For research use only.
Catalog No.S3030 Synonyms: Niclocide
Molecular Weight(MW): 327.12
Niclosamide can inhibit DNA replication and inhibit STAT3 with IC50 of 0.7 μM in a cell-free assay. Niclosamide selectively inhibited the phosphorylation of STAT3 and had no obvious inhibition against the activation of other homologues (e.g., STAT1 and STAT5).
Selleck's Niclosamide has been cited by 18 publications
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Effects of some confirmed hits on IRF7 transcription level in response to IFN-α2a treatment (1 h) in SH-SY5Y cells. Data represent mean expression fold±SEM relative to GAPDH, measured from three independent experiments, each in triplicates. *P<0.05, **P<0.01, and ***P<0.001 compared to IFN-α2a treated cells.
Acta Pharm Sin B, 2018, 8(6):889-899. Niclosamide purchased from Selleck.
(B) H&E images. (C–E) IHC for PCNA, pSTAT3, and pPI3K after the drug treatment. BKM120 treatment showed downregulation of the pPI3K expression. pSTAT3 expression, however, was not completely suppressed by STAT3 inhibitor treatment. Note that pSTAT3 and PCNA were heavily expressed in the same dysplastic area of serial sections (red circles, sections from the same liver tissue). (F) ISH for Appa showing downregulation by STAT3 inhibitors. Bars, 50 μm.
Neoplasia, 2015, 17(7):586-97. Niclosamide purchased from Selleck.
LAMP1 IF analysis. (A) Representative confocal IF images (60×) of LAMP1 (green) in SK-GT-4 cells or (C) FLO-1 cells treated with vehicle or niclosamide (0.5 μM) for 48 hours. Arrows point to cells with peripheral lysosomes, while arrowheads indicate cells with perinuclear lysosomes. (B) Quantification of the percentage of SK-GT-4 cells or (D) FLO-1 cells with either peripheral or perinuclear lysosomes relative to their respective total cell number after treatment with vehicle or niclosamide.
Neoplasia, 2018, 20(10):1008-1022. Niclosamide purchased from Selleck.
Bacterial infection in IPEC-J2 cells. The invasion and attachment of EHECO157:H7 was increased in the IPEC-J2 cells in the presence of 1 μM niclosamide. Data are expressed as the mean ± SEM (n= 6). Differences between groups were determined by paired samples t-test. *P<0.05 compared with the control.
Int Immunopharmacol, 2016, 36:199-204.. Niclosamide purchased from Selleck.
Inhibition of STAT3 phosphorylation by niclosamide in colon cancer cells HCT116 and SW620. Notes: (A) SW620 cells were treated with niclosamide (5 µM) for different lengths of time (0, 2, 4, 6, 8, and 12 h). Total protein was extracted, and the expression levels of P-STAT3, STAT3, and GAPDH proteins were detected by Western blot analysis. (B) HCT116 cells were treated with niclosamide (5 µM) for different lengths of time (0, 2, 4, 6, 8, and 12 h). Total protein was extracted, and the expression levels of P-STAT3, STAT3, and GAPDH proteins were detected by Western blot analysis. (C) SW620 cells were treated with niclosamide at different concentrations (0.5, 1, 2.5, 5, and 10 µM) or vehicle control (DMSO) for 12 h. (D) HCT116 cells were treated with niclosamide at different concentrations (0.5, 1, 2.5, 5, and 10 µM) or vehicle control (DMSO) for 12 h. Total protein was then extracted and detected by Western blot analysis. The data were obtained from 3 independent experiments. *P<0.05.
Onco Targets Ther, 2017, 10:1767-1776. Niclosamide purchased from Selleck.
STAT 3 inhibitor, niclosamide, had the antitumor activity for ovarian clear cell cancer cell lines, KK. (A) Niclosamide had antitumor effect for ovarian clear-cell carcinoma cell line, KK. (B) Western blot analysis revealed the downregulation of p-STAT3, and XIAP proteins and increased expression of cleaved-PARP by treatment with niclosamide in a dose-dependent manner. Cell viability was assessed using MTT assay after 24 h from the treatment with niclosamide. Equivalent amounts (10 µg) of protein were subjected to SDS-PAGE and blotted with anti-STAT3, anti-phospho-STAT3, anti-XIAP, anti-cleaved-PARP, and anti-β-actin antibodies.
Oncol Lett, 2018, 15(4):5772-5780. Niclosamide purchased from Selleck.
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|Description||Niclosamide can inhibit DNA replication and inhibit STAT3 with IC50 of 0.7 μM in a cell-free assay. Niclosamide selectively inhibited the phosphorylation of STAT3 and had no obvious inhibition against the activation of other homologues (e.g., STAT1 and STAT5).|
Niclosamide (< 5 μM) dose dependently inhibits STAT3-mediated luciferase reporter activity with IC50 of 0.25 μM in HeLa cells. Niclosamide(< 2 μM) dose dependently inhibits the phosphorylation of STAT3 in Du145 cells. Niclosamide (1 μM) inhibits the EGF-induced nuclear translocation of STAT3 in Du145 cells. Niclosamide(< 2 μM) dose dependently inhibits the transcription of STAT3 downstream genes in Du145 cells. Niclosamide(< 10 μM) dose dependently induces G0/G1 arrest and apoptosis of Du145 cancer cells.  Niclosamide is able to inhibit SARS-CoV replication at a micromolar concentration in Vero E6 cells infected with SARS-CoV.  Niclosamide(< 7.5 μM) promotes Frizzled1 endocytosis, downregulates Dishevelled-2 protein, and inhibits Wnt3A-stimulated beta-catenin stabilization and LEF/TCF reporter activity in U2OS cells.  Niclosamide inhibits the TNF-induced NF-κB reporter activity in a dose- and time-dependent manner in U2OS cells. Niclosamide(125 nM) inhibits NF-κB activation induced by p65, IKKα, IKKβ, IKKγ, and TAK1 in U2OS cells. Niclosamide(< 500 nM) completely block the time- and dose-dependent TNFα-induced alteration of the NF-κB–DNA complex in HL-60 cells. Niclosamide(< 10 nM) inhibits constitutive NF-κB activation in U266 cells. Niclosamide inhibits TNF-induced degradation of IκBα and relocation of p65 in a dose- and time-dependent manner in HL-60, Molm13, or AML primary cells. Niclosamide(500 nM) decreases TNF-induced NF-κB–dependent gene products involved in cell survival in HL-60 cells. Niclosamide dose dependently inhibits the growth and induces robust apoptosis of AML cells associated with decreased Mcl-1 and XIAP levels and increased intracellular ROS levels. 
|In vivo||Niclosamide(40 mg/kg/d, i.p.) inhibits growth of xenografted AML cells in nude mice bearing HL-60 xenograft tumors. |
Protein Kinase profiling assay:Assay for 22 different proteins kinases is carried out by ProQinase Gmbh. All of the protein kinases are expressed either in Sf9 insect cells or in E.coli as recombinant GST-fusion proteins or His-tagged proteins. Protein kinases are purified by affinity chromatography using either GSH-agarose or Ni_NTH-agarose. A radiometric protein kinase assay is used for measuring the kinase activity of the 22 protein kinases. Briefly, for each protein kinase, 50 μL reaction cocktail containing 60 mM HEPES-NaOH, 3 mM MgCl2, 3 mM MnCl2, 3 μM Na-orthovanadate, 1.2 mM DTT, 50 μg/mL PEG20000, 1 μM [γ-33P]-ATP, Niclosamide, adequate amount of enzyme and its substrate. The PKC-alpha assay additionally contain 1 mM Cacl2, 4 mM EDTA, 5 μg/mL phosphatidylserine and 1 μg/mL 1, 2-Dioleyl-glycerol. The reaction cocktails are incubated at 37 °C for 60 minutes and stop with 50 μL 2% (v/v) H3PO4. Incorporation of 33Pi is determined with a microplate scintillation counter. The activities and the IC50 values are calculated using Quattro Workflow V2.28.
|In vitro||DMF||12 mg/mL warmed (36.68 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
1% DMSO+30% polyethylene glycol+1% Tween 80
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
In vivo Formulation Calculator (Clear solution)
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Working concentration： mg/ml；
Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL，)
Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH2O，mix and clarify.
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