A new research paper was published in Aging (Aging-US) Volume 15, Issue 7, entitled, “Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic.”

The accumulation of senescent cells has an important role in the phenotypical changes observed in aging and in many age-related pathologies. Thus, the strategies designed to prevent these effects, collectively known as senotherapies, have a strong clinical potential. 

Senolytics are a type of senotherapy aimed at specifically eliminating senescent cells from tissues. Several small molecule compounds with senolytic properties have already been identified, but their specificity and range of action are variable. Because of this, potential novel senolytics are being actively investigated. 

Given the involvement of HDACs and the PI3K pathway in senescence, researchers Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip from the University of Leicester, Najran University and Universitat Oberta de Catalunya hypothesized that the dual inhibitor CUDC-907, a drug already in clinical trials for its antineoplastic effects, could have senolytic effects. 

“Here, we show that CUDC-907 was indeed able to selectively induce apoptosis in cells driven to senesce by p53 expression, but not when senescence happened in the absence of p53.” 

Consistent with this, CUDC-907 showed senolytic properties in different models of stress-induced senescence. Their results also indicate that the senolytic functions of CUDC-907 depend on the inhibitory effects of both HDACs and PI3K, which leads to an increase in p53 and a reduction in BH3 pro-survival proteins. Taken together, their results show that CUDC-907 has the potential to be a clinically relevant senolytic in pathological conditions in which stress-induced senescence is involved.

“According to our results, CUDC-907 could be an interesting drug to be used as a senolytic, alone or as part of a targeted approach.”

DOI: https://doi.org/10.18632/aging.204616

Corresponding author - Salvador Macip - sm460@le.ac.uk

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Keywords - aging, senescence, senolytics, HDAC, PI3K, CUDC-907

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Aging (Aging-US)

Characterization of the HDAC/PI3K Inhibitor CUDC-907 as a Novel Senolytic

A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 9, entitled, “In vitro and in vivo effects of zoledronic acid on senescence and senescence-associated secretory phenotype markers.”

Zoledronic acid has been found to reduce fracture risk and, in some studies, to decrease mortality in humans and extend lifespan and healthspan in animals. Because senescent cells accumulate with aging and contribute to multiple comorbidities, the non-skeletal actions of zoledronic acid could be due to senolytic (killing of senescent cells) or senomorphic (inhibition of the secretion of the senescence-associated secretory phenotype (SASP)) actions.

In this new study, researchers Parinya Samakkarnthai, Dominik Saul, Lei Zhang, Zaira Aversa, Madison L. Doolittle, Jad G. Sfeir, Japneet Kaur, Elizabeth J. Atkinson, James R. Edwards, Graham G. Russell, Robert J. Pignolo, James L. Kirkland, Tamar Tchkonia, Laura J. Niedernhofer, David G. Monroe, Nathan K. Lebrasseur, Joshua N. Farr, Paul D. Robbins, and Sundeep Khosla from the Mayo Clinic, Phramongkutklao Hospital and College of Medicine, Eberhard Karls University, University of Minnesota, University of Oxford, and University of Sheffield tested the above hypothesis using multiple complementary approaches (in vitro, in vivo, and in silico) to evaluate possible effects of zoledronic acid on modulating cellular senescence.

The researchers first performed in vitro senescence assays using human lung fibroblasts and DNA repair-deficient mouse embryonic fibroblasts, which demonstrated that zoledronic acid killed senescent cells with minimal effects on non-senescent cells. Next, in aged mice treated with zoledronic acid or vehicle for 8 weeks, zoledronic acid significantly reduced circulating SASP factors, including CCL7, IL-1β, TNFRSF1A, and TGFβ1 and improved grip strength. Analysis of publicly available RNAseq data from CD115+ (CSF1R/c-fms+) pre-osteoclastic cells isolated from mice treated with zoledronic acid demonstrated a significant downregulation of senescence/SASP genes (SenMayo). 

To establish that these cells are potential senolytic/senomorphic targets of zoledronic acid, the team used single cell proteomic analysis (cytometry by time of flight [CyTOF]) and demonstrated that zoledronic acid significantly reduced the number of pre-osteoclastic (CD115+/CD3e-/Ly6G-/CD45R-) cells and decreased protein levels of p16, p21, and SASP markers in these cells without affecting other immune cell populations. 

“Collectively, our findings demonstrate that zoledronic acid has senolytic effects in vitro and modulates senescence/SASP biomarkers in vivo. These data point to the need for additional studies testing zoledronic acid and/or other bisphosphonate derivatives for senotherapeutic efficacy.”

DOI - https://doi.org/10.18632/aging.204701

Corresponding author - Sundeep Khosla - khosla.sundeep@mayo.edu

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Effects of Zoledronic Acid on Senescence and SASP Markers

BUFFALO, NY- March 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Exploring the effects of Dasatinib, Quercetin, and Fisetin on DNA methylation clocks: a longitudinal study on senolytic interventions.”

Senolytics, small molecules targeting cellular senescence, have emerged as potential therapeutics to enhance health span. However, their impact on epigenetic age remains unstudied. In this new study, researchers Edwin Lee, Natàlia Carreras-Gallo, Leilani Lopez, Logan Turner, Aaron Lin, Tavis L. Mendez, Hannah Went, Alan Tomusiak, Eric Verdin, Michael Corley, Lishomwa Ndhlovu, Ryan Smith, and Varun B. Dwaraka from the Institute For Hormonal Balance, TruDiagnostic, Buck Institute for Research on Aging, and Cornell University aimed to assess the effects of senolytic treatments on DNA methylation (DNAm), epigenetic age, and immune cell subsets. 

“[...] this study aims to comprehensively assess the impact of senolytic drugs on epigenetic aging through two longitudinal studies to address our research objective. The initial investigation focuses on a combination treatment of Dasatinib and Quercetin, while the subsequent phase incorporates Fisetin into the treatment regimen.”

In a Phase I pilot study, 19 participants received Dasatinib and Quercetin (DQ) for 6 months, with DNAm measured at baseline, 3 months, and 6 months. Significant increases in epigenetic age acceleration were observed in first-generation epigenetic clocks and mitotic clocks at 3 and 6 months, along with a notable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks. 

Building upon these findings, a subsequent investigation evaluated the combination of DQ with Fisetin (DQF), a well-known antioxidant and antiaging senolytic molecule. After one year, 19 participants (including 10 from the initial study) received DQF for 6 months, with DNAm assessed at baseline and 6 months. Remarkably, the addition of Fisetin to the treatment resulted in non-significant increases in epigenetic age acceleration, suggesting a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging. 

“Furthermore, our analyses unveiled notable differences in immune cell proportions between the DQ and DQF treatment groups, providing a biological basis for the divergent patterns observed in the evolution of epigenetic clocks. These findings warrant further research to validate and comprehensively understand the implications of these combined interventions.”

DOI - https://doi.org/10.18632/aging.205581

Corresponding authors - Varun B. Dwaraka - varun@trudiagnostic.com

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A Longitudinal Study on Dasatinib, Quercetin, and Fisetin Senolytic Interventions

BUFFALO, NY- October 22, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on September 26, 2024, entitled, “Use of the senolytics dasatinib and quercetin for prevention of pelvic organ prolapse in a mouse animal model.”

Pelvic organ prolapse is a common condition among women in the U.S., with a 13% estimated risk of requiring surgery by age 80. Senolytic agents like dasatinib and quercetin (D+Q) target age-related cellular senescence and reduce senescent cell activity in various disease processes.

In their paper, researchers Erryn Tappy, Haolin Shi, Jessica Pruszynski, and Maria Florian-Rodriguez from the University of Texas Southwestern Medical Center, Department of Obstetrics and Gynecology in Dallas, utilized a mouse model of pelvic organ prolapse, Fibulin-5 knockout (Fbln-5-/-) mice, to assess the ability of D+Q to prevent development of prolapse.

The D+Q injections administered did not result in significant differences in prolapse development but did reduce cellular senescence markers in Fbln-5-/- mice. This suggests senolytic agents may help mitigate the role of cellular senescence in tissue dysfunction associated with prolapse. The researchers suggest that further studies are needed to determine optimal timing, dosage, and delivery of senolytics for prolapse prevention.

"This study represents one of the first to evaluate the impact of senolytic agents D+Q on the clinical development of pelvic organ prolapse and expression of proteins associated with cellular senescence in a mouse model.”

DOI - https://doi.org/10.18632/aging.206120

Corresponding author - Maria Florian-Rodriguez - Maria.Florian-Rodriguez@UTSouthwestern.edu

Video short - https://www.youtube.com/watch?v=kTQfjhubx_4

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Keywords - aging, pelvic organ prolapse, cellular senescence, senolytic agents, animal model

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Senolytics Dasatinib and Quercetin for Prevention of Pelvic Organ Prolapse in Mice

BUFFALO, NY—February 18, 2025 — A new #research paper was #published by Aging (Aging-US) on January 8, 2025, in Volume 17, Issue 1, titled “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”

Researchers Kamendra Kumar, Bo-Hyun Moon, Santosh Kumar, Jerry Angdisen, Bhaskar V.S. Kallakury, Albert J. Fornace Jr., and Shubhankar Suman from Georgetown University Medical Center explored whether a drug called ABT-263 could help reduce the risk of gastrointestinal (GI) cancer caused by radiation exposure. Their findings suggest that ABT-263, a senolytic agent, helps eliminate harmful aging cells in the gut, reducing inflammation and lowering cancer risk in mice. These results could lead to potential treatments for people exposed to radiation, including cancer patients and astronauts.

Radiation exposure, whether from medical treatments, environmental sources, or space travel, can damage cells and increase the risk of GI cancer. One key factor in this process is cellular senescence, where damaged cells stop dividing but continue to release harmful molecules that promotes tumor growth. This study tested whether ABT-263, a drug designed to remove these aged cells, could lower cancer risk in a mouse model of GI cancer.

In this study, researchers exposed mice to radiation and found that it increased the number of damaged cells in their intestines, leading to more tumors. However, when the mice were given ABT-263, the number of harmful cells decreased, and they developed fewer tumors. The drug also reduced inflammation and blocked signals that promote cancer growth.

“Oral administration of ABT-263 in Apc1638N/+ mice resulted in a significant reduction in low-LET IR-induced intestinal tumor burden at 5 months post-exposure."

These findings highlight the potential of senolytic drugs like ABT-263 as a preventive treatment for radiation-induced cancers. This approach could be especially beneficial for cancer patients undergoing radiation therapy, astronauts exposed to cosmic radiation, and individuals at risk from environmental sources such as radon gas.

However, while ABT-263 showed promise, it also has known side effects, including reduced platelet counts, which can impact blood clotting. Future research will focus on optimizing senolytic treatments to ensure they are both safe and effective for human use. Scientists are also exploring alternative drugs and combination therapies that might offer the same benefits with fewer risks.

This study provides strong evidence that removing senescent cells could help prevent radiation-related GI cancer. With further research, senolytic drugs may become an important tool in protecting at-risk populations from the long-term effects of radiation exposure.

DOI - https://doi.org/10.18632/aging.206183

Corresponding author - Shubhankar Suman - ss2286@georgetown.edu

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Senolytic ABT-263 Reduces Radiation-Induced Gastrointestinal Cancer

In this #episode of the Longevity & Aging Series, Dr. Shubhankar Suman from the Department of Oncology at Georgetown University Medical Center joins host Dr. Evgeniy Galimov to discuss a #research paper he co-authored in Volume 17, Issue 1 of Aging (Aging-US), titled: “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”

DOI - https://doi.org/10.18632/aging.206183

Corresponding author - Shubhankar Suman - ss2286@georgetown.edu

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Keywords - aging, senescence-associated secretory phenotype, senolytic agent, carcinogenesis, inflammation, β-catenin

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Longevity & Aging Series (S3, E4): Dr. Shubhankar Suman

BUFFALO, NY — June 4, 2025 — A new #editorial was #published in Aging (Aging-US) Volume 17, Issue 5, on May 29, 2025, titled “Rethinking healthcare through aging biology.”

In this scientific editorial, Aging (Aging-US) Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG) and the University of Groningen (RUG), advocates for healthcare reform that addresses the biological drivers of aging rather than individual chronic conditions. The article proposes that targeting the root causes of age-related diseases through aging biology could revolutionize preventive care, extend healthspan, and reduce long-term healthcare costs. This proactive approach aligns with a growing body of aging research focused on improving healthy longevity.

Dr. Demaria explains that today’s disease-focused model is inadequate for aging populations, who often suffer from multimorbidity—the presence of multiple chronic illnesses like cancer, heart disease, and type 2 diabetes. These overlapping conditions, rooted in common aging mechanisms, overwhelm healthcare systems and lead to complex treatments with limited success. The editorial suggests that identifying and intervening in the biological aging process could prevent such diseases before they emerge.

In the editorial, Dr. Demaria outlines three healthcare paradigms. The first is the existing system, which reacts to disease after symptoms appear. The second involves intervening once age-related damage begins, using new tools such as senolytics, which eliminate harmful senescent cells, and rapalogs, which regulate cellular metabolism. The third and most forward-looking model focuses on preventing aging-related damage before it starts. This strategy supports lifelong biological balance and seeks to avoid early molecular decline through continuous health maintenance.

Prevention is key in this model. Lifestyle choices—such as exercise, a healthy diet, quality sleep, and stress reduction—play a vital role in slowing the aging process. Dr. Demaria also points to the promise of biological age diagnostics—tools or tests that estimate a person’s biological age—which allow people to track their physiological aging and adopt personalized interventions. Additionally, optimizing maternal nutrition and early-life health can contribute to lifelong disease prevention.

To support this shift, the editorial calls for major changes in medical education. Physicians must be trained in geroscience, healthspan optimization, and personalized preventive care. This knowledge will prepare future clinicians not just to treat disease, but to delay or prevent it altogether. Collaboration among healthcare providers, researchers, and policymakers will be essential for building this new system.

​​“The third paradigm—preventing aging-related damage—demands a systemic shift toward predictive and preventative research, with an emphasis on multi-omic data, lifestyle interventions, and early-life interventions.”

By redefining medicine around the science of aging, Dr. Demaria’s editorial highlights the path toward healthier aging, longer life expectancy, and a more sustainable healthcare future.

DOI - https://doi.org/10.18632/aging.206262

Corresponding author - Marco Demaria - m.demaria@umcg.nl

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New Vision for Healthcare Focuses on Preventing Aging-Related Diseases

Recent discoveries in #aging research reveal a powerful insight: the biological changes that lead to chronic #diseases begin far earlier than most people realize—often in midlife, well before symptoms appear. This early phase offers a valuable opportunity for prevention. As highlighted in a recent editorial by Marco Demaria, Editor-in-Chief of Aging and a researcher at the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, and the University of Groningen (RUG), the aging process itself – not just the diseases it produces – can and should be a primary focus of healthcare. 

The Problem with Traditional Medicine

While modern healthcare has extended lifespan and improved treatment for many diseases, it tends to be insufficient in addressing the complex needs of aging populations. Older individuals frequently experience multiple chronic conditions simultaneously, such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. This state of multimorbidity complicates care, increases the use of multiple medications, and reduces quality of life. The dominant traditional healthcare system, which typically begins only after symptoms appear, is costly and insufficient for addressing the interconnected nature of these conditions.

A New Model for Healthcare: Insights from the Editorial

In his recent editorial, “Rethinking healthcare through aging biology,” published in Aging Volume 17, Issue 5, Dr. Demaria outlines a shift from disease-specific treatment to targeting the biological mechanisms of aging itself, a more integrated and forward-looking approach. He presents three evolving healthcare models.

Full blog - https://aging-us.org/2025/06/a-new-vision-for-healthcare-addressing-aging-before-disease-begins/

Paper DOI - https://doi.org/10.18632/aging.206262

Corresponding author - Marco Demaria - m.demaria@umcg.nl

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Keywords - aging, healthcare, senolytics, epigenetics, medical education

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A New Vision for Healthcare: Addressing Aging Before Disease Begins

BUFFALO, NY — August 11, 2025 — Aging (Aging-US) is proud to support a milestone event for the global senescence and aging research community.

This coming September 16-19, 2025, Rome, Italy will host two back-to-back events that will define the next chapter of senescence science and translation:

-10th Annual International Cell Senescence Association (ICSA) Conference
-Senotherapeutics Summit – organized with the Phaedon Institute

This combined program could not come at a more important time. The field is entering a transformative phase:

-Multiple clinical trials on senolytics and senomorphics are now reporting results, offering the first real-world evidence of their therapeutic potential.

-Exciting new discoveries in senescence mechanisms, biomarkers, and tissue-specific roles are reshaping our understanding of when and how to target these cells.

For the first time, the leading fundamental science meeting on cellular senescence will be directly connected with a global summit dedicated to the clinical and commercial development of senotherapeutics. This unique integration will allow participants to seamlessly move from bench to bedside discussions, exploring both the latest research and its translation into therapies that could transform how we approach aging and age-related diseases.

Highlights include:

-Keynotes from pioneers driving both discovery science and translational innovation

-Sessions on mechanisms, biomarkers, and emerging targets

-Industry and regulatory panels on clinical trial design, safety, and approval pathways

-Case studies from ongoing and completed human trials

-Networking with leaders from academia, biotech and pharma

Celebrate a decade of ICSA and help chart the path for the next generation of senescence science and therapeutics.

Registration is still open: https://icsa2025rome.com/

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Aging-US Supports Landmark Senescence and Aging Research Events in Rome

Aging (Aging-US) Supports Landmark Senescence and Aging Research Events in Rome

BUFFALO, NY — September 23, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 7, 2025, titled “Senescent cell heterogeneity and responses to senolytic treatment are related to cell cycle status during senescence induction.”

This study, led by first authors Francesco Neri and Shuyuan Zheng, together with corresponding authors Denis Wirtz, Pei-Hsun Wu, and Birgit Schilling from the Buck Institute for Research on Aging, the USC Leonard Davis School of Gerontology, and Johns Hopkins University, reveals that not all aging cells behave the same. The researchers identified key differences between senescent cell subtypes that may influence how well they respond to senolytic drugs. These findings could help guide the development of more effective therapies for age-related diseases.

Senescent cells are aged or damaged cells that stop dividing and accumulate in tissues over time. While they play a role in wound healing and protecting against cancer early in life, they can drive chronic inflammation and tissue decline with age. Researchers are exploring ways to selectively remove these cells using senolytic drugs. However, the large variety of senescent cell types has made it difficult to design treatments that work for all of them. This study aimed to better understand the functional differences among senescent cell subpopulations.

Using high-resolution imaging, the team analyzed thousands of human endothelial and fibroblast cells growing in the lab. They observed that cells that exited the cell cycle (stopped dividing) in a later phase showed stronger signs of senescence and were more sensitive to senolytic treatment. These cells also produced more IL-6, a molecule associated with inflammation. The findings suggest that DNA content, which varies depending on the cell cycle phase, plays an important role in how aging cells function and how they respond to drugs.

“We found that G2-arrested senescent cells feature higher senescence marker expression than G1-arrested senescent cells.”

This is the first clear evidence that senescent cells do not all respond equally to treatment. The results suggest that future senolytic therapies could be more successful if they are designed to target specific subtypes of senescent cells, especially those with greater inflammatory potential.

While this research was conducted in laboratory cell cultures, it provides a foundation for studying how these findings apply to living tissues. Future work will examine whether similar patterns occur in the body and how this knowledge could lead to more precise and effective treatments for age-related conditions. Understanding the diversity of aging cells is key to developing therapies that are both safer and more targeted.

DOI - https://doi.org/10.18632/aging.206299

Corresponding authors - Denis Wirtz — wirtz@jhu.edu, Pei-Hsun Wu — pwu@jhu.edu, and Birgit Schilling — bschilling@buckinstitute.org

Abstract video - https://www.youtube.com/watch?v=x8bhKEFLzqA

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Keywords - aging, cellular senescence, imaging, heterogeneity, senolytics, cell cycle

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