Nine Repurposed Drugs That Could Slow Aging and Extend Healthy Lifespan
A major review identifies nine common drugs—including metformin, aspirin, and dasatinib—with promising anti-aging mechanisms targeting shared biological pathways.
Summary
Researchers from the Chinese Academy of Medical Sciences reviewed nine repurposed drugs for their potential to combat aging itself, not just individual age-related diseases. The drugs—aspirin, atorvastatin, enalapril, metformin, canagliflozin, liraglutide, acarbose, N-acetylcysteine, and dasatinib plus quercetin—work through key longevity pathways including mTOR, AMPK, NF-κB, and SASP. In model organisms, these compounds show evidence of extending healthspan and lifespan by reducing chronic inflammation, improving metabolic efficiency, and boosting cellular stress resistance. The review highlights a paradigm shift: treating aging as a single modifiable biological process rather than managing its downstream diseases one by one. Major translational hurdles remain, including species differences, sex-specific responses, and the absence of validated aging biomarkers.
Detailed Summary
Aging is increasingly recognized not merely as an inevitable decline but as a biological process that may be pharmacologically modifiable. This framing opens the door to treating aging itself as a disease target, potentially compressing morbidity and extending healthy human lifespans at scale.
This comprehensive review from the Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, examines nine drugs already approved for other conditions that show anti-aging promise: aspirin, atorvastatin, enalapril, metformin, canagliflozin, liraglutide, acarbose, N-acetylcysteine, and the senolytic combination of dasatinib plus quercetin. Rather than evaluating each drug in isolation, the authors analyze them through the lens of shared aging biology.
The drugs converge on four major molecular pathways: mTOR (mechanistic target of rapamycin), AMPK (AMP-activated protein kinase), NF-κB (nuclear factor kappa B), and SASP (senescence-associated secretory phenotype). By modulating these pathways, the compounds reduce chronic low-grade inflammation, enhance metabolic efficiency, clear senescent cells, and improve cellular stress resistance—hallmarks of the aging process itself.
In preclinical model organisms, several of these agents demonstrate measurable extensions in both healthspan and lifespan, lending biological plausibility to their repurposing for aging indications. The dasatinib-quercetin combination, in particular, has attracted attention as a senolytic strategy to eliminate dysfunctional aged cells.
Despite this promise, the review is candid about translational barriers. Species-specific biology and sex differences complicate extrapolating animal data to humans. The field also lacks validated, reliable biomarkers of biological aging, making it difficult to measure drug efficacy in clinical trials. Optimal dosing strategies for aging—as opposed to disease treatment—remain undefined. The authors advocate for a paradigm shift that positions aging as a unified, modifiable condition worthy of direct therapeutic targeting.
Key Findings
- Nine repurposed drugs show anti-aging potential by targeting mTOR, AMPK, NF-κB, and SASP pathways.
- Metformin, dasatinib+quercetin, and acarbose extend healthspan and lifespan in model organisms.
- Reducing chronic inflammation and clearing senescent cells are key shared mechanisms.
- Major barriers include species differences, sex variability, and lack of validated aging biomarkers.
- Authors call for treating aging as a single modifiable biological process, not a collection of diseases.
Methodology
This is a narrative review synthesizing preclinical and clinical literature on nine repurposed drugs. No original experimental data were generated; findings are drawn from existing model organism studies and available human data. The review is limited to the abstract, so the full scope of included studies and selection criteria cannot be fully assessed.
Study Limitations
The review is based solely on the abstract, limiting depth of assessment. Translational challenges highlighted by the authors—species specificity, sex differences, and absent aging biomarkers—mean preclinical promise may not translate to human benefit. Optimal dosing and long-term safety profiles for aging-specific use remain unestablished.
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