Medicines already used for allergies, blood pressure, diabetes and other conditions may eventually be repurposed to target some of the biological processes involved in human aging.
A new gene-network study analyzed thousands of longevity-related genes and existing medicines to identify drugs that might influence specific mechanisms associated with aging. The researchers found hundreds of potential candidates, including a smaller group whose effects on gene activity appeared to move cells in a more youthful direction.
The results do not prove that any of these medicines can make people live longer. The study was primarily computational, meaning its predictions must still be tested in laboratory experiments, animals and carefully designed human clinical trials. However, the findings offer researchers a more systematic way to decide which existing drugs deserve further investigation.
How Researchers Mapped the Biology of Aging
The study was published in Nature Aging on June 26, 2026. Researchers from Northeastern University, Harvard Medical School and collaborating institutions developed a network-medicine framework called SHARP to examine how aging-related genes interact with one another and with the targets of existing drugs.
Rather than treating aging as a single condition, the researchers focused on biological mechanisms commonly known as the hallmarks of aging. These include genomic instability, cellular senescence, mitochondrial dysfunction, stem-cell exhaustion, impaired nutrient sensing, loss of protein maintenance and changes in communication between cells.
The team began with 2,358 genes previously associated with longevity, age-related diseases or biological pathways involved in aging. Of these, 1,250 could be connected to at least one recognized hallmark of aging. Many of the genes were linked to more than one hallmark, showing that the different processes involved in aging are closely interconnected.
The researchers then placed these genes within the human interactome, a large map of experimentally observed interactions among human proteins. They found that genes associated with each hallmark tended to form connected neighborhoods rather than appearing randomly throughout the network.
These connected neighborhoods were described as hallmark modules. By locating them, the researchers could investigate whether the targets of existing medicines were positioned close enough to influence particular aging processes.
More Than 6,400 Drugs Were Examined
The researchers compared the aging modules with the known targets of 6,442 approved or clinically tested compounds.
A drug whose targets were located close to a hallmark module was considered more likely to affect that part of the aging process. However, closeness alone could not reveal whether the drug would produce a beneficial or harmful effect.
To solve that problem, the team developed another measurement called pAGE. This metric examined how a drug changes gene expression and compared those changes with the gene-expression patterns normally associated with aging.
A positive pAGE result indicated that the drug appeared to oppose certain age-related gene-expression changes. A negative result suggested that the medicine might reinforce those changes and potentially produce an age-accelerating effect.
Combining the network analysis with pAGE allowed researchers to distinguish drugs that could simply affect an aging pathway from those predicted to push that pathway in a potentially healthier direction.
The Study Identified 21 Potential Pro-Longevity Drugs
The network analysis initially identified 370 drugs whose targets were significantly close to one or more hallmarks of aging.
Only 60 of these medicines had sufficient gene-expression data for the researchers to calculate their pAGE scores. Among those 60, 21 produced positive scores and were classified as potential pro-longevity candidates.
Another 23 drugs produced negative scores and were identified as potentially age-accelerating. The remaining 16 generated inconsistent results, meaning researchers could not determine whether their overall effects were likely to be beneficial or harmful.
The results demonstrate why identifying a drug that interacts with an aging pathway is not enough. A medicine may strongly affect a particular biological mechanism while changing it in an undesirable direction.
Which Existing Medicines Appeared Promising?
The study identified different candidates for different hallmarks of aging rather than finding one medicine capable of reversing the entire aging process.
For stem-cell exhaustion, drugs with positive pAGE scores included olopatadine, amlexanox, acemetacin, guanethidine and several other compounds. Olopatadine is commonly used in allergy treatments, while amlexanox has previously been used for inflammatory conditions.
For altered communication between cells, the candidates included oxymetazoline, terazosin, tetryzoline, cirazoline and synephrine. Oxymetazoline is found in some nasal sprays, while terazosin is prescribed for high blood pressure and symptoms related to an enlarged prostate.
The analysis associated fenoprofen, doconexent and clinofibrate with potentially beneficial effects on epigenetic alterations. Captopril, a blood-pressure medicine, and marimastat were among the candidates associated with changes in the extracellular matrix.
Drugs including tivozanib, pilaralisib and linsitinib were identified as potential candidates for targeting deregulated nutrient sensing. However, several of these medicines were developed for serious conditions such as cancer and may carry substantial risks. Their appearance in the analysis should not be interpreted as evidence that they are safe for healthy people to use for longevity.
The System Recognized Known Longevity Candidates
The researchers tested their framework against medicines already being investigated for possible effects on aging and longevity.
The comparison included metformin, rapamycin, acarbose, aspirin, dasatinib and quercetin. Eleven of 17 compounds currently being studied in healthy-aging trials showed significant proximity to at least one hallmark module.
Aspirin was predicted to influence six hallmarks, while dasatinib was connected to five. Rapamycin was primarily associated with altered communication between cells. Metformin, acarbose and quercetin showed weaker but still potentially meaningful proximity to aging-related modules.
Among the nine clinical-trial drugs for which adequate gene-expression data were available, eight produced positive pAGE results for at least one hallmark. This gave the system encouraging sensitivity when compared with compounds already considered relevant to longevity research.
The framework also successfully recognized several drugs that had improved lifespan or healthspan in independent mouse experiments, including vorinostat, selumetinib and other experimental compounds. However, the researchers acknowledged that the validation groups were small and that larger studies will be needed to measure the model’s accuracy reliably.
Why Repurposing Existing Drugs Could Accelerate Research
Developing a completely new medicine can take many years and requires extensive testing for toxicity, dosage, effectiveness and manufacturing quality.
Existing drugs may offer a faster starting point because researchers already understand much of their chemistry, targets, side effects and behavior in the human body. Some have also been used by patients for decades.
Repurposing does not eliminate the need for clinical trials. A medicine that is safe for treating a serious disease may not be appropriate for long-term use in otherwise healthy people. Dosages suitable for cancer, diabetes or high blood pressure may also be unsuitable when the goal is to slow an aging process.
Nevertheless, beginning with approved or clinically tested compounds could shorten some stages of development and allow researchers to concentrate on whether a medicine can improve healthspan at a tolerable dose. The study authors describe their system as a way to prioritize the strongest candidates rather than testing thousands of drugs through trial and error.
Slowing Aging Is More Complicated Than Finding One Pill
The study reinforces the idea that aging is not controlled by a single gene or biological switch.
Different hallmarks influence one another. Mitochondrial dysfunction can affect inflammation, damaged-cell removal, nutrient sensing and communication between tissues. Cellular senescence can contribute to chronic inflammation, while genomic instability may influence cancer risk and stem-cell decline.
Because of these connections, one medicine is unlikely to improve every aspect of aging. The researchers suggest that future longevity strategies may require multiple interventions aimed at different biological mechanisms.
This does not necessarily mean combining many powerful drugs. It could involve carefully selected treatments administered at different times, doses or stages of life. Any such strategy would require extensive safety testing because drug combinations can produce unexpected interactions.
The Research Does Not Show That People Should Take These Drugs
None of the candidates identified by the study has been proven to slow aging in healthy humans.
The research did not give these drugs to people or measure whether they extended human lifespan. It predicted their potential effects using gene networks, protein interactions and drug-induced changes in gene expression.
Computational predictions can help researchers find patterns that would be difficult to detect manually, but they cannot fully reproduce what happens inside a living person. A drug may affect different tissues in different ways, produce harmful side effects or reach an aging-related target only at an unsafe dose.
Some identified medicines are prescription drugs used for cancer, cardiovascular disease or other serious conditions. Taking them without a valid medical reason could cause severe harm.
The researchers emphasized that their findings provide testable hypotheses and a research roadmap rather than a cure for aging. Each candidate would require laboratory validation followed by animal research and, where justified, controlled human trials.
What the Study Could Mean for Longevity Medicine
The most important contribution of the study may be its method rather than any individual drug on the candidate list.
By combining genetic evidence, protein-interaction networks and drug-related gene-expression changes, the SHARP framework provides a way to investigate aging as a connected biological system.
Researchers could use the approach to identify drugs targeting individual hallmarks, predict whether their effects are potentially beneficial and understand the molecular pathways through which they may work. The framework could also be updated as scientists collect better gene-expression data and discover new relationships between genes and aging.
The study does not show that a widely available anti-aging treatment is ready for use. It does suggest that some of the molecular tools required to influence aging may already exist within today’s collection of medicines.
The next challenge is determining which predictions survive experimental testing and whether any candidate can improve human healthspan without creating risks greater than its potential benefits.
The full research paper is available through Nature Aging. Additional context about the project and its research team is available from Northeastern University’s College of Science.
