In WB-F344 cells, thioacetamide (TAA; 0–10,000 μM; 24 h) exhibits concentration-dependent cytotoxicity[4]. In the early stages, at low (1000 μM) and high (10000 μM) concentrations, thioacetamide (TAA; 1000 and 10000 μM; 0-24 h; WB-F344 cells) contains differentially-expressed genes[4].

In male ICR mice, thioacetamide (TAA; 100 mg/kg; i.p., three times per week) can cause chronic liver fibrosis[2]. In C57BL/6 mice, thioacetamide (200–1200 mg/kg; intraperitoneal; once) causes a hepatic encephalopathy model [3].

Cell Viability Assay[4]
Cell Types: WB-F344 cells
Tested Concentrations: 0-10000 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: Had 20% and 50% cell death at the 1000 and 10000 μM concentrations, respectively.

Animal/Disease Models: Male ICR mice[2]
Doses: 100 mg/kg
Route of Administration: intraperitoneal (ip)injection; three times weekly for eight weeks
Experimental Results: Induced chronic liver fibrosis in male ICR mice and resulted in lower body weight, serum cholesterol and triglycerides as well as increased liver size, ALT, AST and LDH values.

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Animal/Disease Models: Male C57BL/6 mice (20-25g, aged 8-12 weeks )[3]
Doses: 200, 600, and 1,200 mg/kg
Route of Administration: intraperitoneal (ip)injection; once
Experimental Results: Altered the neuropsychiatric state, motor behavior and reflex and sensory functions. Increased in the glutamate release in the cerebral cortex of Hepatic encephalopathy (HE ) mice.

Absorption, Distribution and Excretion
WHEN 5 MG (3)H-THIOACETAMIDE WERE ADMIN ORALLY IN DIET TO MALE ALBINO RATS... RADIOACTIVITY WAS FOUND IN ALL ORGANS EXAMINED (LIVER, KIDNEY & ADRENAL GLAND) & WAS HIGHEST IN LIVER.
WHOLE-BODY AUTORADIOGRAPHY SHOWED THAT AN IV DOSE OF ANTITHYROID AGENT, (35)S-THIOACETAMIDE, WAS TAKEN UP IN LIVER, KIDNEYS (MEDULLA), HEART MUSCLE, HARDERIAN GLANDS, SPLEEN, LYMPH NODES, & GI TRACT OF RATS. ABOUT 80% WAS EXCRETED IN 24-HR URINE.
THE DISTRIBUTION OF LABELED THIOACETAMIDE WAS STUDIED AS A FUNCTION OF TIME IN LIVER, KIDNEYS, PLASMA, AND MUSCLE OF RATS. THE DEVELOPMENT OF CENTRILOBULAR HEPATIC NECROSIS WAS FIRST OBSERVED 6 HOURS AFTER PEAK PLASMA LEVELS OF THIOACETAMIDE-S-OXIDE WERE OBTAINED (9 HOURS AFTER ADMINISTRATION OF THIOACETAMIDE).

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Metabolism / Metabolites
...THIOACETAMIDE IS METABOLIZED IN VIVO TO ACETAMIDE WHICH IS ITSELF CARCINOGENIC...ACETAMIDE IS THEN HYDROLYZED TO ACETATE...
THIOACETAMIDE, A PRE- OR PROCARCINOGEN, MUST UNDERGO BIOCHEMICAL METABOLIC ACTIVATION BY HOST. /FROM TABLE/
HEPATOTOXICITY OF THIOACETAMIDE MAY BE MEDIATED BY ITS METAB TO THIOACETAMIDE SULFINE WHICH IN TURN, IS METABOLIZED TO AN ULTIMATE TOXIC METABOLITE.
THIOACETAMIDE IS OXIDIZED TO THIOACETAMIDE S-OXIDE BY RAT LIVER MICROSOMES & BY A MIXED-FUNCTION OXIDASE SYSTEM.
For more Metabolism/Metabolites (Complete) data for THIOACETAMIDE (9 total), please visit the HSDB record page.

[1]. Standard operating procedures in experimental liver research: thioacetamide model in mice and rats. Lab Anim. 2015 Apr;49(1 Suppl):21-9.

[2]. Hepatoprotection of silymarin against thioacetamide-induced chronic liver fibrosis. J Sci Food Agric. 2012 May;92(7):1441-7.

[3]. A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study. Arq Neuropsiquiatr. 2010 Aug;68(4):597-602.

[4]. Expression analysis of early response-related genes in rat liver epithelial cells exposed to thioacetamide in vitro. J Vet Med Sci. 2009 Jun;71(6):719-27.

Thioacetamide can cause cancer according to an independent committee of scientific and health experts.
Thioacetamide appears as white crystals with a mercaptan odor.
Thioacetamide is a thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur. It has a role as a hepatotoxic agent. It is functionally related to an acetamide.
Thioacetamide is a synthetic, colorless crystalline solid that is soluble in water and ethanol. Thioacetamide is currently only used as a replacement for hydrogen sulfide in qualitative analysis. When heated to decomposition, it emits toxic fumes of nitrogen oxides and sulfur oxides. The primary routes of potential human exposure to thioacetamide are inhalation and dermal contact. It is reasonably anticipated to be a human carcinogen. (NCI05)
A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.

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Mechanism of Action
Multiple injections of thioacetamide ... decrease the synthesis of cytochrome p450b and the amounts of its translatable mRNA.
A factor was isolated from /thioacetamide-induced/ fibrogenic rat liver which stimulates collagen synthesis in cultured fibrolblasts without affecting their rate of proliferation.
Altered transport of nuclear RNA sequences is an early response to carcinogens. Nuclear envelopes were isolated and assayed for nucleoside triphosphatase (NTPase) activity, on the premise that this enzymatic activity participates in RNA transport. A common feature of the action of ... thioacetamide ... at low doses without significant toxicity, was to increase nuclear envelopes NTPase activity and to increase RNA transport, as assessed by the appearance of rapiidly labeled RNA in the cytoplasm and by in vitro assay. The increases in NTPase were specific for the nuclear envelope fraction, and early toxic effects of higher doses initially masked the increases. The induced increases in nuclear envelope NTPase were long-lived. In contrast, increases in nuclear envelope NTPase were observed only during the regenerative phase of carbon tetrachloride intoxication; the CCl4-induced increase was short-lived and returned promptly to control levels. These changes in NTPase activity were not associated with parallel changes in phosphorylation/dephosphorylation of nuclear envelope proteins. Increases in nuclear envelope NTPase and alterations in RNA transport, without attendant nuclear replication, may relate to altered nuclear RNA restriction. This change in a regulatory phenomenon may make these cells more susceptible to further modification, potentially playing a role in the initiation phase of carcinogenesis.

C2H5NS

75.13

75.014

62-55-5

2723949

White to off-white solid powder

1.1±0.1 g/cm3

45.3±23.0 °C at 760 mmHg

108-112 °C(lit.)

-18.8±22.6 °C

363.9±0.1 mmHg at 25°C

1.522

0.12

1

1

0

4

33

0

YUKQRDCYNOVPGJ-UHFFFAOYSA-N

InChI=1S/C2H5NS/c1-2(3)4/h1H3,(H2,3,4)

ethanethioamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

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 (1331.03 mM)
H2O : 50 mg/mL (665.51 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (33.28 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 25.0 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: ≥ 2.5 mg/mL (33.28 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 25.0 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: ≥ 2.5 mg/mL (33.28 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 25.0 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.)