Niclosamide - CAS 50-65-7
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Not Intended for Therapeutic Use. For research use only.
Niclosamide is an oral antihelminthic drug, which has been used to treat tapeworm infection for about 50 years. Niclosamide is also used as a molluscicide for water treatment in schistosomiasis control programs. Recently, several groups have independently discovered that niclosamide is also active against cancer cells. Evidence supports that niclosamide targets multiple signaling pathways (NF-κB, Wnt/β-catenin, Notch, ROS, mTORC1, and Stat3), most of which are closely involved with cancer stem cells. Given its potential antitumor activity, clinical trials for niclosamide and its derivatives are warranted for cancer treatment.
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A crystalline solid
1.Niclosamide blocks glucagon phosphorylation of Ser552 on β-catenin in primary rat hepatocytes via PKA signalling.
Chowdhury MK1, Wu LE1, Coleman JL2, Smith NJ2, Morris MJ1, Shepherd PR3, Smith GC4. Biochem J. 2016 May 1;473(9):1247-55. doi: 10.1042/BCJ20160121. Epub 2016 Mar 10.
Recently, it has been found that glucagon is able to activate the β-catenin signalling pathway leading to increased cyclin D1 and c-Myc expression in liver. Therefore the main aim of the present study is to determine whether the effect of glucagon activating β-catenin signalling leading to increased target gene expression is mediated through cAMP activation of PKA (protein kinase A). Primary rat hepatocytes were incubated with insulin, glucagon or adrenaline (epinephrine) and a range of inhibitors of PI3K (phosphoinositide 3-kinase), Wnt, mitochondrial uncoupler (niclosamide) or PKA inhibitors to dissect out the pathway leading to increased Ser(552) phosphorylation on β-catenin following glucagon exposure. In primary rat hepatocytes, we found that short exposure to glucagon or adrenaline caused a rapid increase in Ser(552) phosphorylation on β-catenin that leads to increased cyclin D1 and c-Myc expression. A range of PI3K and Wnt inhibitors were unable to block the effect of glucagon phosphorylating β-catenin.
2.A network-based drug repositioning infrastructure for precision cancer medicine through targeting significantly mutated genes in the human cancer genomes.
Cheng F1, Zhao J1, Fooksa M2, Zhao Z3. J Am Med Inform Assoc. 2016 Mar 28. pii: ocw007. doi: 10.1093/jamia/ocw007. [Epub ahead of print]
OBJECTIVE: Development of computational approaches and tools to effectively integrate multidomain data is urgently needed for the development of newly targeted cancer therapeutics.
3.[Preliminary study of toxicity of niclosamide ethanolamine salt on wetland creatures along lower reaches of Yangtze River in Nanjing City].
Hang DR, You BR, Huang YX, Mei QF, Jing SB, Hu Heng-guang. Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi. 2015 Oct;27(5):467-9, 509.
OBJECTIVE: To understand the impact of niclosamide ethanolamine salt on the Yangtze River wetland creatures, so as to provide an evidence for the environmental impact assessment of the Oncomelania hupensis control measures.
4.Correction: A Novel High Content Imaging-Based Screen Identifies the Anti-Helminthic Niclosamide as an Inhibitor of Lysosome Anterograde Trafficking and Prostate Cancer Cell Invasion.
Circu ML, Dykes SS, Carroll J, Kelly K, Galiano F, Greer A, Cardelli J, El-Osta H. PLoS One. 2016 Mar 14;11(3):e0151718. doi: 10.1371/journal.pone.0151718.
[This corrects the article DOI: 10.1371/journal.pone.0146931.].
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CAS 50-65-7 Niclosamide

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