Niclosamide: Comprehensive Profile

Al-Hadiya, Badraddin M.H.

doi:10.1016/s0099-5428(05)32002-8

Cited by 77 publications

(61 citation statements)

References 37 publications

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“…Niclosamide has been approved as anthelmintic against cestodes with well tolerated9 in humans for nearly 50 years 10. In recent years, niclosamide has been identified as a potential anti‐cancer agent in thyroid,11 renal,12 ovarian,13 lung,14 and prostate15 cancers.…”

Section: Introductionmentioning

confidence: 99%

A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway

Chen

Huang

et al. 2018

Cancer Medicine

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The incidence and mortality rate of urological cancers is increasing yearly. Niclosamide has been repurposed as an anti‐cancer drug in recent years. Synthesized derivative of niclosamide was testified for its anti‐cancer activity in urological cancers. MTT assay was used to measure the cytotoxicity effect of niclosamide and its derivatives in urological cancer cell lines. Migratory ability was monitored by scratch migration assay. Apoptosis and cell cycle changes were analyzed by annexin V and PI staining. The apoptosis‐related signal proteins were evaluated by western blotting. T24 had the best drug sensitivity with the lowest IC 50 in niclosamide and B17 treatment than DU145 and Caki‐1 cells. After niclosamide and B17 treatment, the mitotic cells were decreased, but apoptotic bodies and morphology changes were not prominent in T24, Caki‐1, and DU145 cells. The migratory ability was inhibited in niclosamide treatment than control group on Caki‐1 cells and niclosamide and B17 treatment than control group on DU145 cells. Early apoptosis cells were increased after niclosamide and B17 treatment than control group without cell cycle changes in T24, Caki‐1, and DU145 cells. Programmed cell death was activated majorly through PAPR and bcl‐2 in T24 and caspase‐3 in Caki‐1 cells, respectively. Niclosamide and B17 derivative had good ability in inhibition proliferation and migratory ability in T24, Caki‐1, and DU145 cells without prominent morphology and apoptotic body changes. UCC cells are more sensitive to niclosamide and B17 treatment. Early apoptosis was induced after niclosamide and B17 treatment through different mechanisms in T24, Caki‐1, and DU145 cells.

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Section: Introductionmentioning

confidence: 99%

A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway

Chen

Huang

et al. 2018

Cancer Medicine

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“…The anthelmintic drug niclosamide has been used in management of tapeworm infections for half a century (Al-Hadiya, 2005). Niclosamide kills tapeworms through inhibition of oxidative phosphorylation and stimulation of adenosine triphosphatese activity in the mitochondria (Al-Hadiya, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Niclosamide kills tapeworms through inhibition of oxidative phosphorylation and stimulation of adenosine triphosphatese activity in the mitochondria (Al-Hadiya, 2005). In recent years, niclosamide has been identified as a potential anticancer agent (Li et al, 2014;Pan et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Metabolism of the anthelmintic drug niclosamide by cytochrome P450 enzymes and UDP-glucuronosyltransferases: metabolite elucidation and main contributions from CYP1A2 and UGT1A1

Zhang

et al. 2015

Xenobiotica

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1. Niclosamide is an old anthelmintic drug that shows potential in fighting against cancers. Here, we characterized the metabolism of niclosamide by cytochrome P450 enzymes (CYPs) and UDP-glucuronosyltransferases (UGTs) using human liver microsomes (HLM) and expressed enzymes. 2. NADPH-supplemented HLM (and liver microsomes from various animal species) generated one hydroxylated metabolite (M1) from niclosamide; and UDPGA-supplemented liver microsomes generated one mono-O-glucuronide (M2). The chemical structures of M1 (3-hydroxy niclosamide) and M2 (niclosamide-2-O-glucuronide) were determined through LC-MS/MS and/or NMR analyses. 3. Reaction phenotyping revealed that CYP1A2 was the main enzyme responsible for M1 formation. The important role of CYP1A2 in niclosamide metabolism was further confirmed by activity correlation analyses as well as inhibition experiments using specific inhibitors. 4. Although seven UGT enzymes were able to catalyze glucuronidation of niclosamide, UGT1A1 and 1A3 were the enzymes showed the highest metabolic activities. Activity correlation analyses demonstrated that UGT1A1 played a predominant role in hepatic glucuronidation of niclosamide, whereas the role of UGT1A3 was negligible. 5. In conclusion, niclosamide was subjected to efficient metabolic reactions hydroxylation and glucuronidation, wherein CYP1A2 and UGT1A1 were the main contributing enzymes, respectively.

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“…It was approved by US FDA for the treatment of worm infections and has been used in human for more than 50 years (Al-Hadiya 2004). The mechanism of anthelminthic activity of niclosamide has been well illustrated.…”

Section: Niclosamidementioning

confidence: 99%

“…The mechanism of anthelminthic activity of niclosamide has been well illustrated. Niclosamide is known to interfere with the production of adenosine triphosphate (ATP) by inhibiting mitochondria (Pearson and Hewlett 1985;Al-Hadiya, 2004). It uncouples oxidative phosphorylation in the parasite mitochondria, thus inhibiting ATP production without affecting the respiratory chain and ATP synthase (Frayha et al 1997).…”

Section: Niclosamidementioning

confidence: 99%

Existing drugs and their application in drug discovery targeting cancer stem cells

Lv¹,

Shim²

2015

Arch. Pharm. Res.

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Despite standard cancer therapies such as chemotherapy and targeted therapy have shown some efficacies, the cancer in many cases eventually relapses and metastasizes upon stopping the treatment. There is a small subpopulation of cancer cells within tumor, with specific characters similar to those found in stem cells. This group of cancer cells is known as tumor-initiating or cancer stem cells (CSCs), which have an ability to self-renew and give rise to cancer cell progeny. CSCs are related with drug resistance, metastasis and relapse of cancer, hence emerging as a crucial drug target for eliminating cancer. Rapid advancement of CSC biology has enabled researchers to isolate and culture CSCs in vitro, making the cells amenable to high-throughput drug screening. Recently, drug repositioning, which utilizes existing drugs to develop potential new indications, has been gaining popularity as an alternative approach for the drug discovery. As existing drugs have favorable bioavailability and safety profiles, drug repositioning is now actively exploited for prompt development of therapeutics for many serious diseases, such as cancer. In this review, we will introduce latest examples of attempted drug repositioning targeting CSCs and discuss potential use of the repositioned drugs for cancer therapy.

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Niclosamide: Comprehensive Profile

Cited by 77 publications

References 37 publications

A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway

A new niclosamide derivatives‐B17 can inhibit urological cancers growth through apoptosis‐related pathway

Metabolism of the anthelmintic drug niclosamide by cytochrome P450 enzymes and UDP-glucuronosyltransferases: metabolite elucidation and main contributions from CYP1A2 and UGT1A1

Existing drugs and their application in drug discovery targeting cancer stem cells

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