FOX04 - DRI - 30mg

SPECIFICATIONS

Product Code: F4D030

Sequence: H-D-Leu-D-Thr-D-Leu-D-Arg-D-Lys-D-Glu-D-Pro-D-Ala-D-Ser-D-Glu-D-Ile-D-Ala-D-Gln-D-Ser-D-Ile-D-Leu-D-Glu-D-Ala-D-Tyr-D-Ser-D-Gln-D-Asn-D-Gly-D-Trp-D-Ala-D-Asn-D-Arg-D-Arg-D-Ser-D-Gly-D-Gly-D-Lys-D-Arg-D-Pro-D-Pro-D-Pro-D-Arg-D-Arg-D-Arg-D-Gln-D-Arg-D-Arg-D-Lys-D-Lys-D-Arg-D-Gly-OH

Molecular Formula: C228H388N86O64

Molecular Weight: 5358.05

CAS: 2460055-10-9

Purity: Technical / Research Grade 98%

Other Details: No TFA Salt

Form: Lyophilized powder

Color: White

Storage Temperature: -20°C

Source: Synthetic

Safety Classification: Standard handling

DESCRIPTION

Prolonged exposure to intense stress and the physiological processes associated with aging are linked to the accumulation of irreversible cellular damage, a phenomenon that may contribute to progressive functional decline. Research indicates that senescent cells, which permanently exit the cell cycle, can influence tissue function over time and may participate in age-associated biological changes.

Unlike apoptotic cells, senescent cells are not efficiently cleared from tissues and may persist for extended periods. These cells often develop a characteristic pro-inflammatory profile known as the senescence-associated secretory phenotype (SASP). In experimental models, long-term accumulation of senescent cells has been associated with disruption of tissue homeostasis and progression of age-related changes.

DNA damage that is not adequately repaired may contribute to cellular dysfunction and accelerated biological aging. Although multiple repair mechanisms exist, these systems are not fully efficient. When repair processes are insufficient, compensatory responses such as senescence and apoptosis help preserve tissue integrity. Senescent cells, however, may accumulate over time and influence aging-related processes.

FOXO4 is a transcription factor belonging to the FOXO family of genes involved in cellular regulation, differentiation, oxidative stress signaling, apoptosis, insulin signaling, and senescence. FOXO4 expression has been identified in multiple tissues, including endocrine, metabolic, and reproductive organs.

FOXO4-DRI is a modified peptide derived from the FOXO4 protein in which naturally occurring L-amino acids are replaced with D-amino acids. This structural modification enhances molecular stability and reduces enzymatic degradation. Despite these changes, the peptide retains the ability to interact with intracellular signaling pathways.

In experimental models, FOXO4-DRI has been shown to disrupt the interaction between FOXO4 and the tumor suppressor protein p53. p53 is a central regulator of cell cycle control and programmed cell death. By interfering with FOXO4–p53 binding, FOXO4-DRI may allow p53 to resume its transcriptional activity and support intrinsic apoptotic pathways.

These effects have been observed predominantly in senescent cells. In preclinical research, selective targeting of senescent cells has been associated with improved tissue function and restoration of cellular environments more favorable to renewal processes.

Additional investigations have explored the relationship between FOXO proteins and insulin signaling pathways involved in metabolism, oxidative stress regulation, and aging-related mechanisms. Alterations in FOXO activity have also been examined in experimental models of neurodegeneration.

Preclinical research has further evaluated age-related endocrine changes. In animal models, FOXO4-DRI exposure has been associated with improved functional markers in aging Leydig cells responsible for testosterone production. These findings continue to support ongoing research into senescence modulation and age-associated biological decline.

All information presented above is derived exclusively from laboratory studies, animal models, and exploratory research. It is provided for scientific and educational purposes only and does not constitute medical advice, diagnostic guidance, or therapeutic claims.

REFERENCES

All information presented above is derived from in vitro experiments, animal studies, and other preclinical research models. These data are intended solely for basic scientific investigation of biological mechanisms and do not imply any therapeutic, diagnostic, preventive, or clinical use in humans or animals.

G. Murtaza et al., "FOXO Transcriptional Factors and Long-Term Living" [PubMed]

M.P. Baar et al., "Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging" [Cell]

C. Zhang et al., "FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice" [PubMed]

S. Lee et al., "FoxO integration of insulin signaling with glucose and lipid metabolism" [PubMed]

W. Hu et al., "Roles of forkhead box O (FoxO) transcription factors in neurodegenerative diseases: A panoramic view" [Progress in Neurobiology]

Y. Huang et al., "Senolytic Peptide FOXO4-DRI Selectively Removes Senescent Cells From in vitro Expanded Human Chondrocytes" [PubMed]

A.L. Bulteau et al., "Age-Dependent Declines in Proteasome Activity in the Heart" [Archives of Biochemistry and Biophysics]

A. Ciechanover et al., "The ubiquitin proteasome system in neurodegenerative diseases: sometimes the chicken, sometimes the egg" [PubMed]

Y. Sun et al., "FOXO4 Inhibits the Migration and Metastasis of Colorectal Cancer by Regulating the APC2/β-Catenin Axis" [PubMed]

P. Krimpenfort et al., "Rejuvenation by Therapeutic Elimination of Senescent Cells" [PubMed]

DISCLAIMER

This product is intended strictly for laboratory research and development use only. This material is not a medicine or drug and has not been evaluated or approved by the FDA, EMA, or any regulatory authority for the prevention, treatment, or cure of any medical condition or disease. Any form of administration to humans or animals is strictly prohibited. Handling is restricted to qualified laboratory professionals.

All product information provided on this website is for informational and educational purposes only.