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Overview
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Background
Niclosamide is an inhibitor of the signal transducer and activator of transcription 3 (STAT3) with IC50 value of 0.7 μM [1].
STATs are a class of transcription factors that regulate fundamental cellular and biological processes, such as cell proliferation, cell survival, immune responses, and angiogenesis, by modulating the expression of specific target genes. STAT3 has been frequently reported to be over-activated in various human cancer types [1].
In HeLa cells, Niclosamide (< 5 μM) inhibited STAT3-mediated luciferase reporter activity with in a dose dependent manner, with IC50 value of 0.25 μM. In Du145 cancer cells, Niclosamide(< 10 μM) dose-dependently induced G0/G1 arrest and apoptosis [1].
In nude mice bearing HL-60 xenograft tumors, Niclosamide treatment (40 mg/kg/d, i.p.) for 15 days potently inhibited the growth of HL-60 tumors. Further, immunoblotting of xenograft tissues from mice revealed a potent inhibitory effect of Niclosamide on the pathway of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [2].[1]. Ren X, Duan L, He Q, et al. Identification of Niclosamide as a New Small-Molecule Inhibitor of the STAT3 Signaling Pathway. ACS Medicinal Chemistry Letters, 2010, 1(9): 454-459.
[2]. Jin Y, Lu Z, Ding K, et al. Antineoplastic mechanisms of niclosamide in acute myelogenous leukemia stem cells: inactivation of the NF-kappaB pathway and generation of reactive oxygen species. Cancer Research, 2010, 70(6): 2516-2527.
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