Niclosamide

Pricing Availability Delivery Time Qty
Cat.No. 4079 - Niclosamide | C13H8Cl2N2O4 | CAS No. 50-65-7
Description: STAT3 inhibitor; also inhibits mTORC1 signaling
Chemical Name: 5-Chloro-N-(2-chloro-4-nitrophenyl)-2-hydroxybenzamide
Purity: ≥99% (HPLC)
Datasheet
Citations (1)
Reviews
Literature
Pathways

Biological Activity

Inhibitor of the STAT3 signaling pathway; inhibits the activation, nuclear translocation and transactivation of STAT3. Displays selectivity for STAT3 over STAT1, STAT5, JAK1, JAK2 and Src kinases. Inhibits the transcription of STAT3 target genes and induces cell growth inhibition, apoptosis and cell cycle arrest of cancer cells with constitutively active STAT3. Also reversibly inhibits mTORC1 signaling and stimulates autophagy in vitro; displays antineoplastic effects in acute myelogenous leukemia (AML) stem cells.

Technical Data

M. Wt 325.99
Formula C13H8Cl2N2O4
Storage Store at +4°C
Purity ≥99% (HPLC)
CAS Number 50-65-7
PubChem ID 4477
InChI Key RJMUSRYZPJIFPJ-UHFFFAOYSA-N
Smiles O=C(NC2=C(Cl)C=C([N+]([O-])=O)C=C2)C1=C(O)C=CC(Cl)=C1

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

All Tocris products are intended for laboratory research use only.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
Solubility
DMSO 3.26 10
ethanol 8.15 25

Preparing Stock Solutions

The following data is based on the product molecular weight 325.99. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.

Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 3.07 mL 15.34 mL 30.68 mL
5 mM 0.61 mL 3.07 mL 6.14 mL
10 mM 0.31 mL 1.53 mL 3.07 mL
50 mM 0.06 mL 0.31 mL 0.61 mL

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Product Datasheets

Safety Datasheet

References

References are publications that support the biological activity of the product.

Balgi et al (2009) Screen for chemical modulators of autophagy reveals novel therapeutic inhibitors of mTORC1 signaling. PLoS One 4 e7124 PMID: 19771169

Jin et al (2010) Antineoplastic mechanisms of niclosamide in acute myelogenous leukemia stem cells: inactivation of the NF-κB pathway and generation of reactive oxygen species. Cancer Res. 70 2516 PMID: 20215516

Ren et al (2010) Identification of niclosamide as a new small-molecule inhibitor of the STAT3 signaling pathway. ACS Med.Chem.Lett. 1 454


If you know of a relevant reference for Niclosamide, please let us know.

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View all STAT Inhibitors

Keywords: Niclosamide, Niclosamide supplier, STAT3, mTORC1, signaling, signalling, pathway, inhibitors, inhibits, anthelmintic, STAT, mTOR, Stem, Cell, Signaling, Autophagy, Cancer, Cells, 4079, Tocris Bioscience

1 Citation for Niclosamide

Citations are publications that use Tocris products. Selected citations for Niclosamide include:

Natarajan et al (2014) STAT3 modulation to enhance motor neuron differentiation in human neural stem cells. PLoS One 9 e100405 PMID: 24945434


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Literature in this Area

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!

*Please note that Tocris will only send literature to established scientific business / institute addresses.


Cancer

Cancer Research Product Guide

A collection of over 750 products for cancer research, the guide includes research tools for the study of:

  • Cancer Metabolism
  • Epigenetics in Cancer
  • Receptor Signaling
  • Cell Cycle and DNA Damage Repair
  • Angiogenesis
  • Invasion and Metastasis
Immunology

Immunology Product Listing

A collection of over 190 products for immunology research, the guide includes research tools for the study of:

  • Chemokine and Cytokine Signaling
  • Chemotaxis
  • Complement System
  • Immune Cell Signaling
  • Inflammation

Pathways for Niclosamide

JAK-STAT

JAK-STAT Signaling Pathway

The JAK-STAT signaling pathway has several roles, including the control of cell proliferation and hematopoiesis. It is the main signal transduction cascade from cytokine receptors.