ID: pinealon
Aliases: PINEALON, EDR peptide, Glu-Asp-Arg
Type: compound
Route/form: regional/research short peptide context; route varies and is not US-approved
Status: research_or_regional
Evidence level: early human
Best data tier: early human
Support scope: human, non-human/mechanistic
Source types: early_human, mechanistic, preclinical
Linked sources: 3
Broad outcomes: Brain / mood / sleep, Longevity / mitochondrial / redox
Reading note: These are curation notes anchored to linked sources, not a clinical recommendation or protocol.
Targets / mechanism
- gene-expression regulation hypothesis
- free-radical suppression in cell models
- neuroprotective peptide-bioregulator claims
Optimization domains
- brain
- longevity
- neuroprotection
- aging
Research basis
- Cell and mechanistic EDR literature gives a rationale for neuroprotective/aging claims.
Limits, risks, and missing evidence
- Human evidence quality and applicability are limited.
- Do not treat as equivalent to approved neurorehabilitation drugs or robust cognitive enhancers.
Risk flags
- regional bioregulator literature
- weak human context
- unapproved context
- identity uncertain
Linked papers, labels, and reviews
- Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes
preclinical / pubmed_pinealon_cell_viability_2011
Cell/organotypic model anchor for Pinealon claims. - EDR peptide: possible mechanism of gene expression and protein synthesis regulation involved in the pathogenesis of Alzheimer disease
mechanistic / pubmed_pinealon_edr_alz_2020
Mechanistic EDR/Pinealon gene-expression paper. - Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission
early_human / pubmed_pinealon_polymorbidity_2015
Older regional human source; interpret cautiously due limited accessibility/generalizability.