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Compare 1 price for FOX04-DRI. Cheapest: £705.48. Average: £705.48.
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| £705.48 | £7.05/mg | In Stock | Free |
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FOXO4‑DRI | D‑retro‑inverso peptide senolytic (FOXO4–p53 interaction inhibitor)
FOXO4‑DRI is a D‑retro‑inverso peptide designed to disrupt the interaction between FOXO4 and p53, a complex that helps senescent cells resist apoptosis. In mouse and cell culture studies, this selective disruption can trigger apoptosis predominantly in senescent cells while sparing non‑senescent counterparts, making FOXO4‑DRI a widely used tool compound in senescence biology.
In senescent cells, FOXO4 physically interacts with p53 (notably via the FOXO4 CR3 domain), tethering p53 in the nucleus and promoting a pro‑survival state. FOXO4‑DRI is a D‑retro‑inverso analog of the FOXO4 CR3 peptide (often coupled to a cell‑penetrating sequence) that competitively binds p53, displacing endogenous FOXO4. This releases p53 from the FOXO4 scaffold, promoting p53‑dependent apoptosis selectively in senescent cells where FOXO4–p53 engagement is elevated, thereby reducing senescence‑associated secretory phenotype (SASP) signaling and senescent cell burden in preclinical models.
Tool for selectively inducing apoptosis in senescent fibroblasts and other cell types by disrupting FOXO4–p53.
Reduces senescent cell markers in tissues of aged or chemotoxicity‑challenged mice.
Mitigates chemotoxicity phenotypes in mice by clearing therapy‑induced senescent cells.
Preclinical studies report improved physical performance and organ markers after senolysis.
Emerging evidence that senescent cell clearance may alleviate tissue degeneration in select models.
Employed in preclinical studies via parenteral routes (e.g., intraperitoneal or intravenous) for systemic exposure; cell‑penetrating design supports intracellular delivery.
| Goal | Dose | Frequency | Route |
|---|---|---|---|
| Senescent cell clearance (rodent) | Dose varies by model; follow study‑specific designs | Intermittent pulse dosing used in several experiments | Parenteral (e.g., IP/IV) |
Alters p53 availability/localization and may modify FOXO4‑DRI’s pro‑apoptotic effects on senescent cells.
Orthogonal senolytic mechanism (intrinsic apoptosis priming) may combine with FOXO4‑DRI for enhanced senescent cell clearance in some models.
Common comparator senolytic regimen; may be used in alternating or sequential designs to probe senolytic specificity across cell types.
mTOR suppression can reduce SASP and senescence burden; timing relative to FOXO4‑DRI may influence readouts.
Increase senescent cell load in models; FOXO4‑DRI often tested post‑insult to remove senescent cells; co‑administration requires careful timing.
May modulate oxidative stress and senescence induction, affecting baseline senescent cell burden prior to FOXO4‑DRI treatment.
Cellular uptake and engagement of p53; in vitro, early apoptosis markers may emerge in senescent cells within 12–24 h.
Reduction in SA‑β‑gal–positive cells and SASP cytokines in vitro; in vivo, initial biomarker shifts may be detectable.
In rodent models, functional improvements (e.g., physical performance, organ function markers) reported following intermittent dosing.
Persistence of reduced senescent cell burden and improved tissue markers observed in some studies; durability depends on model and senescence re‑accumulation.
FOXO4‑DRI disrupted FOXO4–p53 interaction, selectively induced apoptosis in senescent cells, and improved function in aged and chemotherapy‑challenged mice.
Review highlighting senolysis as a strategy; FOXO4‑DRI discussed as a peptide senolytic targeting FOXO4–p53.
Summarizes the FOXO4–p53 interaction and the rationale for D‑retro‑inverso peptides to target senescent cells; positions FOXO4‑DRI among mechanistically targeted senolytics.
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