Absorption, Distribution and Excretion
The volume of distribution was about 1 mL/g, total body clearance was 0.27 mL/min and renal clearance was 0.19 mL/min. Approximately 64 72% of (14)C acetamide was excreted in the urine, while only 0.5 0.8% appeared in exhaled air during the first 6 hr after dosing. Thus, approximately 30% of the administered dose was not recovered and it was suggested that metabolized acetamide enters the acetate pool.
Less than 0.07% of the recovered urinary radioactivity in rats given 100 or 1000 mg/kg bw (14)C acetamide coeluted upon high performance liquid chromatography with an N-hydroxyacetamide standard and this hydroxamic acid could not be detected after incubation of acetamide with rat liver microsomes and NADPH or in primary cultures of rat hepatocytes. (14)C Acetamide does not bind covalently to proteins in the presence of rat liver microsomes and NADPH or cytosolic fraction, whereas hepatocyte cultures contained non extractable radioactivity. This association was inhibited by cycloheximide to the same extent as (14)C acetate incorporation into cellular proteins.

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Metabolism / Metabolites
Acetamide ... was found in small amt in human urine as metabolite of metronidazole.
Metabolism of metronidazole to acetamide was apparently mediated by intestinal flora.
Acetamide is carcinogenic in rats and mice. To clarify the mechanism of carcinogenesis by acetamide, we investigated DNA damage by andacetamide metabolite, acetohydroxamic acid (AHA), using 32P-5'-end-labeled DNA fragments. AHA treated with amidase induced DNA damage in the presence of Cu(II) and displayed a similar DNA cleavage pattern of hydroxylamine. DNA damage was inhibited by both catalase and bathocuproine, suggesting that H2O2 and Cu(I) are involved. Carboxy-PTIO, a specific scavenger of nitric oxide (NO), partially inhibited DNA damage. The amount of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) by amidase-treated AHA was similar to that by hydroxylamine. ESR spectrometry revealed that amidase-treated AHA as well as hydroxylamine generated NO in the presence of Cu(II). From these results, it has been suggested that AHA might be converted into hydroxylamine by amidase. These results suggest that metal-mediated DNA damage mediated by amidase-catalyzed hydroxylamine generation plays an important role in the carcinogenicity of acetamide.

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Biological Half-Life
The half life of radioactivity in blood after intravenous dosing of (14)C acetamide to rats averaged 20.6 + or - 0.3 hr after a 10 mg/kg bw dose and 16.1 + or - 1.6 hr after a 50 mg/kg bw dose.

Toxicity Summary
IDENTIFICATION AND USE: Acetamide is a solid. It is used as a solvent and stabilizer, accelerator in the estimation of bilirubin, antidote against monofluoroacetamide poisoning, and humectant for paper. HUMAN EXPOSURE AND TOXICITY: There are no data available. ANIMAL STUDIES: When acetamide was administered at a concentration of 5% in the diet to 99 male rats, with 2 rats returned to a control diet each week, liver tumors were found after treatment for 14-40 weeks in 22/81 rats. Acetamide-treated rats developed neoplastic nodules and hepatocellular carcinomas. The incidence, speed of onset, and frequency of metastases were greater in males than in females. Acetamide had the least toxic effects in regards to teratogenicity and embryotoxicity, compared to its derivatives. Acetamide produced morphological transformation in Syrian hamster embryo cells without metabolic activation. ECOTOXICITY STUDIES: Acetamide exhibited a selective damaging action on Entosiphon sulcatum.

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Toxicity Data
LC50 (rat) = 16,000 ppm

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Interactions
Two groups of 40 male wistar rats were fed diets containing 2.5% acetamide or 2.5% acetamide + 5.6 l-arginine, & 2 groups of 15 males were fed diet containing 5.6% arginine glutamate or a control diet for 1 yr. In 2/8 rats fed acetamide ... hepatomas ... were observed; 7/16 rats fed acetamide for 1 yr and maintained on control diet for further 3 MO developed liver tumors. In contrast, 1/11 rats that received acetamide + arginine glutamate for 1 yr and control diet for 3 MO had hyperplastic liver nodules. No liver tumors occurred in control group nor in rats fed 5.6% arginine glutamate alone.

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Non-Human Toxicity Values
LD50 Rat oral 7000 mg/kg
LD50 Rat ip 10,300 mg/kg
LD50 Rat sc 10,000 mg/kg
LD50 Rat iv 12,500 mg/kg
For more Non-Human Toxicity Values (Complete) data for ACETAMIDE (9 total), please visit the HSDB record page.

[1]. Acetamide. IARC Monogr Eval Carcinog Risks Hum. 1999;71 Pt 3:1211-21.

[2]. The food contaminant acetamide is not an in vivo clastogen, aneugen, or mutagen in rodent hematopoietic tissue. Regul Toxicol Pharmacol. 2019 Nov;108:104451.

[3]. Acetamide derivatives with antioxidant activity and potential anti-inflammatory activity. Molecules. 2010 Mar 23;15(3):2028-38.

Acetamide can cause cancer according to The World Health Organization's International Agency for Research on Cancer (IARC).
Acetamide appears as colorless crystals with a mousy odor (NTP, 1999). Low toxicity.
Acetamide is a member of the class of acetamides that results from the formal condensation of acetic acid with ammonia. It is a monocarboxylic acid amide, a N-acylammonia and a member of acetamides. It is a tautomer of an acetimidic acid.
Acetamide is used primarily as a solvent and a plasticizer. Workers may be exposed in the plastics and chemical industries. It causes mild skin irritation from acute (short-term) exposure. No information is available on the chronic (long-term), reproductive/developmental, or carcinogenic effects of acetamide in humans. EPA has not classified acetamide for carcinogenicity.
Acetamide has been reported in Convolvulus erinaceus, Haplophyllum acutifolium, and other organisms with data available.
Acetamide is a mineral with formula of CH3CONH2. The corresponding IMA (International Mineralogical Association) number is IMA1974-039. The IMA symbol is Ace.
Acetamide is found in red beetroot. Acetamide (or acetic acid amide or ethanamide), CH3CONH2, the amide of acetic acid, is a white crystalline solid in pure form. It is produced by dehydrating ammonium acetate. Acetamide has been shown to exhibit anti-microbial, anti-inflammatory, anti-arthritic and antibiotic functions. Acetamide belongs to the family of Primary Carboxylic Acid Amides. These are compounds comprising primary carboxylic acid amide functional group, with the general structure RC(=O)NH2. (A3310, A3311, A3311, A3312).
Acetamide is a metabolite found in or produced by Saccharomyces cerevisiae.

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Therapeutic Uses
/EXPL THER/ /The study objective was/ to observe the effect of fluoroacetamide on cardiomyocytes of rat and the antidotal effect of acetamide. Four groups of SD rats were treated with various dosages of fluoroacetamid (p.o.) and 2 groups of them were treated with acetamide (i.p.). The changes of cardiomyocytes and serum AST, LDH, CK, CK-MB and HBDH were measured at different intervals after poisoning. In the group treated with fluoroacetamid 8 mg/kg. bw, serum AST[(589.58 +/- 821.72) U/L], CK[(916.78 +/- 343.55) U/L], HBDH[(504.47 +/- 148.88) U/L] raised obviously compared with control[(187.70 +/- 46.87), (755.65 +/- 498.90), (347.25 +/- 228.40) U/L respectively] (p<0.01), and the pathological findings such as degeneration, liquefactive necrosis and filtration of inflammatory cells in cardiac muscles were observed 24 hours later, while all the male dead within 3 days. In the group treated with fluoroacetamid 4 mg/kg. bw, serum LDH and HBDH rose significantly compared with control (p<0.01) 5 day later. On the day of 10, myocardial enzymes restored in all experiment groups with some interstitial fibroblastic proliferation. The pathological changes were reduced in the group treated with acetamide synchronously (100 mg/kg. bw). Acute intoxication of fluoroacetamide could damage cardiomyocytes while acetamide could reduce the injury of them, but the injury was reversible. ...
/EXPL THER/ /The study objective was/ to investigate the effects of acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid, GABA) and excitatory amino acid (glutamate, Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning. Eighty Sprague-Dawley rats (SPF) were randomly divided into five groups, with 16 rats in each group: saline control group, dimethyl sulfoxide (DMSO) control group, TET exposure group, high-dose (2.8 g/kg/d) acetamide treatment group, and super-high-dose (5.6 g/kg/d) acetamide treatment group. Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting, and were then intramuscularly injected with saline or different doses of acetamide in the following 5 days. The cortex of the temporal lobe was collected at 3 hr, 12 hr, 48 hr, or 7 d after treatment. The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry. ... The OD value of GABA in TET exposure group started to increase at 12 hr after treatment, reached the peak at 48 hr, and decreased to the normal level at 7 d. In the high-dose acetamide treatment group, the increase in OD at 12 hr was not so significant as that in the TET exposure group, OD value decreased to the normal level at 48 hr and was lower than that in the exposure group, and the changes were more like those in the control groups. In the super-high-dose acetamide treatment group, OD value began to increase significantly at 3 hr and was significantly higher than that in the TET exposure group (p<0.01), it reached the peak at 12 hr, and was restored to the normal value at 48 hr. ... The OD value of Glu in TET exposure group at 3 hr after treatment was significantly lower than those in the two control groups, it increased gradually from 12 hr to 48 hr, and recovered to the normal level at the 7th d. The changes in the high-dose acetamide treatment group were similar to those in the TET exposure group, but became more like those in the control groups after 48 hr; the OD value in super-high-dose acetamide treatment group was significantly higher than that in the TET exposure group at 3 hr after treatment (p<0.01), while no significant difference was found at 12 hr; it was significantly lower than those of all other groups at 48 hr and 7 d (p<0.01). Treatment with high dose of acetamide has some curative effect on TET poisoning-induced central nervous lesion, while the effect of super-high-dose acetamide on expression of neurotransmitters is too complex to evaluate.

C2H5NO

59.0672

59.037

60-35-5

Acetamide-15N;1449-72-5;Acetamide-d5;33675-83-1

178

White to off-white solid powder

1.0±0.1 g/cm3

78.4±23.0 °C at 760 mmHg

78-80 °C(lit.)

1.2±22.6 °C

62.4±0.3 mmHg at 25°C

1.418

-0.91

1

1

0

4

33

0

DLFVBJFMPXGRIB-UHFFFAOYSA-N

InChI=1S/C2H5NO/c1-2(3)4/h1H3,(H2,3,4)

acetamide

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)

H2O : ~50 mg/mL (~846.45 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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