) properties of phenyl acetate reflect its role as a metabolite and therapeutic agent. As a small aromatic ester (molecular weight 136.15), it is absorbed and distributed throughout the body. It is metabolized through pathways involving ester hydrolysis and conjugation. Its half-life and bioavailability would be determined in PK studies. It is soluble in DMSO.

Phenyl acetate has a moderate toxicity profile. It is handled as a research chemical with appropriate safety precautions. As a metabolite of phenylalanine, it is naturally occurring in mammals. However, at high concentrations, it may have adverse effects. Standard laboratory safety practices, including the use of gloves and eye protection, should be followed when handling this compound.

Phenolic acetate is a clear, colorless liquid with a sweet solvent odor and is non-flammable. It can be used as a laboratory reagent and in the production of certain organic chemicals. Phenolic acetate is an acetate ester formed by the condensation of phenol and acetic acid. It belongs to the phenylacetate class and benzene compounds, and is functionally related to phenol. Phenolic acetate has been reported to exist in Arabidopsis thaliana and Euglena, and relevant data are available. Phenolic acetate is an aromatic fatty acid metabolite of phenylalanine and has potential antitumor activity. Phenolic acetate is naturally present in mammals and can induce tumor cell differentiation, inhibit their growth, and induce apoptosis. Its mechanism of action includes reducing protein isopreneization, activating peroxisome proliferation-activating receptors, inhibiting DNA methylation, and consuming glutamine. (NCI04) Phenylacetate is a metabolite found or produced in Saccharomyces cerevisiae.

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Phenyl acetate (Acetic acid phenyl ester) is an aromatic fatty acid metabolite of phenylalanine with potential antineoplastic activity. It induces differentiation, growth inhibition, and apoptosis in tumor cells. It is being studied in the treatment of cancer and used as adjunctive therapy for hyperammonemia in urea cycle enzymopathy. The compound is not an approved drug but is available for research use.

C8H8O2

136.15

136.052

122-79-2

Phenyl acetate-d5;22705-26-6

31229

Colorless to light yellow liquid

1.073 g/mL at 25 °C(lit.)

196 °C(lit.)

-30 °C

170 °F

0.418mmHg at 25°C

n20/D 1.501(lit.)

1.611

0

2

2

10

114

0

CC(=O)OC1=CC=CC=C1

IPBVNPXQWQGGJP-UHFFFAOYSA-N

InChI=1S/C8H8O2/c1-7(9)10-8-5-3-2-4-6-8/h2-6H,1H3

phenyl acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 250 mg/mL (1836.21 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (15.28 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (15.28 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (15.28 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)