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Thioacetamide


CAS No. : 62-55-5

(Synonyms: Acetothioamide; TAA; Thiacetamide)

62-55-5
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Cat. No. : HY-Y0698
M.Wt: 75.13
Formula: C2H5NS
Purity: >98 %
Solubility: DMSO : 100 mg/mL (ultrasonic);H2O : 50 mg/mL (ultrasonic)
Introduction of 62-55-5 :

Thioacetamide (TAA) is an indirect hepatotoxin and causes parenchymal cell necrosis. Thioacetamide requires metabolic activation by microsomal CYP2E1 to thioacetamide-S-oxide initially and then to thioacetamide-S-dioxide, which is a highly reactive metabolite, and its reactive metabolites covalently bind to proteins and lipids thereby causing oxidative stress and centrilobular necrosis. Thioacetamide can induce chronic liver fibrosis, encephalopathy and other events model[1][2][3][4]. In Vitro:Thioacetamide (TAA; 0-10000 μM; 24 h; WB-F344 cells) has cytotoxicity in a concentration-dependent manner[4].
Thioacetamide (TAA; 1000 and 10000 μM; 0-24 h; WB-F344 cells) has differentially-expressed genes in the early phases at low (1000 μM) and high (10000 μM) concentrations[4].
In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Thioacetamide can be used in animal modeling to create hepatic tumor and liver fibrosis models. As the dose of Thioacetamide increases, the half-life increases linearly, and the bioactivity of Thioacetamide in rats is characterized by zero-order or saturation kinetics[5][6].

1. Inducing liver tumors[5]
Background
Thioacetamide causes malignant transformation of hepatocytes by inducing DNA damage, cytotoxicity and inflammatory responses.
Specific Modeling Methods
Rat: Adult males • 180-200 g
Administration: 200 mg/kg • intraperitoneal injection • twice a week for 16 weeks
Note
(1) Prepared by dissolving in 0.9% w/v NaCl for intraperitoneal injection[5].
(2) Inhibitors can be used after 13 weeks[5].
Modeling Indicators
Molecular changes: Increased activity of serum ALT, AST, ALP and GGT increased bilirubin concentration, and decreased serum albumin. Increased levels of Wnt3a and β-catenin, decreased levels of GSK 3β and increased levels of Notch1, Smo and Gli2 in liver tissue[5].
Tissue changes: Liver sections showed multiple cirrhotic nodules, abnormal arrangement of hepatic cords, central veins and portal veins separated by thick fibrous tissue, leukocyte infiltration, vascular congestion, obvious bile, and tubular hyperplasia. Strong blue-stained liver fibrosis was observed around cirrhotic or tumor nodules[5].

Opposite Product(s) : Saxagliptin (HY-10285)
2. Induced liver fibrosis model[6]
Background
Thioacetamide is metabolized by the CYP2E1 enzyme system in the liver into active metabolites, which produce ROS, causing oxidative stress, leading to lipid peroxidation of liver cell membranes, damaging liver cells, and the damaged liver cells release pro-inflammatory factors, leading to liver disease.
Specific Modeling Methods
Rat: Adult male Wistar rats • 225-250 g
Administration: 150 mg/kg • intraperitoneal injection • twice per week for 12 weeks
Note
(1) 7.5% saline solution was injected intraperitoneally at 2 ml/kg and the model was established eight weeks later[6].
(2) 36 h after the last injection, blood was drawn by cardiac puncture[6].
Modeling Indicators
Molecular changes: Serum ALT, AST, ALP and GGT activities and total bilirubin levels increased significantly, and liver MDA and 4HNE contents increased[6].
Tissue changes: Obvious vacuolar degeneration, bile duct epithelial proliferation and wide fibrous septa appear [6].
Correlated Product(s): Pheneturide (HY-111177); Isoniazid (HY-B0329)
Opposite Product(s): Nilotinib (HY-10159); Imatinib (HY-15463)

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