Quick Comparison
| AEDG Peptide | Crystagen | |
|---|---|---|
| Half-Life | 1-2 hours | Approximately 30 minutes (acute pharmacology); proposed gene-expression effects outlast plasma exposure |
| Typical Dosage | Oral/sublingual: 10-20 mg once daily. Injectable: 1-10 mg subcutaneous once daily. Typical course: 10-20 days, repeated every 3-6 months. Same protocols as Epithalon. | Oral (capsule): 100-200 mg once daily for 10-30 day cycles, repeated 2-3 times per year. Subcutaneous injection: 1-5 mg per dose, alternate days for 10-20 day cycles. Standard Khavinson cycling protocol. |
| Administration | Subcutaneous injection, oral, or sublingual | Oral capsule or subcutaneous injection (cycled) |
| Research Papers | 8 papers | 1 papers |
| Categories |
Mechanism of Action
AEDG Peptide
AEDG peptide (Ala-Glu-Asp-Gly) is the minimal active sequence of Epithalon and represents the core tetrapeptide responsible for its reported biological effects. According to the Khavinson peptide bioregulator theory, this short sequence has tissue-specific gene-regulatory activity, particularly targeting pineal gland cells and somatic cells capable of telomerase expression.
The primary reported mechanism is activation of telomerase, the ribonucleoprotein enzyme that maintains telomere length. AEDG is proposed to interact with regulatory elements in the hTERT gene promoter (encoding the catalytic subunit of telomerase), enhancing its transcription in somatic cells where hTERT is normally silenced or minimally expressed. Reactivation of telomerase allows cells to add TTAGGG telomeric repeats to chromosome ends, counteracting the progressive telomere shortening that occurs with each cell division and ultimately triggers replicative senescence. Cell culture studies from the Khavinson laboratory have reported that AEDG treatment extends the replicative lifespan of human fibroblasts and increases telomerase activity in peripheral blood mononuclear cells.
The second major reported mechanism involves regulation of pineal gland function. The pineal gland produces melatonin — the circadian rhythm hormone and potent antioxidant — and its function declines markedly with age (pineal calcification and reduced melatonin output). AEDG is proposed to modulate gene expression in pinealocytes, restoring melatonin synthesis toward more youthful levels. This would have downstream effects on circadian rhythm regulation, sleep quality, antioxidant defense, and immune function — all of which are modulated by melatonin. Additional reported effects include upregulation of antioxidant enzyme expression (SOD, catalase) and modulation of cell cycle regulatory genes. As with other Khavinson peptide bioregulators, the research base is predominantly from Russian institutions, and the proposed direct DNA-binding mechanism awaits independent validation.
Crystagen
Crystagen is a short Khavinson tripeptide (Glu-Asp-Pro) positioned as the immune and thymus-targeted bioregulator within the wider Khavinson peptide family. The proposed mechanism follows the standard family framework: short peptides interact with gene promoter sequences in thymic and lymphocyte cell nuclei, modulating expression of genes involved in T cell maturation, cytokine production, and broader immune regulation.
Proposed effects include support for thymic function — particularly relevant given the well-documented age-related thymic involution that contributes to immunosenescence in older adults — alongside modulation of lymphocyte chromatin organisation and immune cell maturation pathways. Russian research has reported crystagen-induced improvements in lymphocyte counts, T helper cell function, and clinical recovery from infections in elderly populations and in patients recovering from immunosuppressive treatments. The peptide is often used alongside thymalin (a related thymic peptide preparation also in this database) as part of broader Khavinson immune-support protocols.
As with the rest of the Khavinson family, the efficacy evidence base sits within Russian gerontology and immunology research with limited independent Western validation. Crystagen is not validated as a treatment for primary immunodeficiency, HIV-related immune dysfunction, or other formally diagnosed immune conditions, and should not displace evidence-based immune therapy. The brief plasma half-life (around 30 minutes) reflects the proposed model of transient signalling triggering longer-lasting transcriptional changes in immune cell populations.
Risks & Safety
AEDG Peptide
Common
injection site irritation, mild drowsiness.
Serious
telomerase activation may promote pre-cancerous cells, limited Western safety data.
Rare
allergic reactions.
Crystagen
Common
generally reported as well tolerated.
Serious
very limited Western clinical data; theoretical concern with use in autoimmune disease (immune-modulating peptides may unpredictably affect autoimmune activity).
Rare
allergic reactions. Should not replace evidence-based immune therapy in serious immunodeficiency.
Full Profiles
AEDG Peptide →
A tetrapeptide (Ala-Glu-Asp-Gly) identical to Epithalon's core active sequence — effectively the same compound. Studied for telomerase activation and pineal gland regulation, promoting melatonin production and potentially slowing cellular aging through telomere maintenance. Part of the Khavinson bioregulator peptide family developed in St. Petersburg.
Crystagen →
A Khavinson tripeptide (Glu-Asp-Pro) developed in Russia as a tissue-specific bioregulator targeting the thymus and broader immune system. Promoted for age-related immune decline (immunosenescence), recovery from immunosuppressive treatments, and as a general immune support during the cold and flu season. Within the same Khavinson family as thymalin and thymosin alpha-1, both already in your database.