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Emerging Research

FOXO4-DRI

Senolytic Peptide | FOXO4-p53 Disruption for Cellular Aging Research

FOXO4-DRI (FOXO4-D-Retro-Inverso) is a synthetic 46-amino acid peptide designed to selectively eliminate senescent cells -damaged cells that accumulate with age and secrete harmful inflammatory factors (SASP). The peptide uses D-amino acids in reversed sequence, making it resistant to proteolytic degradation while maintaining binding function. FOXO4-DRI works by disrupting the FOXO4-p53 interaction that keeps senescent cells alive, causing p53 nuclear exclusion and redirecting it to mitochondria to trigger apoptosis. In mouse studies, it restored fur density, renal function, and physical fitness in aged animals while protecting against chemotherapy-induced toxicity. Notably, it shows 11.73-fold selectivity for senescent over healthy cells. No human clinical trials have been conducted; all efficacy data comes from preclinical animal and cell studies. The peptide was first described by Dr. Peter de Keizer and colleagues at Erasmus University Medical Center in 2017.

Daily dose

~25 mg (anecdotal human translation)

Frequency

Every other day × 3 doses

Cycle length

5 days per cycle

Storage

-20°C (lyophilized)

Key benefits

Selective senescent cell elimination, tissue homeostasis restoration, anti-aging research compound

How it works

Disrupts FOXO4-p53 interaction, causing p53 nuclear exclusion and mitochondrial translocation. Triggers apoptosis specifically in senescent cells with 11.73-fold selectivity over healthy cells.

Dosage protocols

Goal

Mouse Research Protocol

Dose

5 mg/kg · Every other day × 3

Route

IV or IP

Goal

Anecdotal Human Translation

Dose

~25 mg · Every other day × 3

Route

SubQ

Research indications

anti Aging

Senescent Cell ClearanceSelectively eliminates senescent cells that accumulate with age
Tissue RejuvenationMouse studies show restored tissue function in aged animals

cellular

Cellular HealthRemoves damaged cells to potentially allow regeneration

inflammation

SASP ReductionEliminates cells producing inflammatory senescence factors

Administration

injectable

Interactions

Avoid Combination
RapamycinRapamycin may interfere with senolytic effects by modulating autophagy and cellular stress responses. A 1-2 week washout period is recommended before FOXO4-DRI administration.
Avoid Combination
QuercetinQuercetin is itself a senolytic that works through different pathways. Concurrent use may diminish FOXO4-DRI effects. Minimum 96-hour washout, preferably 1-2 weeks.
Monitor Combination
DasatinibDasatinib + Quercetin is an alternative senolytic cocktail. Different mechanism than FOXO4-DRI. Sequential use may be considered but requires washout periods.
Avoid Combination
CorticosteroidsCorticosteroids may suppress the apoptotic cascade required for senolytic activity. Avoid concurrent use; washout period recommended.
Compatible
HumaninDifferent mechanisms -Humanin protects healthy cells while FOXO4-DRI clears senescent ones. May be complementary in aging protocols.
Unknown
MOTS-CBoth target aging pathways but through different mechanisms. MOTS-C focuses on metabolic regulation. No interaction studies available.
Unknown
EpitalonEpitalon works through telomerase activation while FOXO4-DRI eliminates senescent cells. Theoretically complementary but no studies on combination.
Unknown
5-Amino-1MQ5-Amino-1MQ has some senolytic properties through NNMT inhibition. Different mechanism. No data on concurrent use.
Unknown
BPC-157BPC-157 promotes tissue repair while FOXO4-DRI eliminates senescent cells. May be complementary for tissue regeneration but no studies available.
Synergistic
Chemotherapy AgentsMouse studies show FOXO4-DRI protects against doxorubicin-induced liver toxicity and may enhance tumor response when clearing senescent cells post-chemotherapy.

Safety notes

No human clinical trials conducted

All safety data from mouse studies

Avoid Rapamycin, Quercetin, corticosteroids concurrently

Anecdotal: injection site reactions reported

p53 pathway involvement -theoretical oncogenic concerns

May not benefit healthy young individuals

Research studies

Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis (2017)

Mouse | 5 mg/kg IV | 3 doses every other day | Fast-aging & naturally aged mice

Landmark study introducing FOXO4-DRI. Demonstrated 11.73-fold selectivity for senescent cells. In aged mice, restored fur density, normalized renal function (plasma urea/creatinine), increased voluntary running activity, and protected against doxorubicin-induced liver damage. No thrombocytopenia or cardiac abnormalities observed.

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FOXO4-DRI Alleviates Age-Related Testosterone Secretion Insufficiency (2020)

Mouse | 5 mg/kg IP | Every other day × 3 | Aged mice (20-24 months)

Treatment significantly increased serum testosterone levels in aged mice. Enhanced expression of testosterone synthesis enzymes (3β-HSD, CYP11A1). Decreased testicular senescence markers (p53, p21, p16) and reduced inflammatory cytokines (IL-1β, IL-6, TGF-β). No toxicity to normal Leydig cells.

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Senolytic FOXO4-DRI Removes Senescent Human Chondrocytes (2021)

Human cells in vitro | Passaged chondrocytes | Senescence model

Removed over 50% of highly-passaged senescent chondrocytes (PDL9) while not affecting minimally-passaged cells (PDL3). Reduced senescence markers and improved cartilage quality. However, did not enhance chondrogenic potential of treated cells.

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FOXO4-DRI Ameliorates Bleomycin-Induced Pulmonary Fibrosis (2022)

Mouse | BLM-induced fibrosis model | Therapeutic administration

Similar efficacy to approved drug Pirfenidone. Decreased senescent cells, downregulated SASP factors, attenuated collagen deposition. Increased type 2 alveolar epithelial cells while selectively killing TGF-β-induced myofibroblasts.

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FOXO4-DRI Targets ECM Production in Pulmonary Fibrosis (2023)

Mouse | Bleomycin model | ECM pathway analysis

Confirmed FOXO4-DRI resets p53 nuclear distribution and decreases total ECM protein content. Therapeutic administration showed milder pathologic changes and less collagen deposition than untreated fibrosis group.

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