A bacterial reverse mutation assay (Ames test) was conducted using Salmonella typhimurium tester strains TA98, TA100, TA1535, TA1537 and Escherichia coli strain WP2 uvrA.
The test substance Aceturic acid was dissolved in water and tested at a maximum dose of 5000 μg per plate, both in the presence and absence of Aroclor-induced rat liver S9 metabolic activation.
Positive controls included 2-nitrofluorene, sodium azide, 9-aminoacridine, methyl methanesulphonate, and 2-aminoanthracene. Sterile distilled water served as the negative control.
No evidence of mutagenicity was observed at any dose level (ranging from 333 to 5000 μg/plate) with any bacterial strain, with or without S9 activation. Positive controls responded as expected except for 2-aminoanthracene in strain TA100 with S9, which required a doubled concentration (2.0 μg/plate) to produce proper responses. [1]

Bone marrow micronucleus (BMM) assay in mice:
ICR (Crl:CD1) mice (6-8 weeks old, 5 males and 5 females per group) were used. The test substance was administered as a single oral dose at 500, 1000, or 2000 mg/kg body weight. Negative control received 0.5% methylcellulose in purified deionized water. Positive control received cyclophosphamide monohydrate at 50 mg/kg body weight. Mice were euthanized 24 hours after treatment. Additional groups were dosed with water or 2000 mg/kg of Aceturic acid and sacrificed 48 hours after treatment. Femoral bone marrow was collected, and smears were stained with May-Gruenwald-Giemsa stain. Polychromatic erythrocytes (PCEs) were examined microscopically for micronuclei (micronucleated PCEs, MPCEs). [1]
Acute oral toxicity study in rats:
Male and female Crl:CD Sprague-Dawley rats (n=5/sex/group) received a single oral gavage dose of Aceturic acid dissolved in 0.5% methylcellulose at the OECD limit dose of 2000 mg/kg body weight. Control groups received water or glycine at 2000 mg/kg body weight. Animals were observed for 14 days. [1]
Repeated dose (28-day) dietary toxicity study in rats:
Sprague-Dawley rats (10 per sex per group) were fed diets containing Aceturic acid at targeted doses of 100, 500, or 1000 mg/kg body weight/day for 28 days. A glycine control group received 1000 mg/kg body weight/day. Dietary concentrations were adjusted weekly based on mean male body weights and historical mean feed consumption (approx. 28 g/rat/day). Diets were prepared on study days -2, 6, 13, and 20, stored frozen (≤20°C), and used within 7 days. Female rats received the same diet concentrations as males, resulting in slightly higher actual doses. Clinical observations, body weights, feed consumption, functional observational battery, motor activity, hematology, coagulation, serum chemistry, and anatomic pathology were assessed. [1]

---

Bone marrow micronucleus (BMM) assay in mice:
ICR (Crl:CD1) mice (6-8 weeks old, 5 males and 5 females per group) were used. The test substance was administered as a single oral dose at 500, 1000, or 2000 mg/kg body weight. Negative control received 0.5% methylcellulose in purified deionized water. Positive control received cyclophosphamide monohydrate at 50 mg/kg body weight. Mice were euthanized 24 hours after treatment. Additional groups were dosed with water or 2000 mg/kg of Aceturic acid and sacrificed 48 hours after treatment. Femoral bone marrow was collected, and smears were stained with May-Gruenwald-Giemsa stain. Polychromatic erythrocytes (PCEs) were examined microscopically for micronuclei (micronucleated PCEs, MPCEs). [1]
Acute oral toxicity study in rats:
Male and female Crl:CD Sprague-Dawley rats (n=5/sex/group) received a single oral gavage dose of Aceturic acid dissolved in 0.5% methylcellulose at the OECD limit dose of 2000 mg/kg body weight. Control groups received water or glycine at 2000 mg/kg body weight. Animals were observed for 14 days. [1]
Repeated dose (28-day) dietary toxicity study in rats:
Sprague-Dawley rats (10 per sex per group) were fed diets containing Aceturic acid at targeted doses of 100, 500, or 1000 mg/kg body weight/day for 28 days. A glycine control group received 1000 mg/kg body weight/day. Dietary concentrations were adjusted weekly based on mean male body weights and historical mean feed consumption (approx. 28 g/rat/day). Diets were prepared on study days -2, 6, 13, and 20, stored frozen (≤20°C), and used within 7 days. Female rats received the same diet concentrations as males, resulting in slightly higher actual doses. Clinical observations, body weights, feed consumption, functional observational battery, motor activity, hematology, coagulation, serum chemistry, and anatomic pathology were assessed. [1]

Genotoxicity: No evidence of mutagenicity was observed in the bacterial reverse mutation assay (Ames test) with Aceturic acid up to 5000 μg/plate, with or without S9 metabolic activation. [1]
In vivo genotoxicity: In the mouse bone marrow micronucleus assay, no increase in the incidence of micronucleated polychromatic erythrocytes (MPCEs) was observed at 24 or 48 hours following treatment with Aceturic acid at doses of 500, 1000, or 2000 mg/kg body weight. Cyclophosphamide (positive control) produced a significant increase. All mice survived and appeared normal. [1]
Acute oral toxicity: No mortalities or adverse clinical signs were observed in Sprague-Dawley rats following a single oral gavage dose of Aceturic acid at 2000 mg/kg body weight over 14 days. All animals gained weight, and no gross lesions were found in any organs. The acute LD50 is greater than 2000 mg/kg body weight. [1]
Repeated dose (28-day) dietary toxicity: No adverse clinical effects, mortality, or differences in body weight, feed consumption, behavioral responses, or motor activity were observed in rats receiving up to 1000 mg/kg/day (targeted) of Aceturic acid. No biologically significant or test substance-related differences were observed in hematology, coagulation, or serum chemistry variables. The no-observed-adverse-effect-level (NOAEL) for systemic toxicity from dietary exposure to Aceturic acid was determined to be 898.9 mg/kg body weight/day for male rats and 989.9 mg/kg body weight/day for female rats (based on actual mean consumption). [1]

[1]. Toxicology studies with N-acetylglycine. Food Chem Toxicol. 2010 May;48(5):1321-7.

N-acetylglycine is an N-acylglycine, where the acyl group is specifically defined as an acetyl group. It is a human metabolite. It is an N-acetyl amino acid and an N-acylglycine. It is the conjugate acid of N-acetylglycine. N-acetylglycine has been reported to exist in fruit flies, Candida tropicalis, and other organisms with relevant data.

---

Aceturic acid (N-acetylglycine) has been identified as a minor constituent of numerous foods at concentrations ranging from 0.01327 μg/g to 13.65 μg/g. It is a naturally occurring N-acetylated amino acid found in proteins such as cytochrome c, hemoglobin, and ovalbumin. Enzymatic hydrolysis of N-acetylated amino acids into constituent amino acids occurs via aminoacylases present in various tissues including liver, kidney, and brain. No prior toxicology studies had been reported for this substance. The studies were conducted in accordance with Good Laboratory Practice guidelines. [1]

C4H7NO3

117.1033

117.042

543-24-8

N-Acetylglycine-d5;1219805-82-9

10972

White to off-white solid powder

1.2±0.1 g/cm3

405.1±28.0 °C at 760 mmHg

207-209 °C(lit.)

198.8±24.0 °C

0.0±2.0 mmHg at 25°C

1.454

-1.41

2

3

2

8

110

0

OKJIRPAQVSHGFK-UHFFFAOYSA-N

InChI=1S/C4H7NO3/c1-3(6)5-2-4(7)8/h2H2,1H3,(H,5,6)(H,7,8)

2-acetamidoacetic acid

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 : ~100 mg/mL (~853.97 mM)
H2O : ~50 mg/mL (~426.99 mM)

Solubility in Formulation 1: 16.67 mg/mL (142.36 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

---

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