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Análisis de Pureza HPLC
FOX04
CAS: 2460055-10-9
Estudiado para la eliminación selectiva de células senescentes
FOX04 is a research peptide in the anti-aging / longevity category. FOXO4-DRI is a retro-inverso peptide (D-amino acid mirror image in reverse sequence) designed to disrupt the interaction between FOXO4 and p53 in senescent cells. MiPeptidos offers FOX04 in 2 sizes with 99.4% verified purity and full analytical documentation.
- Targets senescent 'zombie' cells
- Research-backed age reversal
- Supports tissue rejuvenation
- Protease-resistant formula
During weeks 1-3, FOX04-DRI works at the cellular level to selectively clear senescent cells — studies report mild fatigue as the body processes debris. By weeks 4-9, research suggests improved tissue function and vitality as zombie cells are removed and healthy cells take over. A 6-week rest period follows each cycle to let the body complete the renewal process.
$144.95/vial · Everything you need to start
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Análisis de Pureza HPLC
Clear Zombie Cells.
9-week targeted senolytic protocol backed by 5 studies and the de Keizer FOXO4 research program
FOX04-DRI (also written FOXO4-DRI) is a D-retro-inverso peptide designed to disrupt the FOXO4-p53 interaction that keeps senescent cells alive. Developed by Dr. Peter de Keizer at Erasmus University Medical Center (Netherlands), FOX04-DRI is the first peptide-based senolytic specifically engineered to trigger apoptosis selectively in senescent cells while sparing healthy cells.
Resultados Publicados
Revisado por ParesResultados cuantificables de investigación clínica publicada.
Lo que Dicen los Expertos
4 MédicosProfesionales e investigadores líderes que han estudiado y prescrito este péptido.
Dr. Peter de Keizer
Principal Investigator, Erasmus University Medical Center / Utrecht University
Developer of FOX04-DRI. Published the landmark 2017 Cell paper demonstrating targeted senescent cell clearance in aged mice. Pioneer of peptide-based senolytics.
FOXO4 is pivotal for the viability of senescent cells. A FOXO4 peptide that perturbs the FOXO4-p53 interaction selectively causes p53 nuclear exclusion and apoptosis in senescent cells. This restored fitness and fur density in fast-aging mice.
Research protocol: 5 mg/kg, 3x per week for 3 weeks, via intraperitoneal injection. In aged mice, this protocol restored renal function, fur density, and exploratory behavior. The D-retro-inverso configuration is essential for protease resistance.
Fuente: Baar et al. (2017) Cell PMID: 28340340
Dr. James Kirkland
Director, Robert and Arlene Kogod Center on Aging, Mayo Clinic
Father of the senolytic field. Published the first paper demonstrating that clearing senescent cells extends healthspan and lifespan. Pioneer of dasatinib + quercetin senolytic therapy.
Senescent cells are a fundamental cause of aging. Clearing them — whether through small molecules or targeted peptides like FOX04-DRI — has the potential to delay, prevent, or alleviate multiple age-related conditions as a group.
Advocates intermittent 'hit-and-run' dosing for senolytics — brief intense treatment followed by long rest periods. Senescent cells take weeks to re-accumulate, so continuous dosing is unnecessary and potentially counterproductive.
Fuente: Kirkland & Tchkonia (2020) EBioMedicine PMID: 32540402; Baker et al. (2016) Nature PMID: 26840489
Dr. Judith Campisi
Professor, Buck Institute for Research on Aging (deceased, 2024)
Pioneer of cellular senescence research. Discovered the Senescence-Associated Secretory Phenotype (SASP). Her work established that senescent cells are not merely arrested but actively destructive through SASP.
Senescent cells are not simply quiet cells that stopped dividing. They produce a complex mix of pro-inflammatory cytokines, chemokines, growth factors, and proteases — the SASP — that disrupts tissue function and promotes age-related pathology.
Her SASP discovery provided the mechanistic rationale for senolytics. Emphasized that the inflammatory secretome of senescent cells is the primary mechanism through which they drive tissue aging, not merely their accumulation.
Fuente: Coppe et al. (2008) PLOS Biology PMID: 19053174; Campisi (2013) Ann Rev Physiol PMID: 23398157
Dr. Andrew Huberman
Professor of Neurobiology, Stanford University
Ph.D. in Neuroscience. Host of Huberman Lab, one of the most popular science podcasts globally.
Senolytics represent one of the most exciting frontiers in longevity science. The idea that you can selectively clear cells that are actively poisoning their neighbors — and that doing so demonstrably reverses aspects of aging — is remarkable.
Discusses senolytics as a key longevity strategy. Notes the importance of intermittent dosing (senescent cells take weeks to return) and the distinction between targeted peptide senolytics (FOX04-DRI) and broad-spectrum small molecule senolytics (D+Q).
Fuente: Huberman Lab Podcast: Senescence & Longevity Science (2023)
Protocolo de Dosificación
3 FasesRégimen de dosificación paso a paso compilado de profesionales líderes e investigación clínica.
Based on the de Keizer mouse protocol (5 mg/kg IP, 3x/week). For a 70 kg individual, this translates to approximately 350 mcg per injection (human equivalent dose calculation with allometric scaling). Administer in the morning. Expect no immediate symptoms — senescent cell apoptosis is a gradual process.
Critical rest period. The body clears apoptotic senescent cells and SASP-mediated inflammation resolves. Immune system processes debris. Senescent cells take 4-8 weeks to re-accumulate. This is the 'hit-and-run' approach advocated by Dr. Kirkland.
Repeat the 3-week active cycle every 2-3 months. Continuous dosing is NOT recommended — senolytics should be used intermittently. Monitor inflammatory markers (CRP, IL-6) to assess SASP clearance.
Add 1 mL bacteriostatic water to 10 mg vial = 10 mg/mL. For a 350 mcg dose (70 kg human equivalent), draw approximately 3.5 units on an insulin syringe. IMPORTANT: Human equivalent dosing is estimated from mouse data using allometric scaling — not clinically validated.
3 weeks on, 6 weeks off (minimum). This 'hit-and-run' senolytic dosing is critical — continuous treatment is counterproductive because (1) senescent cells need time to accumulate before the next cycle, and (2) transient p53 activation is safer than chronic activation.
Lyophilized: -20°C for 24+ months. Reconstituted: 2-8°C, use within 21 days. The D-retro-inverso configuration provides excellent protease resistance and stability.
Subcutaneous injection. The D-amino acid retro-inverso configuration provides protease resistance, extending half-life significantly beyond standard L-amino acid peptides. Cell-penetrating peptide — efficiently crosses cell membranes to reach the nuclear FOXO4-p53 complex.
Cronología de Recuperación
Basado en observaciones de investigación publicada. Los resultados individuales varían. Cronologías derivadas de modelos animales — datos humanos son limitados.
Active Senolytic Phase — Targeted Clearance
- FOX04-DRI disrupts FOXO4-p53 nuclear complexes in senescent cells
- Liberated p53 translocates to mitochondria, initiating intrinsic apoptosis cascade
- Senescent cells selectively undergo apoptosis — healthy cells unaffected
- No immediate symptomatic effects expected — cellular-level process
- Some individuals report mild fatigue as immune system processes apoptotic debris
Base de investigación: Baar et al. (2017) Cell PMID: 28340340
SASP Resolution & Immune Clearance
- Pro-inflammatory SASP factors begin declining as senescent cell burden reduces
- Macrophages phagocytose apoptotic senescent cell debris (efferocytosis)
- Tissue microenvironment inflammation resolves progressively
- Improvements in systemic inflammatory markers (CRP, IL-6) may become measurable
- Energy levels and general well-being may improve as SASP-driven inflammation resolves
Base de investigación: Kirkland & Tchkonia (2020) PMID: 32540402; de Keizer senescence resolution models
Tissue Functional Recovery
- In aged mice: restored renal function (plasma creatinine, BUN normalized)
- Fur density restoration and improved physical appearance in fast-aging models
- Increased exploratory behavior — proxy for improved healthspan and vitality
- SASP-mediated paracrine senescence reduced — neighboring cells recover
- Tissue stem cell niches may resume normal function without SASP suppression
Base de investigación: Baar et al. (2017) PMID: 28340340; Baker et al. (2016) Nature PMID: 26840489
Ongoing Maintenance Cycling
- Senescent cells re-accumulate over 2-3 months — time for next cycle
- Repeat 3-week treatment every 2-3 months for sustained senescent cell clearance
- Cumulative benefit: progressively reduced senescent cell burden with each cycle
- Monitor biomarkers: p16INK4a (senescence marker), inflammatory cytokines, epigenetic age clocks
Base de investigación: General senolytic field consensus; Kirkland 'hit-and-run' dosing paradigm
Mecanismo de Acción
3 vías biológicas distintas a través de las cuales opera este péptido.
FOXO4-p53 Disruption
FOX04-DRI is a D-retro-inverso peptide that competes with endogenous FOXO4 for binding to p53. By displacing FOXO4, it liberates p53 to translocate to mitochondria and trigger intrinsic apoptosis — but only in senescent cells where this interaction exists.
- In senescent cells, FOXO4 binds and sequesters p53 in the nucleus, preventing apoptosis
- FOX04-DRI competitively binds p53, displacing FOXO4 and allowing p53 nuclear exclusion
- Liberated p53 triggers BAX/BAK-mediated mitochondrial outer membrane permeabilization → apoptosis
- Healthy cells do not depend on FOXO4-p53 interaction for survival, so they are unaffected
Baar et al. (2017) PMID: 28340340
Selective Senescent Cell Apoptosis
FOX04-DRI exploits a unique vulnerability of senescent cells — their dependence on the FOXO4-p53 survival axis — to selectively induce apoptosis without harming proliferating or quiescent healthy cells.
- Senescent cells have elevated FOXO4 and p53 expression — the target complex is enriched
- Selectivity ratio: senescent cells undergo apoptosis while healthy cells are unaffected at therapeutic doses
- D-retro-inverso configuration prevents proteolytic degradation, extending biological half-life
- Cell-penetrating peptide efficiently crosses membranes to reach the nuclear target complex
Baar et al. (2017) PMID: 28340340; Zhu et al. (2015) PMID: 25754370
SASP Reduction via Source Elimination
By eliminating the senescent cells that produce SASP, FOX04-DRI reduces chronic tissue inflammation at its source rather than merely suppressing downstream inflammatory signals.
- SASP includes IL-6, IL-8, IL-1α, MMP-3, VEGF, and 40+ other factors
- SASP drives paracrine senescence — one senescent cell can induce senescence in neighbors
- Eliminating the source cells provides more durable inflammation resolution than anti-inflammatory drugs
- Tissue microenvironment improves as SASP-mediated damage ceases
Coppe et al. (2010) PMID: 20551169; Baar et al. (2017) PMID: 28340340
Investigación Publicada
5 estudios revisados por pares de PubMed. Haz clic en cualquier PMID para ver el estudio completo.
Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging
Baar MP, Brandt RMC, Putavet DA, Klein JDD, Derks KWJ, Bourber BRM, et al. — Cell (2017)
Hallazgo Clave: Landmark paper. FOX04-DRI selectively cleared senescent cells in vivo, restoring renal function, fur density, and fitness in fast-aging (XpdTTD/TTD) and naturally aged mice. Demonstrated FOXO4-p53 disruption as the senolytic mechanism.
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan
Baker DJ, Childs BG, Durik M, Wijers ME, Sieben CJ, Zhong J, et al. — Nature (2016)
Hallazgo Clave: Clearance of p16Ink4a-positive senescent cells using genetic ablation extended median lifespan by 24-27% in mice. Delayed tumorigenesis and attenuated age-related deterioration of multiple organs. Established the scientific foundation for senolytic therapy.
The Achilles' heel of senescent cells: from transcriptome to senolytic drugs
Zhu Y, Tchkonia T, Pirtskhalava T, Gower AC, Ding H, Giorgadze N, et al. — Aging Cell (2015)
Hallazgo Clave: First identification of senolytic drugs (dasatinib + quercetin). Demonstrated that senescent cells depend on specific anti-apoptotic pathways (SCAPs) for survival. Established the molecular rationale for why targeted disruption of survival signals (like FOXO4-p53) selectively kills senescent cells.
Senescence and the SASP: many therapeutic avenues
Coppe JP, Desprez PY, Krtolica A, Campisi J — Genes & Development (2010)
Hallazgo Clave: Comprehensive characterization of the Senescence-Associated Secretory Phenotype (SASP). Identified IL-6, IL-8, MMP-3, and VEGF as key SASP components. Established that SASP drives paracrine senescence, chronic inflammation, and tissue dysfunction — the 'why' behind senolytic therapy.
Senolytics in idiopathic pulmonary fibrosis: results from a first-in-human, open-label, pilot study
Justice JN, Nambiar AM, Tchkonia T, LeBrasseur NK, Pascual R, Hashmi SK, et al. — EBioMedicine (2019)
Hallazgo Clave: First human senolytic trial. Dasatinib + quercetin improved physical function (6-minute walk distance, chair-stand time) in patients with idiopathic pulmonary fibrosis. Proof-of-concept that senescent cell clearance provides clinical benefit in humans.
Potencia tu Protocolo de Investigación
4 SinergiasLa investigación sugiere combinar FOX04 con estos péptidos para mecanismos complementarios.
FOX04-DRI clears existing senescent cells while Epithalon prevents new senescence by maintaining telomere length — clearance + prevention.
Two-pronged anti-senescence strategy: active clearance of existing zombie cells (FOX04-DRI) plus prevention of new senescence via telomere maintenance (Epithalon). Addresses the hallmark of cellular senescence from both directions.
Immune function is critical for clearing apoptotic senescent cell debris after FOX04-DRI treatment. TA1 enhances the immune clearance arm of the senolytic response.
Enhanced senolytic efficacy: FOX04-DRI kills the zombie cells, TA1 ensures the immune system cleans up completely. Reduces the risk of inflammation from incomplete debris clearance.
After senescent cell clearance, tissue niches need remodeling support. GHK-Cu drives collagen synthesis and tissue remodeling in the spaces vacated by cleared senescent cells.
Complete tissue rejuvenation cycle: senescent cell clearance (FOX04-DRI) followed by tissue remodeling and regeneration (GHK-Cu). Ensures cleared niches are repopulated with functional tissue, not scar tissue.
BPC-157's tissue repair mechanisms can support recovery in tissues damaged by chronic SASP exposure. Use after the senolytic cycle to accelerate tissue healing.
Sequential rejuvenation: clear the toxic cells first (FOX04-DRI cycle), then repair the tissue damage they caused (BPC-157). Particularly relevant for joint and connective tissue aged by chronic SASP exposure.
Especificaciones
Cómo Funciona FOX04
FOXO4-DRI is a retro-inverso peptide (D-amino acid mirror image in reverse sequence) designed to disrupt the interaction between FOXO4 and p53 in senescent cells. In cellular senescence, FOXO4 accumulates in the nucleus and sequesters p53, preventing p53-mediated apoptosis and keeping senescent cells alive. FOXO4-DRI competitively blocks this interaction, freeing p53 to trigger apoptosis selectively in senescent cells while sparing healthy cells. This makes it a targeted senolytic agent.
Aplicaciones de Investigación
Precios
| Tamaño | Por Vial | Paquete de 10 |
|---|---|---|
2mg | $80.00 | $680.00 |
10mgMejor Valor | $400.00 | $3400.00 |
Precios de paquete de 10 mostrados. Descuentos por volumen para 50+ viales — contáctenos.
Certificado de Análisis
Este COA es una muestra representativa. Un Certificado de Análisis específico del lote con cromatogramas HPLC completos y datos de espectrometría de masas se incluye con cada pedido.
Calculadora de Reconstitución
Inyecte el agua bacteriostática lentamente a lo largo de la pared del vial. Agite suavemente hasta disolver — nunca sacuda. Almacene la solución reconstituida a 2-8°C y use dentro de 30 días.
Reseñas de Clientes
Preguntas Frecuentes
Seguridad y Advertencias
Not FDA-approved for human use
FOX04-DRI is a research peptide with NO human clinical trial data. All efficacy data comes from mouse models. Dosing, safety, and efficacy in humans are completely unestablished. All information is for research and educational purposes.
p53 modulation carries inherent oncogenic risk
p53 is the 'guardian of the genome' — the most important tumor suppressor. Any intervention that modulates p53 localization or activity carries theoretical risk of disrupting cancer surveillance. FOX04-DRI is designed to activate (not suppress) p53 in senescent cells, but off-target effects in pre-malignant cells cannot be excluded.
No human pharmacokinetic or toxicology data
Zero human trials have been conducted with FOX04-DRI. Mouse-to-human dose extrapolation using allometric scaling is an approximation only. Maximum tolerated dose, bioavailability, and organ-specific toxicity are entirely unknown in humans.
Solo para Fines de Investigación y Educación. No es consejo médico. No para consumo humano. Consulte a un médico autorizado antes de tomar cualquier decisión relacionada con la salud.
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