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Name: Dasatinib

Class: Drug (selective tyrosine kinase receptor inhibitor that is prescribed for certain types of leukemia)

Alias(es): CAS# 302962-49-8; Trade names: Sprycel; Dasanix

Background: Dasatinib, sold under the brand names Sprycel and Dasanix, is a synthetic medication available by prescription only, that has been FDA approved since 2006[1], and is currently approved for treating chronic Philadelphia chromosome-positive (Ph+) myeloid leukemia in both adults and children[2,3]. Dasatinib has shown specificity for clearing senescent cells of certain types, i.e. preadipocytes (progenitor fat cells that have hormonal, metabolic, and pro-inflammatory functions) both in vitro in human cells and in vivo in mice and rats. There are no results yet for clinical studies involving dasatinib for treating aging in humans, but preclinical studies involving the combination of dasatinib and another senolytic, quercetin, (D+Q) to target a broader range of senescent cells have shown promising results in terms of extending healthspan and lifespan and ameliorating age-related dysfunctions (see preclinical studies section). 

Is there evidence it works in humans for aging? ID

And Reference

Trial Status




Active, not Recruiting

The Safety and Effectiveness of Quercetin and Dasatinib on the Epigenetic Aging Rates in Healthy Individuals

This prospective non-randomized clinical study will involve participants (≥ 40 yrs.old) taking 500mg Quercetin and 50mg Dasatinib oral capsules on Monday, Tuesday, Wednesday (3 days in a row) per month for the duration of 6 mo.

It will evaluate the change from baseline in epigenetic age test results (to be obtained via the illumina 850k epic array).


Not Yet Recruiting

Pilot Study to Test the Safety and Efficacy of Metformin, Dasatinib, Rapamycin and Nutritional Supplements (Bio-quercetin; Bio-fisetin; Glucosamine; Nicotinamide Riboside; Trans-resveratrol) in Reducing Clinical Measures of Aging in Older Adults

This study is also known as the VIAging Deceleration Trial Using Metformin, Dasatinib, Rapamycin and Nutritional Supplements.

 It will be accepting healthy volunteers ≥ 65 years old.


This study will involve first taking metformin and gradually increasing the dose. Then dasatinib, bio-quercetin, and bio-fisetin will be added. Then glucosamine, NR, and resveratrol will be added. And lastly rapamycin will be taken, at which point the subjects will continue on this intervention (taking all of these compounds) for 12 months. 

The study will evaluate: adverse effects of treatments, DEXA scans of visceral adipose tissue, systolic blood pressure, senescent cell levels, glucose control, and DNA methylation via GrimAge.

Estimated study completion date is December 2023.

Is there evidence it works in preclinical studies for aging?

Dasatinib + Quercetin (D+Q) preclinical studies: Benefits of D+Q for aging (as demonstrated in preclinical studies) include reduction of senescent cell burden and inflammatory markers, and improvements in cardiovascular health, gut microbiome, fatty liver disease, bone health and disc degeneration, strength and physical health, and cognitive health. See table below for references and details.





Mice and human cells


  • Dasatinib more effectively targeted senescent human preadipocytes, but was much less effective in senescent HUVECs while Quercetin was less effective in the former and more in the latter.

  • D+Q combo is more effective than either D or Q alone at targeting a broader range of human and mouse senescent cell types in vitro.

  • Single dose of D+Q (oral) was effective at reducing senescent cell burden in vivo in mice, although not all senescent cells were removed.

  • Following irradiation of one leg of wild-type mice:

    • Single dose with D+Q reduced p16 expression in muscle and SA-βGal+ cells in fat at the site of localized ionizing radiation/

    • Single dose of D+Q led to sustained improvement in exercise endurance for 7  months.

  • Treatment of 24-month-old mice with a single dose of D+Q significantly improved left ventricular ejection fraction and fractional shortening (measures of heart function). 

  • D+Q caused statistically significant improvements in vascular endothelial function.

  • D+Q, yielded physiologically important and consistent improvements in vascular smooth muscle sensitivity to nitroprusside.

  • D+Q significantly extended healthspan in progeroid (Ercc1-/Δ) mice.

Zhu et al., 2015



Chronic D+Q (oral) cleared some types of senescent cells, and alleviated vasomotor dysfunction in naturally aged mice and mice with established atherosclerosis via modulation of nitric oxide (NO). D+Q reduced aortic intimal plaque calcification but did not affect plaque fibrosis.

Roos et al., 2016

Mice (aged)

In Vivo

D+Q treatment significantly reduced intestinal senescence (as measured by markers p16Ink4a and p21Cip1) and inflammation (as measured by markers Cxcl1, Il1β, Il6, Mcp1, and Tnfα), and it altered the gut microbiome composition in aged mice (suggests it may treat age-related dysbiosis). Placebo-controlled.

Saccon et al., 2017



Found that accumulation of senescent cells promotes accumulation of fat in the liver and steatosis (liver fat build-up). Thus aging is a contributing factor in causing non-alcoholic fatty liver disease (NAFLD). D+Q effectively reduced overall liver steatosis by removing senescent cells. Mechanism: mitochondria in senescent cells inefficiently metabolize fatty acids, but senolytic therapy with D+Q therapeutically addresses this.

Ogrodnik et al., 2017

Mice, human cells


  • In vitro

    • D+Q effectively reduced senescent cell levels (TAF+, p16INK4A-highly expressing, and SA-βgal+ cells) in human fat tissue from obese individuals by inducing apoptosis. 

    • D+Q did not change senescent cell levels in macrophages.

    • D+Q reduced levels of pro-inflammatory cytokines including SASP, but did not reduce levels of factors required for adipose tissue function and viability. 

    • D+Q was more effective than either D or Q alone.

  • In vivo:

    • D+Q prevented and eliminated physical dysfunction induced by senescent cell transplantation in mice.

    • D+Q cleared senescent cells, alleviated age-related physical dysfunction, and increased late-life survival of aged mice (36% post-treatment median lifespan extension) without extending morbidity (increased median lifespan and healthspan).

Xu et al., 2018

Mice C57BL/6 (aged)

In Vivo

  • Weekly injection of D+Q until 23 months of age and beginning at 6 and 14, but not 18 months of age, resulted in lower incidence of disc degeneration and significant decreases in senescence (markers:  p16INK4a, p19ARF). This suggests that there is a window for successful D+Q treatment (about mid-age in human years) of disc degeneration. However, in established disc degeneration, D+Q treatment may be too late.

  • D+Q resulted in lower circulating levels of certain inflammatory cytokines in all treatment groups, although it was most pronounced in the groups treated from a younger age.

  • D+Q treatment from 14 months of age lowered SASP levels (IL-6 and MMP13), preserved healthy extracellular matrix (ECM), decreased age-related aggrecan degradation, lowered the incidence of disc fibrosis, and modified transcription of key pathways in disc cells to more closely resemble younger cells.   

  • Increased strength in 6mo (young) treatment group.

  • No adverse effects of long-term treatment.

Novais et al., 2021 

Mice (aged)


D+Q improved bone forming capacity of bone marrow mesenchymal stem cells (BSMCs) from aged mice both in vitro and in vivo.

Zhou et al., 2021

Mice (C57Bl/6J)


D+Q injected bi-weekly into young (3mo) and old (20mo) mice following injury resulted in blunted muscle regeneration in young mice, but improved muscle regeneration in old mice. Additionally, D+Q treated old mice had significantly less senescence levels than old controls. In vitro experiments showed that D+Q improved  myogenic progenitor cell proliferation.

Dungan et al., 2021



There is an age-dependent increase in p16Ink4a-positive senescent cells and SASP (inflammation) in brains of mice. Aged mice also experience cognitive decline.Study used INK-ATTAC mice, in which a drug (AP20187) can eliminate p16Ink4a-positive senescent cells. Both D+Q (given orally) and the AP20187 drug (via injection) resulted in a decrease in p16Ink4a-positive microglia and SASP factors in the hippocampus brain region of naturally aged mice, and both treatments significantly improved cognitive function. This suggests that brain inflammation and cognitive decline may be successfully treated with systemic senescent-cell clearance via oral D+Q.

Ogrodnik et al., 2021

Mice (male)


In vivo: D+Q once per month for 4 months significantly lowered senescence levels (p16ink4a mRNA) in bone and the percentage of senescent osteocytes in aged (20mo old) mice vs controls. Significantly cleared senescent cells in 24mo old treated mice, improved spine and femur bone morphology, and improved femur thickness and strength. Lower osteoclast numbers and bone resorption were observed.

Farr et al, 2021

Mice (SAMP10)


In vivo, D+Q (oral) results in improved frailty index, motor and cognitive function, and hippocampal senescent cell levels in SAMP10 (brain-aging model) mice. In vitro, inducing senescence via oxidative stress in differentiated muscle and neuronal cells, then treating with D, Q, or D+Q, resulted in decreased p16Ink4a  expression and number of senescent cells (SABG assay) via apoptosis. D+Q treatment was more effective than D or Q alone.

Ota et al., 2022

Wistar rats


  • D+Q (oral) improved age-related cognitive impairment in old rats & lasted 5 weeks after stopping D+Q; had no effect on younger rats.

  • D+Q decreased peripheral inflammation including SASP factors in aged rats.

  • Mechanism: Did not find decreased senescent cell burden in brain tissue, but found increased synaptic plasticity and modification of H3 histone

Krzystyniak et al, 2022

Dasatinib Mechanism:

The figure above is from a review by Martel et al., 2020. It shows the pathways inhibited by senolytic supplements, such as Quercetin, and drugs, such as Dasatinib, that lead to reduced viability of senescent cells and/or apoptosis of senescent cells.

Dasatinib (D) is a synthetic src-tyrosine kinase inhibitor, and has been found to be senolytic against human pre-adipocytes without affecting non-senescent cells[4]D promotes apoptosis of senescent cells by targeting Src family tyrosine kinases, (i.e. BCR/ABL, Src, c-Kit, ephrin), which are known to be Senescent Cell Anti-Apoptotic Pathway (SCAP) components, a pro-survival network utilized by senescent cells to avoid apoptosis[5]. The senolytic activity of D reduces levels of Senescence-Associated Secretory Phenotype (SASP), an inflammatory and damaging property of senescent cells. D is commonly used in combination with quercetin (Q), a flavonoid senolytic that targets senescent endothelial cells, to achieve a broader senolytic effect than when either are used alone[6].

Are there known safety concerns?

In a 2018 human study involving treating idiopathic pulmonary fibrosis (IPF) patients (ages 55-84) with intermittent DQ (D:100 mg/day, Q:1250 mg/day, three-days/week over three-weeks), all patients were retained for the study course with no D+Q discontinuation. Although there was no placebo arm, the adverse events reported were consistent with previous placebo arms in trials for IPF, and there was only one serious adverse event (pneumonia and edema) which was completely resolved after hospitalization. There were no changes in laboratory tests to indicate any liver or kidney toxicity and pulmonary function did not change.

Dasatinib has been FDA approved since 2006[1], and is currently approved for treating chronic Philadelphia chromosome-positive (Ph+) myeloid leukemia in both adults[2] and children[3].

The drug label for SPRYCEL describes known side effects of use for dasatinib, although it is limited mainly to use in cancer patients: 


Literature Cited

1. Drug Approval Package: Sprycel (Dasatinib) NDA #021986 & 022072. (n.d.). Retrieved April 4, 2022, from  

2. Research, C. for D. E. and. (2018). 2010 Notifications. FDA.

3. Research, C. for D. E. and. (2019). FDA approves dasatinib for pediatric patients with CML. FDA.

4. Kirkland, J. L., & Tchkonia, T. (2020). Senolytic drugs: From discovery to translation. Journal of Internal Medicine, 288(5), 518–536.

5. Song, S., Tchkonia, T., Jiang, J., Kirkland, J. L., & Sun, Y. (2020). Targeting Senescent Cells for a Healthier Aging: Challenges and Opportunities. Advanced Science, 7(23), 2002611.

6. Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., Palmer, A. K., Ikeno, Y., Hubbard, G. B., Lenburg, M., O’Hara, S. P., LaRusso, N. F., Miller, J. D., Roos, C. M., Verzosa, G. C., LeBrasseur, N. K., Wren, J. D., Farr, J. N., Khosla, S., … Kirkland, J. L. (2015). The Achilles’ heel of senescent cells: From transcriptome to senolytic drugs. Aging Cell, 14(4), 644–658.

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