Review: repurposing niclosamide against inflammaging and cellular senescence
This review of molecular and preclinical evidence describes six proposed mechanisms by which niclosamide may target inflammaging and cellular aging, and notes that randomized placebo-controlled trials are still needed. [1]
Automatic summary · not editorially reviewed
The key findings
The review consolidates molecular and preclinical evidence on niclosamide's repurposing for inflammaging and evaluates reformulated oral formulations reaching sustained plasma concentrations of 0.5–3 µmol/L. [1]
The review lists six interconnected mechanisms, including mild reversible mitochondrial uncoupling, mTORC1 inhibition, restored autophagic flux, senolytic and senomorphic effects, Wnt/β-catenin blockade and immune rebalancing. [1]
The authors state that randomized, placebo-controlled trials targeting inflammaging, frailty and biological age biomarkers are an immediate translational priority. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- Molecular and preclinical evidence on niclosamide, plus data from reformulated oral formulations; no human trial participants are described.
- Summary based on
- Study abstract
- Original publication
- June 11, 2026
Review scope: niclosamide and inflammaging pathways
The review asks whether niclosamide, a WHO-listed anthelmintic with a long safety record, could be repurposed against inflammaging, the chronic low-grade inflammation linked to age-related multimorbidity. It consolidates molecular and preclinical evidence on whether the drug can engage core pathways of cellular aging and inflammation at the same time. The authors note that historical poor absorption limited systemic use, and they also evaluate recent data from reformulated oral formulations reaching sustained plasma concentrations of 0.5–3 µmol/L. This is a review of existing evidence, not a new trial.
Supporting source [1]
Six proposed mechanisms in preclinical evidence
The review lists six interconnected mechanisms: mild reversible mitochondrial uncoupling that limits reactive oxygen species and cGAS-STING activation; mTORC1 inhibition via lysosomal deacidification, with indirect IGF-1/IGF-1R modulation through AMPK; restored autophagic flux and lysosomal biogenesis via TFEB nuclear translocation; selective senolytic and senomorphic effects that suppress NF-κB and STAT3, neutralize the senescence-associated secretory phenotype and reduce IL-6, IL-1β and TNF-α; blockade of canonical Wnt/β-catenin signaling to prevent tissue fibrosis; and rebalanced aged immune function by downregulating PD-1/PD-L1 and upregulating Vasorin to inhibit TGFβ-mediated fibrosis. The authors describe this as a polypharmacological profile unlike single-pathway agents.
Supporting source [1]
Translational gap: trials still needed
The authors conclude that reformulated niclosamide combines multi-target anti-inflammaging activity with a decades-long safety record. However, the evidence summarized is molecular and preclinical, and the reformulation data concern plasma concentrations rather than demonstrated human outcomes. The review states that randomized, placebo-controlled trials targeting inflammaging, frailty and biological age biomarkers are now an immediate translational priority. No such trial results are reported here, so the proposed benefits for human aging remain untested in this source.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The summarized evidence is molecular and preclinical, and the reformulation data concern plasma concentrations, not demonstrated human outcomes. No randomized trial results are reported, so benefits for human aging remain untested here.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Alameen AAM, Al-Kuraishy HM, Abdelaziz AM, Batiha GE. · europepmc.org · June 11, 2026