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Thioacetamide

MCE China：Thioacetamide

Brand：MedChemExpress (MCE)

Cat. No.HY-Y0698

CAS：62-55-5

Synonyms：Acetothioamide; TAA; Thiacetamide

Purity：98.0%

Storage：4°C, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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：β-Amyloid (1-40) can be used in animal modelling to construct models of Alzheimer's disease. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } 1. Induction of liver tumors[5] Background Thioacetamide causes malignant transformation of hepatocytes by inducing DNA damage, cytotoxicity and inflammatory responses. Specific Mmodeling Methods Rats: Adult males • 180-200 gDosage: 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]. Correlated Product(s): / Opposite Product(s): Saxagliptin (HY-10285) .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } 2. Induction of 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 Mmodeling Methods Rats: Adult male Wistar rats • 225-250 gAdministration: 150 mg/kg • intraperitoneal injection • twice a 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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References：

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

[2]. Chen IS, et, al. Hepatoprotection of silymarin against thioacetamide-induced chronic liver fibrosis. J Sci Food Agric. 2012 May;92(7):1441-7.  [Content Brief]

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

[4]. Yeom HJ, et, al. 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.  [Content Brief]

[5]. Ahmed G Abd Elhameed, et al. Saxagliptin defers thioacetamide-induced hepatocarcinogenesis in rats: A novel suppressive impact on Wnt/Hedgehog/Notch1 signaling. Environ Toxicol Pharmacol  [Content Brief]

[6]. Mohamed E Shaker, et al. Nilotinib counteracts thioacetamide-induced hepatic oxidative stress and attenuates liver fibrosis progression. Fundam Clin Pharmacol. 2011 Apr;25(2):248-57.  [Content Brief]