ID: foxo4_dri
Aliases: FOX04, FOX04-DRI, FOXO4 D-retro-inverso peptide, FOXO4 peptide
Type: compound
Route/form: preclinical/research peptide; no approved human route
Status: research
Evidence level: preclinical
Best data tier: non-human experimental
Support scope: non-human/mechanistic
Source types: in_vitro, preclinical
Linked sources: 2
Broad outcomes: Hormones / fertility / sexual health, Longevity / mitochondrial / redox, Muscle growth / performance / recovery
Reading note: These are curation notes anchored to linked sources, not a clinical recommendation or protocol.
Targets / mechanism
- FOXO4-p53 interaction disruption hypothesis
- senescent cell apoptosis
- SASP reduction
Optimization domains
- longevity
- senolytic
- aging
- hormones
- joint health
Research basis
- Preclinical and human-cell studies support a senolytic mechanism for FOXO4-DRI in selected models.
- Aged-mouse Leydig-cell work is directly relevant to endocrine-aging claims seen in communities.
Limits, risks, and missing evidence
- No mature human anti-aging efficacy base.
- Senescent-cell biology can be context-dependent, and blanket senolysis may not be benign.
Risk flags
- preclinical only
- senolytic context
- unknown long term safety
- unapproved context
Linked papers, labels, and reviews
- FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice
preclinical / pubmed_foxo4dri_leydig_2020
Aged-mouse endocrine senolytic rationale for FOXO4-DRI. - Senolytic peptide FOXO4-DRI selectively removes senescent cells from in vitro expanded human chondrocytes
in_vitro / pubmed_foxo4dri_chondrocytes_2021
Human-cell senolytic support; no direct anti-aging clinical evidence.