What is FOXO4-DRI?
FOXO4-DRI is a synthetic senolytic peptide designed to selectively eliminate senescent cells — aged, dysfunctional cells that have permanently exited the cell cycle but stubbornly refuse to die through normal apoptotic mechanisms. The “DRI” in its name stands for D-retro-inverso, a specific structural modification strategy in which the peptide is constructed using D-amino acids (the mirror-image isomers of the naturally occurring L-amino acids) and the sequence is written in reverse order. This seemingly subtle change has profound consequences for the molecule’s behavior in biological systems: D-amino acids are not recognized by the proteases that routinely break down naturally occurring peptides, giving FOXO4-DRI exceptional metabolic stability and a dramatically extended functional lifespan in vivo compared to a conventional L-amino acid peptide of the same sequence.
The therapeutic concept behind FOXO4-DRI emerged from research conducted at Erasmus University Medical Center in Rotterdam, Netherlands, primarily from the laboratory of Peter de Keizer, Jan Hoeijmakers, and colleagues. Their key insight was that senescent cells remain alive not by accident, but by actively resisting apoptosis — and that a specific protein-protein interaction between FOXO4 and p53 is central to that resistance. In normal healthy cells, p53 functions as a tumor suppressor and apoptosis inducer. But in senescent cells, FOXO4 sequesters p53 in a transcriptional complex and redirects its activity away from the mitochondria-targeting genes that would otherwise trigger programmed cell death. By disrupting this interaction competitively, FOXO4-DRI releases p53 to do what it does in healthy stressed cells — drive the cell toward apoptosis through the intrinsic pathway.
What makes this approach scientifically distinctive is its selectivity. Senescent cells overexpress FOXO4 relative to their non-senescent neighbors, which means that competitive displacement of p53 from FOXO4 complexes preferentially affects cells where that interaction is most active. Normal, healthy proliferating cells express FOXO4 at much lower levels, making them far less sensitive to FOXO4-DRI’s pro-apoptotic activity. This selectivity window is the theoretical foundation for the entire senolytic strategy.
The biology of cellular senescence, and why its accumulation in aging tissues contributes to dysfunction, is explored in more detail in the Peptide Database’s aging and longevity section. For context on how FOXO4-DRI fits into the broader landscape of longevity-focused compounds being researched today, the AI Coach can provide a comparative overview.
Research Benefits
- Selective clearance of senescent cells: FOXO4-DRI appears to preferentially induce apoptosis in senescent cells while sparing healthy proliferating and quiescent cells, addressing one of the primary challenges of senolytic drug development.
- Restoration of physical fitness and exercise capacity: Mouse studies using fast-aging XpdTTD/TTD models showed improved running distance and grip strength following FOXO4-DRI treatment, suggesting functional restoration of muscle and metabolic performance.
- Improved renal function in aging models: Treated aged mice showed improvements in glomerular filtration and renal histology, consistent with clearance of senescent cells from kidney tissue where their accumulation contributes to fibrosis and inflammation.
- Fur density and coat quality restoration: Treated fast-aging mice in the Erasmus studies recovered lost fur density — a visually striking finding that reflects improved skin stem cell and dermal fibroblast function following senescent cell clearance.
- Reduction of SASP markers: Elimination of senescent cells reduces local secretion of the senescence-associated secretory phenotype (SASP), including pro-inflammatory cytokines like IL-6, IL-8, and MMP3 that damage surrounding tissue and drive chronic low-grade inflammation.
- Protease resistance enabling in vivo activity: The D-retro-inverso structure provides resistance to endogenous proteases, allowing FOXO4-DRI to remain functionally intact long enough to reach and act on senescent cell populations — a practical advantage over conventional L-amino acid senolytic peptides.
- Potentially reversible aging phenotypes: The de Keizer lab studies provided early evidence that some aging-associated tissue phenotypes are not merely the result of cumulative damage but are actively maintained by living senescent cells — and that clearing those cells can reverse, not just slow, certain manifestations of aging.
- Complementarity with small-molecule senolytics: FOXO4-DRI operates through a distinct mechanism from small-molecule senolytics like dasatinib+quercetin or navitoclax, raising the possibility that combination senolytic approaches could cover a broader spectrum of senescent cell subtypes.
How FOXO4-DRI Works
D-Retro-Inverso Structure and Protease Resistance
To understand why FOXO4-DRI is engineered the way it is, you need to appreciate the fundamental problem facing any peptide-based therapeutic: natural proteases in blood, tissues, and cellular compartments are extraordinarily efficient at degrading L-amino acid peptides. A conventional peptide constructed from natural L-amino acids might have a functional half-life measured in minutes to hours in a biological environment before enzymes like aminopeptidases, endopeptidases, and serum proteases cleave it into inactive fragments. For a drug designed to reach intracellular targets in specific cell populations, that’s a serious liability.
The D-retro-inverso strategy elegantly sidesteps this problem. D-amino acids are the stereochemical mirror images of the L-amino acids that make up all naturally occurring proteins. Because the active sites of proteolytic enzymes evolved to bind and cleave L-amino acid substrates in a specific spatial configuration, D-amino acid peptides are essentially invisible to those enzymes — they occupy the same chemical space but present the wrong stereochemical face for enzymatic recognition. The “retro” part of the DRI strategy (reversing the sequence direction) helps preserve the overall three-dimensional shape and surface charge distribution of the interaction domain, so that despite being built from mirror-image building blocks in reverse order, the molecule can still engage its biological target (the FOXO4:p53 interface) with appropriate affinity. The result is a peptide that maintains biological activity while dramatically resisting degradation — a key engineering achievement that translates directly into in vivo efficacy.
For researchers interested in the chemistry of peptide modifications and how structural changes affect stability and potency, the Peptide Database covers D-amino acid and retro-inverso approaches across multiple compound classes.
Competitive p53 Displacement from FOXO4 Complexes
The central mechanism of FOXO4-DRI is competitive displacement of p53 from its interaction with FOXO4 in senescent cells. Understanding why this matters requires understanding why senescent cells don’t die on their own despite expressing high levels of DNA damage markers and other signals that would normally trigger apoptosis.
In senescent cells, FOXO4 is upregulated and forms a nuclear complex with p53. Within this complex, p53 is directed toward the transcription of pro-survival FOXO4 target genes and held away from its mitochondria-associated pro-apoptotic functions. Specifically, p53 that is engaged in the FOXO4 complex cannot effectively translocate to the mitochondria to interact with pro-apoptotic BCL-2 family members and initiate the intrinsic apoptosis cascade. The FOXO4:p53 interaction therefore functions as a molecular lock that keeps senescent cells in their persistently living state.
FOXO4-DRI is designed to mimic the FOXO4 interaction domain that contacts p53, but as a free competitive inhibitor rather than a full-length FOXO4 protein. When FOXO4-DRI is present at sufficient concentration, it outcompetes endogenous FOXO4 for p53 binding. This displaces p53 from the nuclear FOXO4 complex, freeing it to relocate to the mitochondria. The displaced p53 then engages its canonical apoptotic functions at the mitochondrial outer membrane, triggering the conformational changes in BAX and BAK that initiate the intrinsic apoptosis pathway. The key selectivity element is that senescent cells have much higher FOXO4-p53 complex levels than normal cells — so the dose of FOXO4-DRI needed to reach therapeutic competition in senescent cells still falls well below the threshold that would meaningfully disrupt the lower-level FOXO4-p53 interactions present in normal tissue.
BAX/BAK Activation and the Intrinsic Apoptotic Pathway
Once p53 is released from the FOXO4 complex and translocates to the mitochondria, the downstream cascade follows the well-characterized intrinsic apoptosis pathway. p53 at the mitochondria interacts with pro-apoptotic BCL-2 family members BAX and BAK. Under normal homeostatic conditions in senescent cells, BAX and BAK are held in inactive states by anti-apoptotic BCL-2 family members (BCL-2, BCL-XL, MCL-1). When p53 tip the balance toward activation, BAX and BAK undergo conformational changes that allow them to oligomerize and insert into the outer mitochondrial membrane.
This insertion creates pores that permeabilize the mitochondrial outer membrane — a process called mitochondrial outer membrane permeabilization (MOMP). MOMP is the point of no return in intrinsic apoptosis. Cytochrome c and SMAC/DIABLO are released from the mitochondrial intermembrane space into the cytoplasm. Cytochrome c assembles with APAF-1 and procaspase-9 to form the apoptosome, which activates caspase-9. Active caspase-9 then cleaves and activates the effector caspases 3 and 7, which execute the orderly cellular disassembly that characterizes apoptosis. Importantly, this pathway produces a clean, immunologically quiet form of cell death (in contrast to necrosis), which means the senescent cells are eliminated without triggering the intense inflammatory response that necrotic death would provoke in surrounding tissue. The result — from the perspective of the tissue as a whole — is reduced cell number and reduced SASP burden, without an acute inflammatory insult to compensate for.
Research Findings
The Erasmus University Mouse Studies: Physical Fitness and Fur Restoration
The seminal FOXO4-DRI research published by de Keizer and colleagues in 2017 in the journal Cell used two distinct mouse aging models to evaluate the compound’s in vivo effects. The first was a cohort of naturally aged mice (approximately 2 years old in mouse terms, roughly equivalent to late middle age in humans). The second was the XpdTTD/TTD fast-aging model — mice carrying a mutation in the nucleotide excision repair gene XPD that causes accelerated accumulation of DNA damage and an aging phenotype that manifests earlier and more severely than in wild-type animals.
In both models, FOXO4-DRI treatment produced striking phenotypic improvements. Fast-aging mice that had lost significant fur density — a readout of impaired hair follicle stem cell function — regrew fur following treatment. Running capacity and grip strength, both of which decline with aging and cellular senescence in muscle and connective tissue, were substantially improved in treated mice compared to vehicle-treated controls. The magnitude of the functional recovery was not subtle: treated fast-aging mice showed performance metrics that more closely resembled younger wild-type animals than age-matched untreated fast-aging controls. These findings generated considerable excitement in the aging research community because they demonstrated not just slowing of deterioration but apparent reversal of established functional deficits — suggesting that at least some aging phenotypes are not solely the result of irreversible structural damage but are actively maintained by the continued presence and SASP activity of senescent cells.
Renal Function Restoration in Aged Mice
The Erasmus studies also examined renal function, using serum creatinine and blood urea nitrogen levels as functional readouts alongside histological analysis of kidney tissue. Aged mice treated with FOXO4-DRI showed improvements in these markers consistent with a reduction in senescent cell burden in the kidney. Histological examination revealed reduced evidence of fibrotic changes and glomerular abnormalities, consistent with the known contribution of renal tubular epithelial cell senescence to age-related kidney dysfunction.
This finding has particular translational significance because age-related kidney disease is both highly prevalent and strongly associated with mortality and quality-of-life decline in older adults. Senescent cells accumulate progressively in kidney tissue with aging and following acute kidney injury events, where they drive persistent inflammation and fibrosis through SASP secretion. The FOXO4-DRI renal function data provided one of the first demonstrations that a senolytic peptide approach could produce measurable improvements in organ-level functional endpoints — not just in biomarker levels or cell counts, but in physiological measures with clear clinical analogues.
SASP Reduction and Inflammatory Environment Normalization
One of the most consequential effects of senescent cell accumulation in aging tissues is the SASP — the senescence-associated secretory phenotype. Senescent cells secrete a characteristic cocktail of pro-inflammatory cytokines (including IL-6, IL-1β, TNF-α), chemokines (IL-8, MCP-1), matrix metalloproteinases (MMP1, MMP3), and growth factors that collectively create a chronic low-grade inflammatory environment in aging tissues. This “inflammaging” environment impairs tissue stem cell function, disrupts extracellular matrix integrity, promotes insulin resistance, and may contribute to the malignant transformation of neighboring cells by creating a permissive niche for pre-cancerous cells to expand.
When FOXO4-DRI eliminates senescent cells, the source of SASP factors is removed. Tissues treated with FOXO4-DRI in the Erasmus studies showed reduced expression of canonical SASP markers at both the mRNA and protein level, consistent with a genuine reduction in the senescent cell population rather than merely a suppression of SASP secretion without cell death. This distinction matters because senescent cells that are kept alive while their SASP is suppressed (as achieved by some SASP-modifying compounds) may remain capable of reinducing their full secretory program if suppression is withdrawn — whereas dead cells cannot resume SASP activity. Elimination rather than suppression represents a more durable approach to addressing the downstream consequences of cellular senescence.
Selectivity Profiling: Sparing of Normal Cells
The selectivity of FOXO4-DRI — its ability to kill senescent cells without harming healthy normal cells — is both its key claimed advantage and an area that requires careful scrutiny. The Erasmus studies included assessments of normal tissue integrity following FOXO4-DRI treatment, and did not observe significant toxicity in liver, spleen, intestinal epithelium, or hematopoietic compartments at the doses used. Flow cytometric analysis showed selective induction of apoptosis in senescent (p21-positive, p16-positive) cell populations with minimal apoptosis in co-cultured normal proliferating cells, supporting the concept that the FOXO4-p53 complex selectivity window translates into differential sensitivity in mixed cell populations.
However, it is important to note that these selectivity experiments were conducted in vitro and in specific mouse models with well-characterized senescent cell burdens. The generalizability of the selectivity window to other cell types, tissue contexts, and human senescent cell populations with varying FOXO4 expression levels is an active area of investigation. Certain cell types that rely on FOXO4 for normal quiescence or stress resistance might show unexpected sensitivity — a consideration that must be addressed in any clinical translation effort.
Comparison with Small-Molecule Senolytics
FOXO4-DRI’s mechanism-based approach to senolysis contrasts instructively with the small-molecule senolytic strategies that have been more extensively characterized in human studies. The dasatinib+quercetin (D+Q) combination — currently the most clinically studied senolytic regimen — works by inhibiting pro-survival kinases (BCR-ABL, SRC, and others with dasatinib) and flavonoid-mediated pathways (with quercetin) that support senescent cell survival. Navitoclax (ABT-263) targets BCL-2/BCL-XL directly. These compounds have different senescent cell type selectivity profiles, different toxicity concerns (navitoclax causes dose-limiting thrombocytopenia due to platelet dependence on BCL-XL), and different dosing strategies.
FOXO4-DRI’s advantage is mechanistic precision: by targeting the FOXO4:p53 complex specifically, it addresses a molecular feature that is directly mechanistically linked to the senescent cell survival phenotype rather than inhibiting a broadly expressed kinase or survival factor. Its disadvantage relative to small molecules is the inherent complexity and cost of peptide synthesis and the in vivo delivery considerations, including the need for injectable administration. The field’s trajectory points toward combination senolytic approaches that exploit complementary mechanisms to achieve broader senescent cell coverage — and FOXO4-DRI represents one potential component of such combinations.
Dosage and Administration
Doses Used in Preclinical Studies
In the de Keizer 2017 Cell paper, FOXO4-DRI was administered to mice via intraperitoneal injection at doses of approximately 5 mg/kg. Treatments were not continuous but rather intermittent — typically administered on specific days over a defined period rather than as a daily chronic regimen. This intermittent dosing approach reflects the senolytic concept: you are not trying to maintain constant receptor occupancy or sustained pharmacodynamic effect, but rather to trigger apoptosis in the senescent cell population during a treatment window and then allow the body to clear the apoptotic debris and normalize tissue function. The benefit, once the senescent cell burden is reduced, persists beyond the dosing period because the cells are dead rather than merely suppressed. This is analogous in principle to how antibiotic treatments can achieve lasting outcomes once an infection is cleared, rather than requiring indefinite administration.
Route of Administration
All preclinical FOXO4-DRI work to date has used intraperitoneal injection, which is a standard route in mouse studies but not clinically practical in humans. Subcutaneous injection would be the most likely translation route for human use, given that the D-retro-inverso structure provides stability against subcutaneous tissue proteases. Intravenous administration would offer better bioavailability but carries higher complexity and risk. No human pharmacokinetic studies of FOXO4-DRI have been published as of early 2026, so the optimal human dose, route, and frequency remain entirely uncharacterized from a clinical standpoint. Calculations for any experimental peptide reconstitution math can be explored through the Peptide Calculator.
Cycle Frequency and Duration
The preclinical data suggests that intermittent treatment windows — rather than continuous dosing — are consistent with the senolytic mechanism. Since the goal is senescent cell elimination rather than ongoing receptor engagement, there is a theoretical rationale for treatment courses separated by recovery periods that allow tissue remodeling and assessment before re-treating. Small molecule senolytic clinical trials have explored protocols such as two-day on, five-day off dosing cycles for D+Q, which reflects a similar intermittent logic. What an appropriate FOXO4-DRI treatment interval would look like in humans is unknown and would need to be determined through carefully designed phase 1 dose-finding studies. For context on how current senolytic clinical trials are structured, the AI Coach can summarize the available literature on human senolytic study designs.
Research Status and Human Application
FOXO4-DRI is currently a preclinical research compound with no completed human clinical trials as of early 2026. It is available from research peptide vendors for laboratory research purposes. Its use in human subjects outside of a formal clinical trial setting is entirely experimental, uncontrolled, and not informed by any human safety or efficacy data. The scientific community’s enthusiasm for the mechanistic concept is justified by the preclinical data, but the translation from mouse senolytic studies to human clinical benefit has not been established and carries substantial uncertainty. Anyone encountering this compound through research peptide markets should understand that they would be operating well outside the available evidence base. The Peptide Database maintains current information on the regulatory and research status of compounds in this category.
Safety and Side Effects
Preclinical Safety Profile
In the Erasmus mouse studies, FOXO4-DRI was reported to be well-tolerated at the doses used (approximately 5 mg/kg by intraperitoneal injection) with no significant toxicity observed in major organ systems including liver, kidney, spleen, gut epithelium, or bone marrow. Body weights were maintained in treated animals, and no overt signs of systemic toxicity were reported. Histological analyses of tissues from treated mice did not reveal evidence of widespread apoptosis in normal cell populations, consistent with the selectivity claims. However, the toxicological characterization available from these initial publications is relatively limited — the studies were primarily designed to demonstrate efficacy, not to provide comprehensive multi-dose, multi-timepoint safety profiling. More extensive preclinical toxicology studies, including maximum tolerated dose determinations and repeat-dose toxicology in multiple species, would be prerequisites for any serious clinical development program.
Theoretical Risks of Senolytic Strategies
Beyond the compound-specific safety profile, there are theoretical risks inherent to any senolytic strategy that deserve consideration. Senescent cells, despite their pathological contributions to aging, are not uniformly harmful. There is growing evidence that cellular senescence plays beneficial roles in specific contexts: wound healing (where transient senescence of fibroblasts contributes to proper tissue remodeling before immune clearance), embryonic development (where senescence of specific cell populations is required for tissue morphogenesis), and possibly in the acute response to certain infections and cancer. Aggressive senolytic activity that eliminates senescent cells indiscriminately across all tissue contexts could conceivably impair these beneficial functions. The FOXO4-DRI approach’s relative selectivity for persistently senescent cells (rather than transiently senescent ones) may mitigate some of these concerns, but the distinction between beneficial transient senescence and harmful chronic senescence is not always cleanly addressable through a pharmacological targeting approach.
Considerations for the Aging Research Community
FOXO4-DRI represents a scientifically elegant but early-stage concept in aging intervention research. The Erasmus studies from 2017 demonstrated compelling proof-of-concept results that generated deserved excitement, but several years of subsequent research have not yet produced a human clinical trial. The gap between striking mouse aging reversal data and human clinical benefit is a well-recognized challenge in the aging biology field — mouse models of aging, particularly fast-aging genetic models, do not always translate to the complex, multifactorial pathology of human aging. Responsible engagement with this research requires holding the enthusiasm generated by preclinical findings alongside genuine uncertainty about how and whether they will translate. The scientific community working on FOXO4-DRI and related senolytic approaches is actively working to close this translation gap, and the field is worth watching closely.
Frequently Asked Questions
DRI stands for D-retro-inverso. This describes a specific peptide engineering strategy in which the compound is built using D-amino acids (the mirror-image stereoisomers of naturally occurring L-amino acids) and the sequence is assembled in the reverse direction. This combination preserves the three-dimensional shape and biological activity of the peptide’s interaction domain while rendering it invisible to the naturally occurring proteases that would rapidly degrade a conventional L-amino acid peptide. The result is a compound with markedly improved metabolic stability and a much longer functional lifetime in biological environments.
Cellular senescence is a state in which cells permanently exit the cell cycle — they stop dividing — in response to various stressors including DNA damage, oxidative stress, oncogene activation, and telomere shortening. While senescence initially evolved as a tumor suppression mechanism (stopping damaged cells from proliferating and becoming cancerous), senescent cells that are not cleared by the immune system accumulate in aging tissues and drive pathology through the SASP — a chronic secretion of pro-inflammatory cytokines, matrix-degrading enzymes, and growth factors that impair tissue function, disrupt stem cell niches, and contribute to the systemic low-grade inflammation associated with aging. Clearing senescent cell accumulation is the central goal of senolytic therapy.
As of early 2026, no published human clinical trials of FOXO4-DRI have been completed. The compound has been studied extensively in mouse models, where it has produced compelling evidence of efficacy. The translation to human use requires extensive additional work: pharmacokinetic studies in human subjects, dose-finding and safety studies, and ultimately efficacy trials with relevant aging biomarkers or functional endpoints as primary outcomes. Several groups and companies are working on senolytic clinical development, but FOXO4-DRI specifically has not yet entered registered clinical trials to the knowledge available at this writing.
Dasatinib+quercetin (D+Q) is the most clinically advanced senolytic combination, with phase 1 and early phase 2 human studies completed. It works through a different mechanism than FOXO4-DRI: dasatinib inhibits pro-survival tyrosine kinases (including SRC and BCR-ABL) that senescent cells exploit for survival, while quercetin provides complementary flavonoid-mediated effects. The mechanistic difference means the two strategies may have different senescent cell type coverage — some populations may be more sensitive to one than the other. D+Q has the advantage of being further along in clinical evaluation and using commercially available pharmaceutical-grade compounds. FOXO4-DRI has the theoretical advantage of mechanism-based specificity for the FOXO4:p53 interaction that is directly linked to senescent cell survival, but remains in preclinical territory.
The elevated FOXO4 expression in senescent cells appears to be a direct component of the senescent cell survival program — a way the cell actively maintains its resistant-to-apoptosis state. Under various stress conditions that induce senescence (DNA damage, oncogene activation, etc.), transcription factor networks that regulate stress responses are reconfigured. FOXO4 is upregulated as part of this reconfiguration, forming the protective complex with p53 that prevents p53-mediated apoptosis. This upregulation appears to be functional rather than incidental: experimental knockdown of FOXO4 in senescent cells re-sensitizes them to apoptosis, confirming that the elevated FOXO4-p53 interaction is necessary for senescent cell survival. This necessity is what makes the FOXO4:p53 interface a rational therapeutic target.
This is a speculative but scientifically interesting question. Senescent cells within tumors — including therapy-induced senescent cancer cells generated by conventional chemotherapy or radiation — contribute to treatment resistance and tumor recurrence through SASP-mediated paracrine effects. If FOXO4-DRI could selectively eliminate therapy-induced senescent tumor cells, it might enhance the durability of cancer treatment responses. Several research groups have explored “one-two punch” strategies in which conventional therapy induces tumor cell senescence (which is anti-proliferative in the short term) followed by senolytic treatment to eliminate the residual senescent population. FOXO4-DRI has not been specifically characterized in this oncology context, but the mechanistic logic is applicable and represents an area worth watching in the research literature.
The senescence-associated secretory phenotype (SASP) is the characteristic pattern of inflammatory and matrix-modifying molecules that senescent cells secrete constitutively. Key SASP components include cytokines (IL-6, IL-1β, TNF-α, IL-8), chemokines that recruit immune cells, matrix metalloproteinases that degrade extracellular matrix, and various growth factors. The SASP was initially understood as a mechanism to recruit immune cells to clear senescent cells — but when immune clearance fails (as in aging, where immune surveillance declines), accumulating senescent cells create a persistent pro-inflammatory niche that impairs regenerative stem cell function, promotes insulin resistance, accelerates tissue fibrosis, and may create permissive conditions for neighboring pre-cancerous cells. Eliminating senescent cells eliminates the SASP source, which is one reason that senolytic approaches can produce broad tissue benefits beyond the direct effects of removing the senescent cells themselves.
The Peptide Database includes entries on epitalon, GHK-Cu, and other compounds being researched in aging contexts, with detailed mechanism and literature summaries for each. The AI Coach can provide a comparative analysis of senolytic strategies and help contextualize where FOXO4-DRI sits within the broader longevity research landscape. For basic peptide handling and reconstitution questions, the Peptide Calculator is a useful practical resource.
References
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- Childs BG, et al. “Senescent cells: an emerging target for diseases of ageing.” Nature Reviews Drug Discovery. 2017;16(10):718–735. PubMed
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- Zhu Y, et al. “The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs.” Aging Cell. 2015;14(4):644–658. PubMed
- Justice JN, et al. “Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study.” EBioMedicine. 2019;40:554–563. PubMed
- López-Otín C, et al. “The hallmarks of aging.” Cell. 2013;153(6):1194–1217. PubMed
- Demaria M, et al. “An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA.” Developmental Cell. 2014;31(6):722–733. PubMed
- Kirkland JL, Tchkonia T. “Senolytic drugs: from discovery to translation.” Journal of Internal Medicine. 2020;288(5):518–536. PubMed