Sacred Lotus Chinese en Integratieve Geneeskunde

Relationship Graph

Sacred Lotus connections

Updated
Sep 2026

Drug: Senolytica

My Plan
◆ Frontier

Senolytica zijn stoffen die bedoeld zijn om senescente cellen te verwijderen, versleten cellen die stoppen met delen maar niet afsterven. Ze hopen zich op in verouderend weefsel en lekken ontstekingssignalen. Bij muizen zijn de resultaten sterk: het opruimen van deze cellen hield meerdere organen gezonder en verlengde bij normaal verouderde dieren de mediane levensduur. Bij mensen bestaat het werk uit twee kleine pilotstudies.

De ene schreef 14 patiënten met longfibrose in, de andere 9 met diabetische nierziekte. Beide maten cellulaire markers en fysiek functioneren; geen van beide mat overleving. De middelen bestrijken een breed spectrum, van dasatinib, een receptplichtig kankermedicijn, tot fisetine en quercetine, flavonoïden die als gewone supplementen worden verkocht. Van geen enkel senolyticum is aangetoond dat het het menselijk leven verlengt of een ouderdomsgerelateerde ziekte voorkomt.

Cost
Low to HigherLow to Higher · Cheap fisetin to costly dasatinib · intermittent dosing · claimed aging benefit unproven over years
Effort
Easy to ModerateEasy to Moderate
Results In
Months to LongerMonths to Longer

Findings & Outcomes

What It Is

Senolytics are compounds that clear senescent cells, sometimes called zombie cells: cells that stop dividing but do not die off, so they pile up in tissue as the body ages. Cellular senescence is one of the twelve recognized hallmarks in the biology of aging, the processes whose buildup defines growing old.

Senescent Cells and How Senolytics Target Them

1Cells stop dividing but do not die off

With age and stress, some cells enter senescence. They stop dividing, switch on survival programs that block the usual self-destruct signal, and remain in the tissue instead of being cleared away.

2They leak the SASP

These lingering cells secrete a mix of inflammatory signals, the senescence-associated secretory phenotype, or SASP. In this way a small number of non-dividing cells can irritate neighboring healthy tissue and sustain a low, steady background of inflammation.

3Senolytics trigger senescent-cell death

Senolytic compounds block the survival programs that senescent cells depend on, so those cells finally self-destruct as they were blocked from doing. The aim is to remove them while leaving healthy dividing cells largely alone.

What the Research Shows

The strongest data are in mice, and they show cause. The most convincing studies used a genetic on-switch that deletes senescent cells with no drug involved. Only that design can prove the cells actively drive aging. Deleting the cells kept several organs healthier, and in normally aged animals it raised median lifespan. Among aging interventions this is one of the more mechanistically grounded, and the causal mouse data are unusually clean. The mouse drug studies are one step weaker. They tested dasatinib plus quercetin, fisetin, and navitoclax against measures of function, tissue health, and lifespan.

In people the evidence is thinner: two small, open-label pilots, neither with a control group. The first enrolled 14 patients with idiopathic pulmonary fibrosis, tracked cellular markers and short physical-function tests, and reported better physical function, such as walking distance. The second enrolled nine patients with diabetic kidney disease and followed senescence markers and mobility over days to weeks. Neither pilot measured survival or a disease outcome.

Strong results in mice have often failed to carry over to people.

Both pilots, and the review most often cited on the topic, come mostly from one research group at the Mayo Clinic. Some of its members hold patents or financial interests in senolytic drugs.

The Research & Studies

Everything here is based on the research we have collected and checked, sorted into groups and ordered with the strongest evidence first. Click any claim to open the studies behind it.

How it works

Senescent cells leak inflammatory SASP signals that harm nearby tissueModerate · mixed
In plain terms

Worn-out cells that do not clear out leak inflammatory signals that irritate the healthy tissue around them.

In detail

Senescent cells that linger in tissue secrete a mix of inflammatory cytokines, chemokines, growth factors and proteases, defined as the senescence-associated secretory phenotype (SASP). This secretion lets a small number of non-dividing cells disturb surrounding healthy tissue and sustain low-grade inflammation. The SASP is well characterized in cell and tissue studies; how much of any one person's age-related decline it drives, versus the other aging processes, is harder to isolate.

The study · 1

Coppé 2008, PLoS Biology · PLoS Biology, 2008

Senolytics switch off the survival programs senescent cells rely onModerate · mixed
In plain terms

Senescent cells stay alive by switching on survival programs; senolytics switch those off so the worn-out cells self-destruct.

In detail

Senescent cells survive by turning up anti-apoptotic (pro-survival) networks. Mapping those networks identified dasatinib and quercetin as the first senolytics, compounds that block the survival signals so senescent cells undergo the programmed death they had been resisting, while dividing cells are largely spared. The selectivity is partial and differs by cell type: no single compound removes only senescent cells cleanly, and the best drug targets are still being defined.

The study · 1

Zhu 2015, Aging Cell · Aging Cell, 2015

Navitoclax blocks BCL-2 survival proteins and cleared senescent cells in miceModerate · mixed
In plain terms

Navitoclax blocks a survival protein senescent cells depend on, which cleared them and refreshed aged stem cells in mice.

In detail

Navitoclax (ABT263) inhibits the BCL-2 and BCL-xL survival proteins that senescent cells rely on. In aged and irradiated mice it cleared senescent cells and rejuvenated aged blood-forming and muscle stem cells. BCL-xL is also needed by platelets, so this on-target action lowers platelet counts, a dose-limiting effect that has shaped how the drug is tested.

The study · 1

Chang 2016, Nature Medicine · Nature Medicine, 2016

A three-day course cut senescent-cell counts in nine people with diabetic kidney diseasePreliminary
In plain terms

A short senolytic course measurably reduced the count of worn-out cells in human tissue, the first direct proof the drugs clear senescent cells in people.

In detail

In an open-label pilot in people with diabetic kidney disease, three days of dasatinib plus quercetin reduced the number of senescent cells in fat and skin biopsies and lowered several circulating SASP inflammatory factors when measured 11 days later. Only nine participants completed it, there was no control group, and it measured cell counts, not kidney function or any health outcome.

The study · 1

Hickson 2019, EBioMedicine · EBioMedicine, 2019

Longevity And Mortality

Clearing senescent cells delayed fat, muscle and eye aging in micePreliminary
In plain terms

Clearing senescent cells kept aging mice healthier for longer, delaying loss of muscle and fat tissue and the onset of cataracts.

In detail

In genetically engineered mice, switching on the removal of p16-positive senescent cells delayed the onset of age-related changes in fat, skeletal muscle and the eye, and slowed progression of disorders already under way. This used a genetic on-switch to delete the cells, not a senolytic drug, so it proves that senescent cells drive these disorders; it does not show that any pill does.

The study · 1

Baker 2011, Nature · Nature, 2011

Clearing senescent cells extended median lifespan in aged micePreliminary
In plain terms

Removing senescent cells let ordinary aged mice live meaningfully longer and kept several organs working better.

In detail

Clearing p16-positive senescent cells from normally aged mice extended median lifespan across two genetic backgrounds and delayed age-related deterioration of the kidney, heart and fat, without a rise in late-life illness. The clearance was again genetic, not a drug, and mouse lifespan results have often failed to carry over to people; this is a strong animal signal, not a human one.

The study · 1

Baker 2016, Nature · Nature, 2016

Fisetin lowered senescence markers and extended lifespan in aged micePreliminary
In plain terms

Fisetin, a plant compound, lowered senescent-cell markers and lengthened life in aged mice.

In detail

Fisetin, a flavonoid found in strawberries and other plants, reduced senescence markers in several tissues of aged mice and extended median and maximum lifespan even when started late in life. The doses were high relative to what diet provides, the work is in mice, and a supplement bought at nutritional doses is not the same as the intervention that was tested.

The study · 1

Yousefzadeh 2018, EBioMedicine · EBioMedicine, 2018

No human trial has yet shown senolytics extend life or prevent diseasePreliminary · mixed
In plain terms

In people, senolytics have moved cellular markers and small function tests so far, and no study has shown they make anyone live longer or get sick less.

In detail

Across the field, senolytic human trials remain early-phase and small, and have measured biomarkers such as senescent-cell counts and physical-function tests, not survival, disease-free years, or other hard outcomes. No trial has yet shown that senolytics extend human life or prevent an age-related disease. This describes where the trials currently stand, and several larger studies are under way; it is a statement about what has been measured, not a conclusion that the effect is absent.

The study · 1

Kirkland 2020, Journal of Internal Medicine · Journal of Internal Medicine, 2020

Muscle And Strength

Dasatinib plus quercetin improved walking speed and strength in aged micePreliminary
In plain terms

The dasatinib-and-quercetin combination made old mice faster, stronger and more active, and even a few senescent cells were enough to weaken young mice.

In detail

Intermittent dasatinib plus quercetin improved walking speed, endurance and grip strength in naturally aged mice, and transplanting a small number of senescent cells into young mice was enough to cause physical dysfunction that senolytics then reduced. These are mouse measures of function; the same intermittent dosing has not been shown to improve strength or mobility in healthy people.

The study · 1

Xu 2018, Nature Medicine · Nature Medicine, 2018

Respiratory

In 14 pulmonary fibrosis patients, walking distance and gait speed improved while lung function did notPreliminary
In plain terms

In the first human trial, people with a serious lung-scarring disease could walk a little further and move a little faster after senolytics, though their lung function itself did not change.

In detail

In the first human senolytic study, 14 patients with idiopathic pulmonary fibrosis took intermittent dasatinib plus quercetin over three weeks. Measures of physical function improved, including six-minute walk distance and gait speed, while lung function and other clinical measures did not change. It was small, open-label and had no control group, so the improvement could reflect expectation or practice on the tests; it shows feasibility and a signal, not a demonstrated benefit.

The study · 1

Justice 2019, EBioMedicine · EBioMedicine, 2019

How It Works

For most of the 20th century, senescent cells were seen as protective. A cell that has stopped dividing cannot turn into a tumor, so senescence suppresses cancer, and that role still holds. The harm shows up later, once these cells accumulate in aging tissue and stay there.

The agents reach the cell by different routes. Dasatinib and quercetin are given together, called D plus Q, because the two cover different cell types: dasatinib hits some senescent cells harder, quercetin others. Navitoclax works another way, blocking the BCL-2 family of survival proteins head-on.

The dosing follows from that biology. Senolytics are given in short, intermittent courses spaced weeks apart. A senescent cell takes weeks to build back up, so one short course can clear a batch without the drug needing to stay in the body. Short exposure keeps side effects low.

Go Deeper

  • The biology of aging: where cellular senescence sits among the twelve hallmarks, and why clearing it is one idea among many.
  • Autophagy: the cell's routine recycling of its own worn parts, a related but separate arm of cellular housekeeping.
  • Urolithin A: another compound aimed at cellular renewal, with small human trials and outsized marketing.

The Chinese Medicine View

The tradition predates the concept of a senescent cell, so it names no herb or channel for one. Two of its broader ideas still sit near where senolytics act.

The first is turnover. Chinese medicine treats health partly as the free movement of the body's substances. The classics count the buildup of the stale, the stagnant, and turbidity among the roots of disease. Clearing senescent cells so healthy tissue can renew is a loose parallel.

The second is the Kidney and its store of Jing, the essence, the deep constitutional reserve a person draws down across a lifetime. The classics describe its decline in signs close to what modern medicine calls aging.

Chinese medicine does not treat clearing as always good. The tradition separates draining, meant to clear the body out, from tonifying, meant to build a depleted person back up. Classical texts caution that draining a weak or depleted person can do harm. A cold, draining method in someone depleted injures that deep reserve.

Cautions For This Practice

Everything to be aware of is here, in one place. This practice suits most healthy people; a few situations call for real care.

Dasatinib is a prescription cancer drug

Dasatinib is an approved leukemia chemotherapy, and it carries the side effects of one, including fluid around the lungs, lowered blood counts, and bleeding risk. In senolytic research it is used only in monitored clinical trials, in short intermittent courses.

Navitoclax lowers platelet counts

Navitoclax blocks a survival protein that platelets also rely on, so it reduces the platelet count and raises bleeding risk. It remains an investigational drug studied under close monitoring.

Senolytic doses of fisetin and quercetin are not established

Fisetin and quercetin are sold as ordinary supplements at nutritional doses. Senolytic research uses far larger, intermittent doses. Their safety and benefit in people are not established.

This is not a do-it-yourself protocol

The senolytic trials are run in monitored clinical settings, with medical screening, defined doses, and follow-up. A dasatinib course sourced outside that setting skips every one of those safeguards.

These compounds interact with medications

Quercetin and dasatinib both affect the enzymes and transporters that clear other drugs, so they can change the blood levels of medicines a person already takes. Anyone on prescription drugs would want a pharmacist or clinician to check for interactions.

No safety data in pregnancy or breastfeeding

None of these compounds has safety data at senolytic doses during pregnancy or breastfeeding, so they are best avoided in those periods.

Start slow, be smart, read the research, and consult a professional if you have any concerns. This is here to inform your choice, not make it for you.

Common Questions

Will senolytics extend human lifespan?

Not on current evidence. In mice, clearing senescent cells raised median lifespan and kept organs healthier, but the effect has not been tested in people. The human pilots followed markers and function over a few weeks; neither followed survival. The larger, outcome-powered human trials now under way are the first designed to answer it.

Explore Related

Other pages this one connects to, by the evidence they share, the outcomes they touch, and the ground they cover.

Shares a source · 2 shared Two plant flavonoids sold as anti-aging senolytics. Fisetin has striking mouse results and no human efficacy trial; quercetin has a modest record, a few mmHg off blood pressure, and a long-known absorption problem.
Shares a source Aging is a set of cellular processes you can partly slow with basic health habits. What the twelve hallmarks mean, and where anti-aging molecules really stand.
Related evidence Quitting smoking is the biggest single improvement most people can make to their health, and the body starts recovering within a day. What quitting does, and the methods ranked by how well they work.
Related evidence What GLP-1 and dual GLP-1/GIP drugs like semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro, Zepbound) do for weight, blood sugar and the heart, how they work on appetite, the trade-offs (gut effects, muscle loss, regain after stopping, cost), what is not yet known, the Chinese medicine view, and why starting one is a decision made with a prescriber.
Related evidence Metformin is a cheap, decades-old diabetes drug that lowers blood sugar, cut heart attacks and deaths in overweight type 2 diabetes, and cut progression from prediabetes to diabetes by about a third.
Related evidence Rapamycin extends lifespan in mice more reliably than any other drug, even when started late in life, and it is an approved medicine for organ transplant and for a few specific diseases.

All 10 sources on this page independently checked and cross-referenced.

Thomas Dehli, Founder & Editor, Sacred Lotus

Sacred Lotus has published Chinese medicine reference material since 2001. Integrative pages are held to the same standard as the herb and formula library: cite the source, grade the claim at its real strength, and say where the research has not looked. This page is educational and it is not medical advice. Last reviewed and updated August 9, 2026.