FOXO4-DRI Research & Scientific Overview

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FOXO4-DRI Molecular Structure & Chemical Properties

FOXO4-DRI (FOXO4 D-Retro-Inverso) represents a breakthrough in senolytic peptide research, designed specifically to selectively eliminate senescent cells that accumulate with aging and contribute to age-related tissue dysfunction. First reported in 2017 by researchers at Erasmus University Medical Center, this synthetic peptide disrupts the interaction between FOXO4 transcription factor and p53 protein, enabling targeted apoptosis of senescent cells while sparing healthy cells. The peptide’s unique D-retro-inverso structure – featuring reversed amino acid sequence composed entirely of D-amino acids – provides exceptional resistance to enzymatic degradation, allowing prolonged biological activity that distinguishes it from conventional L-amino acid peptides. Studies across multiple organ systems have demonstrated that FOXO4-DRI can restore tissue homeostasis in models of accelerated aging, chemotherapy-induced damage, and natural aging, establishing it as one of the most extensively characterized senolytic compounds in preclinical research.

Chemical Structure

[IMAGE PLACEHOLDER] Insert 2D chemical structure image here Image URL: https://pubchem.ncbi.nlm.nih.gov/image/imgsrv.fcgi?cid=167312269&t=l Alt text: FOXO4-DRI molecular structure diagram showing D-retro-inverso peptide configuration Source credit: PubChem Position: Center-aligned below heading

2D molecular structure (Source: PubChem)

Technical Specifications

Property

Value

CAS Number

2460055-10-9

Molecular Formula

C228H388N86O64 (subscripted)

Molecular Weight

5358.1 g/mol

Amino Acid Sequence

DLeu-DThr-DLeu-DArg-DLys-DGlu-DPro-DAla-DSer-DGlu-DIle-DAla-DGln-DSer-DIle-DLeu-DGlu-DAla-DTyr-DSer-DGln-DAsn-Gly-DTrp-DAla-DAsn-DArg-DArg-DSer-Gly-Gly-DLys-DArg-DPro-DPro-DPro-DArg-DArg-DArg-DGln-DArg-DArg-DLys-DLys-DArg-Gly (all D-amino acids)

Half-Life (Plasma)

Not fully characterized; D-amino acid structure confers enhanced stability

Stability

Highly stable due to D-retro-inverso design; resistant to proteolytic degradation

Solubility

Water soluble; soluble in PBS and physiological buffers

Storage

Lyophilized: -20 degrees C; Reconstituted: 2-8 degrees C (stability varies by formulation)

The peptide’s D-retro-inverso structure involves reversing the amino acid sequence and using exclusively D-amino acids, creating a mirror image of the native FOXO4 binding domain that maintains biological activity while achieving dramatically improved resistance to peptidase degradation. The peptide incorporates an HIV-TAT cell-penetrating sequence to facilitate cellular uptake and intracellular accumulation.

FOXO4-DRI Mechanism of Action

FOXO4-DRI functions through a highly selective mechanism that exploits a unique vulnerability in senescent cells: their dependence on the FOXO4-p53 protein interaction for survival. Research has demonstrated that FOXO4-DRI acts as a competitive antagonist that disrupts the FOXO4-p53 complex, causing p53 nuclear exclusion and subsequent translocation to mitochondria where it triggers apoptosis specifically in senescent cells. This selectivity arises because senescent cells exhibit elevated FOXO4 expression and altered p53 regulation compared to healthy proliferating cells, creating a therapeutic window for targeted elimination.

Primary Cellular Pathways
FOXO4-p53 Interaction Disruption – Selective Senolysis

The core mechanism involves competitive inhibition of the endogenous FOXO4-p53 interaction. Studies using nuclear magnetic resonance spectroscopy revealed that FOXO4-DRI binds to the p53 transactivation domain with higher affinity than native FOXO4, dose-dependently displacing FOXO4 from the complex[1]. Key aspects include:

Competitive binding to p53 that prevents FOXO4 from sequestering p53 in the nucleus
Disruption of p53 localization within PML bodies and DNA-SCARS (DNA segments with chromatin alterations reinforcing senescence)
Selectivity index of 11.73-fold higher potency against senescent versus normal cells in fibroblast models
Rapid effect onset with apoptosis induction occurring 24-36 hours after administration

The D-retro-inverso modification ensures both the FOXO4-derived domain and the cell-penetrating sequence contribute to p53 binding, creating a two-component interaction that enhances specificity[2].

p53 Nuclear Exclusion and Mitochondrial Translocation

Following FOXO4-DRI treatment, active p53 is excluded from the nucleus and redirected to mitochondria. Research demonstrated that:

Ser15-phosphorylated p53 (active form) relocates from nuclear foci to the cytoplasm within hours of FOXO4-DRI exposure[3]
Mitochondrial p53 induces transcription-independent apoptosis through direct interaction with Bcl-2 family proteins
This pathway activates caspase-3/7, confirmed by real-time imaging showing senescent cells displaying bright green fluorescence from activated caspase-3 within 8 hours of treatment
Normal cells remain unaffected due to lower baseline FOXO4 expression and different p53 regulation
Cell-Penetrating Mechanism via HIV-TAT

FOXO4-DRI incorporates the HIV-TAT sequence to enable cellular entry through energy-independent mechanisms. Studies tracking peptide uptake showed:

Cellular accumulation detectable 2-4 hours after administration
Peptide remains intracellularly abundant and stable for at least 72 hours
High intracellular concentrations achieved despite relatively brief plasma half-life
Effective penetration across multiple cell types including fibroblasts, chondrocytes, and Leydig cells
Senescence-Associated Secretory Phenotype (SASP) Reduction

Beyond direct apoptosis induction, FOXO4-DRI treatment reduces inflammatory signaling from senescent cells. Research in aged mouse models demonstrated:

Decreased expression of IL-1 beta, IL-6, and TGF-beta in tissues following FOXO4-DRI administration[4]
Reduction in tissue-level inflammatory markers including TNF-alpha
Improved tissue microenvironment that supports healthy cell function
Preferential targeting of high-SASP-expressing senescent cell subpopulations
p53-Dependent Caspase Activation

The apoptotic cascade initiated by FOXO4-DRI operates through established p53-mediated death pathways. Mechanistic studies revealed:

Apoptosis is completely p53-dependent (eliminated by p53 knockdown)
Caspase activation is essential (blocked by pan-caspase inhibitors)
Both intrinsic mitochondrial and death receptor pathways may contribute
Cell death is cell-intrinsic apoptosis rather than necrosis or other forms of cell death

[CALLOUT BOX – Highlighted] Key Mechanistic Insight: FOXO4-DRI’s selectivity for senescent cells arises from their elevated FOXO4 expression and altered p53 regulation rather than recognition of a senescence-specific marker, creating a mechanistic vulnerability that healthy cells do not share. This represents a novel approach to senolysis distinct from BCL-2 family inhibitors or other senolytic strategies. [END CALLOUT BOX]

FOXO4-DRI Research Applications & Key Findings
Accelerated and Natural Aging Research
Fast-Aging Mouse Models

Groundbreaking research in XpdTTD/TTD mice (modeling trichothiodystrophy syndrome with accelerated aging) demonstrated dramatic improvements following FOXO4-DRI treatment[5]. Key findings include:

Restoration of fur density in mice that had experienced age-related hair loss
Improved exploratory behavior and increased running wheel activity
Enhanced kidney function with reduced plasma urea and creatinine levels
Decreased senescent cell burden in renal tubular cells (quantified by p16 expression and SA-beta-gal staining)

These mice normally exhibit a lifespan approximately half that of wild-type mice and develop aging phenotypes at only a few months of age, making them an ideal model for testing senolytic interventions.

Natural Aging in Wild-Type Mice

Studies in naturally aged wild-type mice (20-24 months old) confirmed that benefits extend beyond genetic aging models[6]:

Kidney function restoration comparable to effects in accelerated aging models
Increased physical activity and willingness to explore novel environments
Improved fur quality and density
Reduced interstitial senescence markers in kidneys
Decreased renal IL-6 expression

These findings demonstrated that therapeutic removal of senescent cells can restore tissue homeostasis even after age-related decline has already occurred.

Chemotherapy-Induced Damage and Tissue Repair
Doxorubicin Chemotoxicity Models

Research examined FOXO4-DRI’s ability to mitigate chemotherapy-induced senescence and organ damage. Investigations in doxorubicin-treated mice revealed[7]:

Complete neutralization of doxorubicin-induced liver damage (normalized AST levels, reduced IL-6 expression)
Prevention of body weight loss associated with chemotherapy
Reduction in hepatocyte senescence burden
Well-tolerated at doses that provided complete protection against chemotoxic effects

These results suggested potential applications in reducing treatment-related side effects in cancer therapy contexts.

Radiation-Induced Pulmonary Fibrosis

Studies in bleomycin-induced pulmonary fibrosis models demonstrated FOXO4-DRI effects on radiation-damaged tissue[8]:

Comparable efficacy to pirfenidone (approved anti-fibrotic medication)
Decreased senescent cell accumulation in lung tissue
Reduced collagen deposition and morphological changes
Increased type 2 alveolar epithelial cells and decreased myofibroblast populations
Downregulated SASP factor expression
Musculoskeletal and Cartilage Research
Senescent Chondrocyte Removal

Investigations relevant to autologous chondrocyte implantation (ACI) for cartilage repair examined FOXO4-DRI’s effects on expanded human chondrocytes. Research showed[9]:

Selective removal of over 50% of senescent cells in late-passage (PDL9) chondrocytes
No significant cell loss in early-passage (PDL3) non-senescent chondrocytes (selectivity demonstrated)
Significantly reduced SA-beta-gal staining in treated populations
Decreased expression of p53, p16, and p21 senescence markers
Lower SASP factor expression in cartilage tissue generated from treated chondrocytes

While chondrogenic potential enhancement was not observed, the reduction in pro-inflammatory secretory factors suggested potential benefits for tissue quality.

Reproductive Aging Research
Leydig Cell Senescence and Testosterone Production

Studies addressing male late-onset hypogonadism examined FOXO4-DRI effects on aged testicular tissue. Research in naturally aged mice (18-24 months) demonstrated[10]:

Selective apoptosis induction in senescent Leydig cells (11.73-fold selectivity over normal cells)
Improved testicular microenvironment with decreased interstitial SA-beta-gal activity
Reduced levels of senescence-associated proteins (p53, p21, p16)
Decreased inflammatory SASP factors (IL-1 beta, IL-6, TGF-beta) in testicular tissue
Alleviation of age-related testosterone secretion insufficiency

FOXO4 was specifically expressed in human Leydig cells, with nuclear translocation observed in elderly human testes correlating with decreased testosterone synthesis.

Cancer-Associated Fibroblast Research
Radiosensitization of Non-Small Cell Lung Cancer

Investigations explored FOXO4-DRI’s potential to target therapy-induced senescent cancer-associated fibroblasts (CAFs). Studies revealed[11]:

Senescence-like CAFs following radiotherapy promote cancer cell radioresistance through JAK/STAT pathway activation
FOXO4-DRI selectively induced apoptosis in senescence-like CAFs
Remarkable radiosensitizing effects on NSCLC cells both in vitro and in vivo
Simultaneous therapeutic effect on radiation-induced pulmonary fibrosis (RIPF)
Dual benefit: decreased cancer radioresistance and reduced normal tissue damage

[CALLOUT BOX – Highlighted] Critical Research Limitation: Despite extensive preclinical research across multiple organ systems and disease models, FOXO4-DRI has NO published human clinical trials in peer-reviewed literature. All efficacy and safety data derive exclusively from cell culture and animal models, primarily mice. Human safety profile, optimal dosing, pharmacokinetics, and therapeutic efficacy remain completely unestablished. [END CALLOUT BOX]

FOXO4-DRI Pharmacokinetics & Metabolism
Absorption & Distribution

FOXO4-DRI exhibits pharmacokinetic properties strongly influenced by its D-retro-inverso structure and cell-penetrating sequence. Following administration in preclinical models:

Intraperitoneal injection shows rapid systemic distribution in rodent studies
Cellular uptake detectable within 2-4 hours of administration
Intracellular accumulation persists for at least 72 hours despite peptide clearance from plasma
D-amino acid composition provides resistance to peptidase degradation in circulation and tissues

Distribution studies using immunohistochemistry demonstrated preferential accumulation in tissues with high senescent cell burdens, suggesting injury-site or senescence-associated targeting mechanisms. The HIV-TAT sequence enables energy-independent cellular entry through transient membrane pore formation, achieving high intracellular concentrations.

Metabolism & Elimination

The metabolic fate and clearance pathways of FOXO4-DRI remain incompletely characterized in published literature. Available research indicates:

D-amino acid structure confers enhanced metabolic stability compared to L-amino acid peptides
Standard proteolytic enzymes show reduced activity against D-amino acid substrates
Exact plasma half-life not published for FOXO4-DRI specifically
Biological effects persist significantly longer than would be predicted from typical peptide pharmacokinetics

A notable pharmacokinetic paradox exists: while the peptide likely undergoes relatively rapid plasma clearance (typical for peptides without specific modifications for extended circulation), intracellular persistence of 72+ hours and biological effects lasting days after single administration suggest either tissue retention, formation of active complexes, or persistent downstream signaling cascade activation.

Excretion Pathways

Limited published data characterize FOXO4-DRI excretion. Based on general peptide pharmacology and the available evidence:

Likely renal filtration and excretion of intact peptide and metabolites
D-amino acid degradation products may follow different excretion kinetics than L-amino acids
No accumulation detected in repeat-dosing studies in mice (administered every other day)
Complete characterization of excretion pathways requires further investigation

The disconnect between presumed rapid clearance and prolonged biological activity represents an important area requiring mechanistic clarification for translational development.

FOXO4-DRI Research Protocols & Administration
Dosing in Published Research

Research investigations have employed FOXO4-DRI across diverse dosing regimens depending on species, model, and research objective:

Mouse models: 5 mg/kg most common dose (range: 5-10 mg/kg)
In vitro cell culture: 25 micromolar standard concentration for senescent cell elimination
Aged mouse treatment protocols: 5 mg/kg every other day for 3 administrations typical
Chronic dosing studies: Once monthly administration sufficient for maintained effects in some models
Dose-response studies: Selectivity index maintained across range of concentrations with optimal therapeutic window

Important: These are experimental doses used in animal studies and cannot be extrapolated to other species due to significant differences in metabolism, receptor density, pharmacokinetics, peptide degradation rates, and tissue distribution. Species-specific factors including body surface area, metabolic rate, and senescent cell burden profoundly influence both efficacy and safety profiles. Human dosing parameters remain completely unestablished.

Administration Routes in Research

Multiple delivery methods have been investigated in preclinical studies:

Intraperitoneal injection – Most common route in mouse studies; reliable systemic delivery with rapid distribution
Subcutaneous injection – Used in some protocols; may provide slower absorption and more sustained levels
Intravenous injection – Employed primarily for pharmacokinetic characterization studies
Local application – Investigated for specific applications requiring tissue-targeted delivery

The optimal administration route for clinical translation remains to be determined and may vary by therapeutic indication.

Common Model Organisms

FOXO4-DRI has been studied across multiple experimental systems:

Mice – Primary research model (C57BL/6J background most common, also XpdTTD/TTD accelerated aging model); vast majority of published data
Cell culture models – Human IMR90 fibroblasts (radiation-induced senescence), TM3 Leydig cells, human chondrocytes, various cancer cell lines, cancer-associated fibroblasts
Ex vivo tissue – Human testicular tissue, cartilage explants
Research Limitations & Regulatory Status
Critical Gaps in Current Evidence

Despite promising preclinical research demonstrating senolytic activity and tissue homeostasis restoration in multiple mouse models, FOXO4-DRI faces substantial translational barriers that prevent clinical application and limit confident extrapolation of findings.

Lack of Human Clinical Data

The most significant limitation is the complete absence of human clinical trial data:

No Phase I, II, or III human trials published in peer-reviewed literature or registered in clinical trial databases
Human safety profile completely unestablished (no toxicology, maximum tolerated dose, or adverse event data)
Optimal human dosing unknown (cannot be reliably extrapolated from mouse studies)
Pharmacokinetics in humans uncharacterized
Long-term effects of senescent cell clearance in humans unstudied
Potential for off-target effects in human tissues unknown

While the lead researcher mentioned intentions to move toward human testing starting with glioblastoma applications, no published results have emerged as of 2025.

Mechanistic Understanding Gaps

Fundamental aspects of FOXO4-DRI’s mechanism and biological effects require clarification:

Tissue-specific FOXO4 expression patterns may create unexpected vulnerabilities (FOXO4 expressed in human testis, placenta, and muscle according to Human Protein Atlas)
Potential cardiac effects from muscle FOXO4 expression remain inadequately characterized
Whether chronic senescent cell clearance affects tissue regeneration or stem cell function over extended periods unknown
Interaction between senescent cell removal and normal tissue homeostasis incompletely understood
Optimal treatment frequency and duration for different indications undefined
Selectivity and Off-Target Concerns

While FOXO4-DRI demonstrates impressive selectivity in cell culture (11.73-fold), translational questions remain:

Ten-fold selectivity considered insufficient by the lead researcher for use in relatively healthy populations
Potential for killing approximately 1 in 10 healthy cells if dosing is not perfectly optimized
Fourth-generation variants with improved selectivity under development (target: 100-fold selectivity)
Effects on rapidly dividing healthy cell populations not fully characterized
Long-term consequences of repeated treatments unknown
Long-Term Safety Considerations

Critical safety questions remain unanswered:

Chronic senescent cell removal effects beyond several weeks unstudied even in animals
Potential effects on tumor surveillance or cancer development uninvestigated
Reproductive toxicity inadequately characterized despite FOXO4 expression in testis and placenta
Effects in developing organisms or during pregnancy completely unknown
Potential for accelerated tissue aging or impaired injury responses with excessive senescent cell depletion
Regulatory & Competitive Sport Status
FDA Position

FOXO4-DRI has not received FDA approval for any indication:

Classified as an unapproved investigational compound
Not recognized as safe or effective for any medical use
Not legally available for medical compounding or prescription use in the United States
No established therapeutic application
Not approved for veterinary use

As an experimental research peptide, FOXO4-DRI lacks the regulatory pathway clearance required for clinical use or marketing as a therapeutic agent.

WADA Prohibition Status

While specific WADA classification of FOXO4-DRI is not explicitly published in readily available sources, as an unapproved investigational peptide with potential performance-enhancing or anti-aging effects:

Likely falls under WADA Section S0 (Non-Approved Substances) prohibited category
No approved medical use would preclude Therapeutic Use Exemptions
Athletes should assume prohibition status given the compound’s senolytic and potential performance-modulating effects

Research Classification: FOXO4-DRI is available only for laboratory research use. It is not intended for human consumption, medical use, or veterinary applications. All research must be conducted under appropriate ethical oversight and regulatory compliance with institutional review board approval where applicable.

Lead Researcher Spotlight
Dr. Peter L.J. de Keizer, PhD

Assistant Professor of Molecular Biology

University Medical Center Utrecht, Utrecht, Netherlands

Dr. Peter de Keizer is the principal investigator who designed and characterized FOXO4-DRI, leading the research team that published the landmark 2017 Cell paper demonstrating selective senescent cell elimination and tissue homeostasis restoration in aged mice. He received his PhD from Utrecht University Medical Center in 2009 for work on FOXO transcription factors in tumor suppression, followed by postdoctoral training at the Buck Institute for Research on Aging in California where he was elected as a fellow of the Dutch Cancer Society in 2010. In 2012, he joined Erasmus University Medical Center in Rotterdam where he developed the FOXO4-DRI peptide and was awarded the prestigious “Talent Extraordinary Award” in 2014. In 2018, he moved to University Medical Center Utrecht to continue his research program focused on cellular senescence in aging and cancer.

Dr. de Keizer’s research contributions include:

Design and characterization of FOXO4-DRI as the first FOXO4-p53 interaction inhibitor for selective senolysis
Demonstration that therapeutic senescent cell removal can restore tissue function after aging-related decline has occurred
Identification of FOXO4 as a critical regulator of senescent cell viability
Research on senescence-stem lock model for aging and tissue dysfunction
Investigation of senescent cell heterogeneity and SASP variation
Co-founding Cleara Biotech to develop next-generation senolytic compounds with improved selectivity

His laboratory continues developing fourth-generation variants of FOXO4-DRI with enhanced specificity and reduced potential for off-target effects, working toward clinical translation for age-related diseases and cancer applications.

Disclaimer: This spotlight is provided for educational purposes to acknowledge scientific contributions to FOXO4-DRI research. Cenexa Labs has no affiliation with Dr. de Keizer, University Medical Center Utrecht, or Cleara Biotech, and this information does not constitute an endorsement of any products or services.

References
Bourgeois, B., Spreitzer, E., Platero-Rochart, D., Paar, M., Zhou, Q., Usluer, S., de Keizer, P.L.J., Burgering, B.M.T., Sanchez-Murcia, P.A., & Madl, T. (2025). The disordered p53 transactivation domain is the target of FOXO4 and the senolytic compound FOXO4-DRI. Nature Communications, 16(1), 60844-9. PubMed

Baar, M.P., Brandt, R.M.C., Putavet, D.A., Klein, J.D.D., Derks, K.W.J., Bourgeois, B.R.M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D.A., van der Pluijm, I., Essers, J., van Cappellen, W.A., van IJcken, W.F., Houtsmuller, A.B., Pothof, J., de Bruin, R.W.F., Madl, T., Hoeijmakers, J.H.J., Campisi, J., & de Keizer, P.L.J. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1), 132-147. PubMed

Zhang, C., Xie, Y., Chen, H., Lv, L., Yao, J., Zhang, M., Xia, K., Feng, X., Li, Y., Liang, X., Sun, X., Deng, C., & Liu, G. (2020). FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice. Aging, 12(2), 1272-1284. PubMed

Meng, J., Li, Y., Wan, C., Sun, Y., Dai, X., Huang, J., Hu, Y., Gao, Y., Wu, B., Zhang, Z., Xu, W., Tang, L., Liang, Y., Zhang, H., de Keizer, P.L.J., Fu, Z., & Zhou, Z. (2021). Targeting senescence-like fibroblasts radiosensitizes non-small cell lung cancer and reduces radiation-induced pulmonary fibrosis. JCI Insight, 6(23), e146334. PubMed

Baar, M.P., Brandt, R.M.C., Putavet, D.A., Klein, J.D.D., Derks, K.W.J., Bourgeois, B.R.M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D.A., van der Pluijm, I., Essers, J., van Cappellen, W.A., van IJcken, W.F., Houtsmuller, A.B., Pothof, J., de Bruin, R.W.F., Madl, T., Hoeijmakers, J.H.J., Campisi, J., & de Keizer, P.L.J. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1), 132-147. PubMed

Baar, M.P., Brandt, R.M.C., Putavet, D.A., Klein, J.D.D., Derks, K.W.J., Bourgeois, B.R.M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D.A., van der Pluijm, I., Essers, J., van Cappellen, W.A., van IJcken, W.F., Houtsmuller, A.B., Pothof, J., de Bruin, R.W.F., Madl, T., Hoeijmakers, J.H.J., Campisi, J., & de Keizer, P.L.J. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1), 132-147. PubMed

Baar, M.P., Brandt, R.M.C., Putavet, D.A., Klein, J.D.D., Derks, K.W.J., Bourgeois, B.R.M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D.A., van der Pluijm, I., Essers, J., van Cappellen, W.A., van IJcken, W.F., Houtsmuller, A.B., Pothof, J., de Bruin, R.W.F., Madl, T., Hoeijmakers, J.H.J., Campisi, J., & de Keizer, P.L.J. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell, 169(1), 132-147. PubMed

Han, X., Xu, T., Fang, Q., Zhang, H., Yue, L., Hu, G., & Sun, L. (2022). FOXO4 peptide targets myofibroblast ameliorates bleomycin-induced pulmonary fibrosis in mice through ECM-receptor interaction pathway. Journal of Cellular and Molecular Medicine, 26(11), 3131-3142. PubMed

Huang, Y., He, Y., Makarcyzk, M.J., & Lin, H. (2021). Senolytic peptide FOXO4-DRI selectively removes senescent cells from in vitro expanded human chondrocytes. Frontiers in Bioengineering and Biotechnology, 9, 677576. PubMed

Zhang, C., Xie, Y., Chen, H., Lv, L., Yao, J., Zhang, M., Xia, K., Feng, X., Li, Y., Liang, X., Sun, X., Deng, C., & Liu, G. (2020). FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice. Aging, 12(2), 1272-1284. PubMed

Meng, J., Li, Y., Wan, C., Sun, Y., Dai, X., Huang, J., Hu, Y., Gao, Y., Wu, B., Zhang, Z., Xu, W., Tang, L., Liang, Y., Zhang, H., de Keizer, P.L.J., Fu, Z., & Zhou, Z. (2021). Targeting senescence-like fibroblasts radiosensitizes non-small cell lung cancer and reduces radiation-induced pulmonary fibrosis. JCI Insight, 6(23), e146334. PubMed

All references open in new window. These citations are provided for educational and research purposes only. This information is not intended to diagnose, treat, cure, or prevent any disease. FOXO4-DRI is intended for laboratory research use only.