FOX-04 DRI
$233.99
10mg
FOXO4-DRI (FOXO4-D-Retro-Inverso) is a synthetic peptide engineered using D-amino acids in a retro-inverso configuration to increase stability against enzymatic degradation. It has been studied in preclinical research for its interaction with the FOXO4–p53 pathway and its role in cellular senescence signaling mechanisms. To date, published data are limited to cell and animal studies.
Usage Disclaimer: Research Use Only. This product is intended strictly for laboratory research and in-vitro studies. It is not for human or animal consumption, medical use, or diagnostic purposes. Any unauthorized use of this product is strictly prohibited.
FDA Compliance: FDA Notice. The statements made regarding these products have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease.
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.
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.
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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