ArticlePLoS pathogens2012
Nitazoxanide stimulates autophagy and inhibits mTORC1 signaling and intracellular proliferation of Mycobacterium tuberculosis.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04498936 (Efficacy of Adding Sofosbuvir/Ledipasvir Combination, or Nitazoxanide to the Standard of Care in Treatment of COVID-19), which is not on this map. Cited by 86 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Efficacy of Adding Sofosbuvir/Ledipasvir Combination, or Nitazoxanide to the Standard of Care in Treatment of COVID-19: A Randomized Controlled Trial
Who cites it
86 citing papers in PubMed, 145 citations in OpenAlex.
- Sofosbuvir/ledipasvir in combination or nitazoxanide alone are safe and efficient treatments for COVID-19 infection: A randomized controlled trial for repurposing antivirals.Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology · 2022Trial
- Early Bactericidal Activity Trial of Nitazoxanide for Pulmonary Tuberculosis.Antimicrobial agents and chemotherapy · 2020Trial
- Exploiting autophagy-targeting natural compounds for potential antimicrobial actions.Autophagy · 2026Review
- Nitazoxanide activates BMP9-ALK1-SMAD signaling cascade and improves HHT vascular pathology.bioRxiv : the preprint server for biology · 2026Article
- Host-directed therapeutics against antimicrobial-resistant bacterial infections: emerging roles of multi-omics and systems biology.Frontiers in pharmacology · 2026Review
- Nitazoxanide alleviates collagen-induced arthritis by inhibiting STAT3-dependent Th17 cell differentiation and inflammatory cytokines production.Frontiers in pharmacology · 2026Article
- Autophagy: mechanisms, roles in human diseases, and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- Combination nitazoxanide and auranofin treatment has synergistic anticancer activity in anaplastic thyroid cancer through enhanced activation of oxidative stress that leads to apoptosis.Cancer letters · 2025Article
- Host-directed therapy for tuberculosis.European journal of medical research · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Repurposing Nitazoxanide for Potential Treatment of Rare Disease Lymphangioleiomyomatosis.Biomolecules · 2024Article
- Glycogen synthase kinase 3 inhibition controlsiScience · 2024Article
- Tristetraprolin mediates immune evasion of mycobacterial infection in macrophages.FASEB bioAdvances · 2024Article
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- TargetingMicrobiology (Reading, England) · 2024Review
- Divergent responses of human intestinal organoid monolayers using commercial in vitro cytotoxicity assays.PloS one · 2024Article
- The pipeline for drugs for control and elimination of neglected tropical diseases: 2. Oral anti-infective drugs and drug combinations for off-label use.Parasites & vectors · 2023Review
- Review
- Article
- The FDA-approved drug nitazoxanide is a potent inhibitor of human seasonal coronaviruses acting at postentry level: effect on the viral spike glycoprotein.Frontiers in microbiology · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Tuberculosis, caused by Mycobacterium tuberculosis infection, is a major cause of morbidity and mortality in the world today. M. tuberculosis hijacks the phagosome-lysosome trafficking pathway to escape clearance from infected macrophages. There is increasing evidence that manipulation of autophagy, a regulated catabolic trafficking pathway, can enhance killing of M. tuberculosis. Therefore, pharmacological agents that induce autophagy could be important in combating tuberculosis. We report that the antiprotozoal drug nitazoxanide and its active metabolite tizoxanide strongly stimulate autophagy and inhibit signaling by mTORC1, a major negative regulator of autophagy. Analysis of 16 nitazoxanide analogues reveals similar strict structural requirements for activity in autophagosome induction, EGFP-LC3 processing and mTORC1 inhibition. Nitazoxanide can inhibit M. tuberculosis proliferation in vitro. Here we show that it inhibits M. tuberculosis proliferation more potently in infected human THP-1 cells and peripheral monocytes. We identify the human quinone oxidoreductase NQO1 as a nitazoxanide target and propose, based on experiments with cells expressing NQO1 or not, that NQO1 inhibition is partly responsible for mTORC1 inhibition and enhanced autophagy. The dual action of nitazoxanide on both the bacterium and the host cell response to infection may lead to improved tuberculosis treatment.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.