AEDG tetrapeptide raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
Literature searches for this compound must account for several spelling variants. Indexing databases contain epitalon, epithalon, epithalone, and AEDG, and relevant records are scattered across Russian-language and English-language journals that do not consistently cross-cite. Early publications describe the parent extract as a mixture of many peptides, whereas later work addresses the single synthetic tetrapeptide. That shift in nomenclature complicates comparison between studies, because extract data and tetrapeptide data are sometimes cited interchangeably. A search strategy omitting the alternate spellings will return an incomplete set of references.
Reported biological findings come mainly from cell culture and rodent experiments. Those studies describe changes in telomerase catalytic subunit expression, melatonin rhythm amplitude, and antioxidant enzyme activity after peptide exposure. Human data are sparse and consist of small trials with limited blinding and inconsistent endpoints. The proposed mechanisms remain hypotheses rather than established facts, and there is no consensus on whether effects observed in animals carry over to people. Independent replication outside the original research groups is limited, which is a recognised gap in the published literature.
The parent extract epithalamin was characterised as a low-molecular-weight fraction of pineal tissue rather than a single defined chemical entity. Researchers fractionated it and tested successive fragments for activity, a screening approach typical of peptide discovery work in that era. Epitalon emerged from that process as one of the shorter sequences of interest. Because the original extract was never fully resolved into individual components, claims about which constituent drives a given effect rest on inference. This distinction matters when reading older reports that attribute extract observations to the tetrapeptide itself.
The compound is generally presented as a synthetic fragment of epithalamin, a pineal gland extract investigated in the former Soviet Union from the 1970s onward. Vladimir Khavinson and colleagues in Saint Petersburg developed short peptides modelled on such extracts, and epitalon became the most widely cited of those sequences. Most primary reports appeared in Russian-language journals or in proceedings with limited international circulation. Independent replication in laboratories outside that network remains sparse, and much repeated secondary material traces back to a small number of originating groups.
Laboratory work has examined effects on telomerase activity in cultured cells, on melatonin rhythms in animals, and on markers of oxidative stress. Some experiments report measurable changes while others show none, and the reported findings rest largely on small studies. The absence of large independent trials means the generality of these results is unresolved rather than settled. Review articles occasionally apply the label geroprotector, a term that reflects a research hypothesis about ageing rather than an established clinical finding.
Epitalon is the common name for a synthetic tetrapeptide with the sequence alanine-glutamate-aspartate-glycine, usually abbreviated AEDG. All four residues are proteinogenic amino acids, and the free peptide has a calculated mass near 390 grams per mole. Because the chain is short and carries no modifications, it is assembled readily by solid-phase synthesis and is distributed mainly as a freeze-dried solid for laboratory work. Catalogue listings use the spellings epitalon, epithalone, and simply AEDG, and the three refer to the same sequence.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic tetrapeptide | Four amino acid residues |
| Residue sequence | Ala-Glu-Asp-Gly | Abbreviated AEDG |
| Approximate mass | 390.35 Da | Monoisotopic, free base form |
| Parent preparation | Epithalamin extract | Derived from pineal tissue |
| Common spelling variants | Epithalon, epithalone, AEDG | Affects literature retrieval |
The published literature is dominated by a small number of research groups, much of it in Russian-language journals, and independent replication outside those groups is limited. Studies are typically small, use cultured cells or rodent models, and report endpoints that differ between papers, which makes comparison difficult. Large randomised human trials have not appeared in the indexed literature. Questions about absorption, distribution and clearance are therefore still treated as open in reviews that mention the compound.
Epitalon is a synthetic tetrapeptide with the sequence alanine–glutamate–aspartate–glycine, commonly abbreviated AEDG. Its design traces to epithalamin, a peptide fraction prepared from bovine pineal gland extracts that researchers in Saint Petersburg began investigating in the 1970s. The compound has a molecular formula of C14H22N4O9 and a nominal molecular mass near 390 daltons. It holds no approved drug status in the United States or the European Union, and material sold under this name is generally offered as a research chemical rather than a finished pharmaceutical product.
Proposed mechanisms centre on cell-culture observations rather than a defined receptor interaction. Several reports describe increased expression of the telomerase catalytic subunit after exposure of cultured human cells, and the authors attributed the effect to short peptide fragments entering the nucleus and influencing gene transcription. No receptor for the tetrapeptide has been identified, and the free peptide is expected to be degraded rapidly by plasma peptidases. Whether any measurable fraction reaches intact tissues after administration remains an unresolved question rather than an established finding.
Published evidence comes mainly from Russian-language journals and from a single research group, with small sample sizes and limited independent replication. A few laboratories outside that group have examined related peptides and reported weaker or absent telomerase effects, so the central claim is best described as contested rather than settled. Rodent studies report modest changes in some ageing markers and in survival, but designs vary and control conditions are often sparse. No large randomised trial in humans has been published, and long-term safety data in healthy populations are correspondingly thin.
Epitalon is a synthetic tetrapeptide with the sequence alanine-glutamate-aspartate-glycine, commonly abbreviated AEDG. It was designed at the St. Petersburg Institute of Bioregulation and Gerontology as a short, chemically defined analogue of epithalamin, a fraction obtained from bovine pineal tissue. Small peptide bioregulators of this type formed a long-running line of work there from the 1980s onward. Because the molecule is produced by solid-phase synthesis rather than extraction, its composition is exact and its purity can be measured directly.
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=== Category:EC 3.2 (act on sugars - glycosylases) === Category:EC 3.2.1 Amylase (EC 3.2.1.1) Sucrase (EC 3.2.1.10) Chitinase (EC 3.2.1.14) Lysozyme (EC 3.2.1.17) Maltase (EC 3.2.1.20) Lactase (EC 3.2.1.23) Beta-galactosidase (EC 3.2.1.23) Hyaluronidase (EC 3.2.1.35)
== Biochemistry == 3-Methylhistidine is a metabolic product that is produced in the body via the enzymatic methylation of histidine during peptide bond synthesis and the methylation of actin and myosin.
Analytical chemistry (or chemical analysis) is the branch of chemistry concerned with the development and application of methods to identify the chemical composition of materials and quantify the amounts of components in mixtures. It focuses on methods to identify unknown compounds, possibly in a mixture or solution, and quantify a compound's presence in terms of amount of substance (in any phase), concentration (in aqueous or solution phase), percentage by mass or number of moles in a mixture of compounds (or partial pressure in the case of gas phase). It encompasses both classical techniques (e.g. titration, gravimetric analysis) and modern instrumental approaches (e.g. spectroscopy, chromatography, mass spectrometry, electrochemical methods). Modern analytical chemistry is deeply intertwined with data analysis and chemometrics, and is increasingly shaped by trends such as automation, miniaturization, and real-time sensing, with applications across fields as diverse as biochemistry, medicinal chemistry, forensic science, archaeology, nutritional science, agricultural chemistry, chemical synthesis, metallurgy, chemical engineering and materials science. In the age of "big data", analytical chemistry, along with chemometrics and bioinformatics, has become central to interpreting complex results from high-throughput techniques like gas chromatography-mass spectrometry (GCMS), high-performance liquid chromatography, inductively coupled plasma mass spectrometry, and high-resolution mass spectrometry.
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Formation of additional capillaries and larger blood vessels (angiogenesis) is a major mechanism by which a cancer may help to enhance its own growth. Disorders of retinal capillaries contribute to the pathogenesis of age-related macular degeneration. Reduced capillary density (capillary rarefaction) occurs in association with cardiovascular risk factors and in patients with coronary heart disease.
Ni + 4 CO → Ni(CO)4 (1 bar, 55 °C) Fe + 5 CO → Fe(CO)5 (100 bar, 175 °C) Nickel tetracarbonyl is formed with carbon monoxide already at 80 °C and atmospheric pressure, finely divided iron reacts at temperatures between 150 and 200 °C and a carbon monoxide pressure of 50–200 bar. Other metal carbonyls are prepared by less direct methods.
Other techniques for determining the dosage of CPA have validated this extrapolation, for instance affinity studies and prostatic CPA levels. The affinity of CPA for the AR is around 20-fold lower than that of DHT, and an excess of CPA levels of around 20 to 30 times those of DHT would hence be expected to maximally neutralize androgen signaling. In accordance, different publications have stated based on preclinical experiments that a 2- to 5-fold excess of CPA can inhibit the effects of testosterone by 50%, a 3- to 10-fold excess of CPA can reduce the effects of "potent androgens" (presumably testosterone and/or DHT) by 50%, and a 10-fold excess of CPA can inhibit the effects of testosterone by "almost 100%". High-dose CPA has been found to achieve prostatic levels that are at least 30-fold those of DHT. One study found that levels of CPA in the prostate gland in men being treated with 200 mg/day oral CPA were about 28 times those of DHT. In accordance with the preceding findings, it has been stated that oral doses of CPA of at least 300 mg/day may achieve a combined androgen blockade action in the treatment of prostate cancer. At a dosage of CPA of 100 mg/day in men with prostate cancer, circulating levels of CPA (e.g., 350 ng/mL) are on the order of 200-fold higher than circulating levels of testosterone (e.g., 100 ng/dL). In men who have undergone orchiectomy, 50 mg/day oral CPA results in a 500-fold excess of circulating CPA relative to circulating testosterone.
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== Mechanism of action == C-terminal CendR motif engages with widely expressed neuropilin-1 receptors to trigger an increased permeability of the vasculature and penetration of tissue parenchyma by an endocytotic/exocytotic transport mechanism. The CendR pathway starts with an endocytosis step that is distinct from known endocytosis pathways. It most closely resembles macropinocytosis, but unlike macropinocytosis, the CendR pathway is receptor (neuropilin)-initiated and its activity is controlled by the nutrient status of the cell or tissue. CendR is an active transport process that requires energy. It is not limited to extravasation, but also includes penetration of tissue parenchyma, potentially via cell-to-cell transport. CendR elements that are not C-terminally exposed are unable to bind to neuropilin-1. However, such cryptic CendR elements can be activated by proteolytic cleavage (e.g. by furin, urokinase type plasminogen activator, and other proteases of suitable substrate specificity).
== Further reading == Hagedorn, Henry H.; Kunkel, Joseph G. (1979). "Vitellogenin and Vitellin in Insects". Annual Review of Entomology. 24 (4): 475–505. doi:10.1146/annurev.en.24.010179.002355. Wheeler, Diana E.; Kawooya, John K. (1990). "Purification and characterization of honey bee vitellogenin". Archives of Insect Biochemistry and Physiology. 14 (4): 253–267. doi:10.1002/arch.940140405. PMID 2134180. "Vitellogenin Gene Expression in Male Fathead Minnow as an Indicator of Exposure to Endocrine Disrupting Chemicals (EDC) in an Aquatic Environment". EPA.gov. 2006. Amdam, G. V.; Norberg, K.; Omholt, S. W.; Kryger, P.; Lourenço, A. P.; Bitondi, M. M. G.; Simões, Z. L. P. (November 2005). "Higher vitellogenin concentrations in honey bee workers may be an adaptation to life in temperate climates". Insectes Sociaux. 52 (4): 316–319. doi:10.1007/s00040-005-0812-2. S2CID 25197924. Seehuus, S.-C.; Norberg, K.; Gimsa, U.; Krekling, T.; Amdam, G. V. (17 January 2006). "Reproductive protein protects functionally sterile honey bee workers from oxidative stress". Proceedings of the National Academy of Sciences. 103 (4): 962–7. doi:10.1073/pnas.0502681103. PMC 1347965. PMID 16418279. Nelson, C. Mindy; Ihle, Kate E; Fondrk, M. Kim; Page, Robert E; Amdam, Gro V; Chittka, Lars (6 March 2007). "The Gene vitellogenin Has Multiple Coordinating Effects on Social Organization". PLOS Biology. 5 (3): e62. doi:10.1371/journal.pbio.0050062. PMC 1808115. PMID 17341131. Corona, M.; Velarde, R. A.; Remolina, S.; Moran-Lauter, A.; Wang, Y.; Hughes, K. A.; Robinson, G. E. (16 April 2007).
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Drugs continue to be taken off the market due to late discovery of hepatotoxicity. Due to its unique metabolism and close relationship with the gastrointestinal tract, the liver is susceptible to injury from drugs and other substances. 75% of blood coming to the liver arrives directly from gastrointestinal organs and the spleen via portal veins that bring drugs and xenobiotics in near-undiluted form. Several mechanisms are responsible for either inducing hepatic injury or worsening the damage process. Many chemicals damage mitochondria, an intracellular organelle that produces energy. Its dysfunction releases excessive amount of oxidants that, in turn, injure hepatic cells. Activation of some enzymes in the cytochrome P-450 system such as CYP2E1 also lead to oxidative stress. Injury to hepatocyte and bile duct cells lead to accumulation of bile acid inside the liver. This promotes further liver damage. Non-parenchymal cells such as Kupffer cells, collagen-producing stellate cells, and leukocytes (i.e. neutrophil and monocyte) also have a role in the mechanism.
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Sources: en.wikipedia.org
It is based on epithalamin, a peptide-rich preparation obtained from pineal gland tissue and studied in the former Soviet Union. Researchers later identified the tetrapeptide AEDG as a constituent fragment of that material. Modern supplies are produced by chemical synthesis rather than tissue extraction.
No. Epithalamin is a heterogeneous extract containing many peptides, while epitalon is a single synthesised tetrapeptide. Publications sometimes treat findings from the two as equivalent, which is a common source of confusion. Their compositions differ and they are not interchangeable in analytical terms.
Most published work uses cell cultures or rodents because those models are faster and less costly to run. The few human trials that have been reported are small, and several lack control groups or blinding. This restricts what can reasonably be concluded about effects in people.
It is a four-amino-acid peptide with the sequence alanine-glutamate-aspartate-glycine. The chain is unmodified and contains only standard proteinogenic residues, which makes it straightforward to produce by solid-phase synthesis and to characterise by standard peptide methods.