Evidence map›Paper›PMID 42274789›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

Repurposing niclosamide to mitigate inflammaging: a review of multi-target mechanisms in cellular senescence and age-related decline.

Ayman Ali Mohammed Alameen, Hayder M Al-Kuraishy, Ahmed M Abdelaziz, Gaber El-Saber Batiha

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Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Ayman Ali Mohammed AlameenDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, P.O. Box 2014, Sakaka, KSA, Saudi Arabia. aaalameen@ju.edu.sa.
Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Al-Mustansiriyah University, Baghdad, Iraq.
Ahmed M AbdelazizDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Sinai University-Arish Branch, Arish, 45511, Egypt. ahmed.abdelaziz@su.edu.eg.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhur University, Damanhur, 22511, AlBeheira, Egypt. dr_gaber_batiha@vetmed.dmu.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic low-grade inflammation, or inflammaging, drives age-related multimorbidity and cellular decline, yet pharmacological interventions targeting its root causes are lacking. Niclosamide, a WHO-listed anthelmintic with a long safety record, has recently emerged as a multi-target geroprotector with potent anti-inflammatory properties, though historical poor absorption limited its systemic use.

objectivesThis review consolidates molecular and preclinical evidence supporting niclosamide's repurposing for inflammaging, focusing on its ability to simultaneously engage core pathways of cellular aging and inflammation. It also evaluates recent data from reformulated oral formulations that achieve sustained plasma concentrations (0.5-3 µmol/L) sufficient for systemic effects. KEY

findingsNiclosamide acts through six interconnected mechanisms: (1) mild reversible mitochondrial uncoupling, limiting ROS and cGAS-STING activation; (2) mTORC1 inhibition via lysosomal deacidification, with indirect IGF-1/IGF-1R modulation through AMPK activation; (3) restoration of autophagic flux and lysosomal biogenesis via TFEB nuclear translocation; (4) selective senolytic and senomorphic effects, suppressing NF-κB and STAT3 to neutralize the senescence-associated secretory phenotype (SASP) and reduce IL-6, IL-1β, and TNF-α; (5) blockade of canonical Wnt/β-catenin signaling to prevent tissue fibrosis; and (6) rebalancing of aged immune function by downregulating PD-1/PD-L1 and upregulating Vasorin to inhibit TGFβ‑mediated fibrosis. Unlike single-pathway agents, niclosamide offers a unique polypharmacological profile that mitigates sterile inflammation at its source.

conclusionsReformulated niclosamide combines multi-target anti-inflammaging activity with a decades-long safety record. Randomized, placebo‑controlled trials targeting inflammaging, frailty, and biological age biomarkers are now an immediate translational priority.

Indexed as

AgingAnti-Inflammatory AgentsCellular SenescenceInflammationNiclosamideAnimalsDrug RepositioningHumansAnti-Inflammatory AgentsNiclosamideCellular senescenceImmunosenescenceInflammagingMitochondrial uncouplingmTORC1NiclosamideSenescence-associated secretory phenotype (SASP)

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Registered trials

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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 Socratic graph.