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NEW ARTICLE: RESEARCH: NICLOSAMIDE in CANCER and other diseases - 2025 Review Paper from Henan, China
NICLOSAMIDE was approved by FDA in 1982 for treating tapeworm infections, and was designated an essential drug by WHO.
NICLOSAMIDE in CANCER Mechanisms:
1. Mitochondrial uncoupling - this is its major anti-cancer mechanism
Niclosamide acts like a mild “leak” in the mitochondrial membrane, letting protons slip across without making ATP. This increases oxygen use, lowers ATP levels, raises AMP/ATP ratio & activates AMPK (energy sensor) to inhibit mTOR (slows down cancer cell growth).
Cancer cells, which often rely on inefficient energy pathways (Warburg effect), are especially vulnerable.
This can lead to inhibition of ATP synthesis, exhausting cellular energy reserves, metabolic stress, and cell death.
2. Signal pathway modulation - It inhibits several “pro-cancer” pathways, including:
- Wnt/β-catenin (important in cancer proliferation, especially colorectal).
- mTOR (controls cell proliferation, growth and metabolism).
- Notch pathway (controls proliferation, growth, angiogenesis and cellular migration)
- STAT3, NF-κB, etc. (cancer survival, proliferation).
- Promotes apoptosis (programmed cell death) and reduce inflammation.
3. Combination with existing chemotherapies
4. Addresses Multi-Drug Resistance - by enhancing production of reactive oxygen species.
OTHER DISEASES - beyond cancer, Niclosamide’s versatility includes:
Anti-bacterial - strong in vitro activity against resistant gram-positive bacteria.
its antibacterial activity involves altering bacterial morphology, reducing intracellular ATP, and inhibiting α-HL secretion (Staph Aureus)
it inhibits all three toxins of Clostridium difficile by targeting a host process essential for toxin entry into colonocytes. In a mouse model, it reduced both primary disease and recurrence without affecting gut microbiota diversity
it demonstrates marked inhibition of vancomycin-resistant Enterococcus faecium (VRE)
It effectively eliminates H. pylori adhesion/invasion
Anti-Fungal - demonstrates impressive antifungal effects in vitro and in vivo niclosamide effectively disrupted and removed biofilms of drug-resistant Candida albicans and Candida auris by targeting mitochondrial respiration
Anti-Viral - Niclosamide could have action against SARS-CoV, MERS, Zika, Hepatitis C, Ebola, EBV
Niclosamide inhibits viral replication by reducing mTOR activation and prevents viral entry
inhibits virion production in EBV-infected cells while showing cytotoxicity and inducing cell cycle arrest
demonstrates strong activity against RSV in vitro, with a 94 % inhibition rate
suppresses Hepatitis C replication and reduces viral load
Metabolic disorders (e.g., Type II Diabetes, fatty liver): Mitochondrial effects and AMPK activation can improve energy balance and reduce fat accumulation.
Diabetes: modulates metabolic pathways, improves insulin sensitivity
Fatty liver (NASH, NAFLD) - reduces hepatic inflammation
Neuropathic Pain - reduces inflammation by inhibiting NF-kB, STAT3
alleviates pain and nerve damage
Rheumatoid Arthritis - inhibits NF-kB activation
reduces secretion of IL-6 and other inflammatory cytokines,
blocks migration and invasion of RA fibroblast-like synoviocytes.
Psoriasis - inhibits keratinocyte hyperproliferation and reduces inflammation by downregulation of STAT3, NF-kB.
Airway Diseases (Asthma, Cystic Fibrosis, COPD)
Niclosamide inhibits certain Ca-activated Cl channels involved in mucus hypersecretion & bronchoconstriction (reduces mucus production & secretion.
it blocks release of mucus and inflammatory mediators which reduces bronchoconstriction.
anti-fibrotic agent for lung fibrosis - Niclosamide downregulates expression of collagen proteins and inhibits pro-fibrotic cytokines.
Endometriosis - Niclosamide targets STAT3 and NF-kB, reduces proinflammatory cytokines and reduces endometriotic lesion growth.
ALS
In vivo experimentation involving two ALS mouse models demonstrated slowed disease progression, enhanced survival rates, and reduced motor neuron loss and muscle atrophy.
At the molecular level, niclosamide inhibited dysregulated pathways such as STAT3 and mTOR, reduced gliosis, and dampened inflammatory signaling
niclosamide has shown remarkable potential by efficiently inhibiting the expression of S100A4, a Ca2+-binding protein frequently upregulated in reactive microglia and astrocytes in ALS models. This inhibition contributes to reduced microglial reactivity, cytoskeletal changes & inflammation in ALS
Systemic Sclerosis - inhibits STAT3, AKT, and Wnt/β-catenin pathways
reduced immune cell activation
reversal of skin and lung fibrosis and reduced rate of inflammation
CONCLUSION:
Ivermectin, Mebendazole and Fenbendazole are leading the repurposed drug revolution
but Niclosamide is the most promising of the other anti-parasitics!
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