This is a working overview of AEDG, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-06-26 and is reviewed periodically as new material appears.
Chemically, the molecule consists of four amino acid residues joined by three peptide bonds, with a free N-terminal amino group and a free C-terminal carboxyl group. Its molecular formula is C14H22N4O9, and its monoisotopic mass is approximately 390 daltons. The acidic glutamate and aspartate side chains give the peptide a net negative charge near neutral pH, a property that shapes its chromatographic behaviour and solubility profile. No disulfide bridges or other post-translational modifications are present, so the primary sequence alone defines the structure.
Most experimental work has been carried out in cell culture and animal models. Several reports describe changes in telomerase activity and proliferation in cultured cells, while rodent studies have examined lifespan, melatonin rhythm and reproductive endpoints. Human data remain limited, and much of the published clinical material consists of small trials with incomplete reporting of methods and controls. Whether the cell and animal findings translate into measurable effects in people is an open question, and the mechanistic basis of the reported telomerase changes is not fully established.
Short peptides such as AEDG are normally supplied as a freeze-dried solid and are kept dry, cold, and shielded from light. Holding at minus twenty degrees Celsius is common for the long term, while a refrigerator suffices for brief periods before use. The material takes up moisture to some degree, so containers should stay sealed and be allowed to reach room temperature before opening, which limits condensation on the contents. Repeated warming and cooling of a single container is discouraged because it admits water and can lower the amount of intact peptide.
Dissolution is usually performed in water or a suitable aqueous buffer, and the resulting liquid is divided into single-use portions before freezing. Freeze-thaw cycling is a recognised source of loss for short peptides, since each cycle can encourage aggregation or adsorption onto container walls. Working solutions are generally kept cold and used within a short window, although published stability data specific to epitalon are thin. Containers should be marked with concentration and date, and solutions examined for cloudiness before use.
Identity is normally established by reversed-phase high-performance liquid chromatography combined with mass spectrometry, a pairing that separates components and confirms molecular mass at once. Purity is quoted as a percentage from the chromatogram, and figures above ninety-five percent are a frequent commercial specification. Amino acid analysis or sequencing supplies further confirmation when required. Because many short peptides behave similarly under chromatography, retention time alone does not establish sequence; the mass measurement is what separates one tetrapeptide from another, and certificates should report both.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Linear tetrapeptide | Four residues joined by three peptide bonds |
| Sequence | Ala-Glu-Asp-Gly | Commonly abbreviated AEDG |
| Molecular formula | C14H22N4O9 | Free acid form |
| Monoisotopic mass | Approximately 390 Da | Matches values reported from mass spectrometry |
| Net charge near neutral pH | Negative | Contributed by glutamate and aspartate side chains |
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.
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.
The most frequently cited laboratory finding is that AEDG increased telomerase activity and extended telomere length in cultured human somatic cells. That work used fetal fibroblast strains and reported changes in enzyme activity alongside altered division counts. Replication by unrelated groups has been limited, and the published record is largely a single-laboratory series rather than a multi-centre programme. The result supports a hypothesis about peptide influence on gene expression in cell culture; it does not by itself establish an effect on telomere length in living animals or in people.
Animal and clinical reports appear mainly in Russian-language journals from the 1990s and 2000s, covering endpoints such as melatonin rhythm, lifespan in aged rodents, and retinal function. Many of these papers involve small groups, lack blinding or placebo comparison, and are difficult to retrieve through indexed databases. Review articles published in English generally summarise the claims without reanalysing the underlying data. Because no large randomised trial exists, the clinical importance of these reported effects stays unresolved and is properly described as an open question.
== History and discovery == "Ultraviolet" means "beyond violet" (from Latin ultra, "beyond"), violet being the color of the highest frequencies of visible light. Ultraviolet has a higher frequency (thus a shorter wavelength) than violet light. UV radiation was discovered in February 1801 when the German physicist Johann Wilhelm Ritter observed that invisible rays just beyond the violet end of the visible spectrum darkened silver chloride-soaked paper more quickly than violet light itself. He announced the discovery in a very brief letter to the Annalen der Physik and later called them "(de-)oxidizing rays" (German: de-oxidierende Strahlen) to emphasize chemical reactivity and to distinguish them from "heat rays", discovered the previous year at the other end of the visible spectrum. The simpler term "chemical rays" was adopted soon afterwards, and remained popular throughout the 19th century, although some said that this radiation was entirely different from light (notably John William Draper, who named them "tithonic rays"). The terms "chemical rays" and "heat rays" were eventually dropped in favor of ultraviolet and infrared radiation, respectively. In 1878, the sterilizing effect of short-wavelength light by killing bacteria was discovered. By 1903, the most effective wavelengths were known to be around 250 nm. In 1960, the effect of ultraviolet radiation on DNA was established.
A gonadotropin release inhibitor is a substance that reduces the secretion of gonadotropins by the anterior pituitary gland. In particular, this means that it reduces the amount of luteinizing hormone (LH) and/or follicle stimulating hormone (FSH) released. Gonadotropins are hormones that signal to the gonads and play a crucial role in the process of gonadal development and function in vertebrates. In birds and mammals, luteinizing hormone (LH) regulates sex steroid production as well as ovulation, whereas follicle stimulating hormone (FSH) promotes spermatogenesis and ovarian follicle maturation. Their release is primarily induced by gonadotropin-releasing hormone (GnRH) (a hypothalamic decapeptide isolated from the mammalian brain in the early 1970s), however several other GnRHs have also been identified in the brains of other vertebrates. Some neurochemicals and peripheral hormones (e.g.gamma-aminobutyric acid (GABA), opiates, gonadal sex steroids, inhibin) can modulate gonadotropin release, but a more specific hypothalamic inhibitory hormone was only identified more recently. In birds, a peptide Gonadotropin-inhibitory hormone was found to suppress gonadotropin release, and later homologous neuropeptides were discovered in mammals, coded by the gene NPVF.
=== Structure-based === Structure-based drug design (or direct drug design) relies on knowledge of the three dimensional structure of the biological target obtained through methods such as x-ray crystallography or NMR spectroscopy. If an experimental structure of a target is not available, it may be possible to create a homology model of the target based on the experimental structure of a related protein. Using the structure of the biological target, candidate drugs that are predicted to bind with high affinity and selectivity to the target may be designed using interactive graphics and the intuition of a medicinal chemist. Alternatively, various automated computational procedures may be used to suggest new drug candidates. Current methods for structure-based drug design can be divided roughly into three main categories. The first method is identification of new ligands for a given receptor by searching large databases of 3D structures of small molecules to find those fitting the binding pocket of the receptor using fast approximate docking programs. This method is known as virtual screening. A second category is de novo design of new ligands. In this method, ligand molecules are built up within the constraints of the binding pocket by assembling small pieces in a stepwise manner. These pieces can be either individual atoms or molecular fragments. The key advantage of such a method is that novel structures, not contained in any database, can be suggested. A third method is the optimization of known ligands by evaluating proposed analogs within the binding cavity.
Sources: en.wikipedia.org
=== Geroprotective activity === Didymin is the principal flavonoid constituent of Monarda didyma L. (scarlet beebalm) extract, occurring at concentrations approximately 80-fold higher than the only other detectable flavonoid, isosakuranetin. In a randomized clinical trial, supplementation with 100 mg/day of Monarda didyma L. extract over 12 weeks was associated with reduced telomere attrition and improvements in markers of biological aging and quality of life, with the effects attributed primarily to didymin.
=== CNO-II === In a minor branch of the above reaction, occurring in the Sun's core 0.04% of the time, the final reaction involving 157N shown above does not produce carbon-12 and an alpha particle, but instead produces oxygen-16 and a photon and continues
However, it is described as a "clear-headed candyflip", with entactogenic-like effects, LSD-like effects such as visuals, but a very clear head space. In addition, it is said to not have the same kind of forceful positive mood push that MDMA has, and to be a little more unpredictable and capable of causing bad trips or negative head spaces. 2C-B is said to be more of a "party drug", to be more recreational drug, and to have less likelihood of challenging, emotional-breakthrough, or mystical-type experiences, relative to psychedelics like psilocybin and LSD. Formal clinical studies have found that 2C-B produces a mixture of psychedelic, some possible entactogen-like, and some stimulant effects. Specific effects in these studies have included slight hallucinogenic states, perceptual changes, ego dissolution, time dilation, increased creativity, stimulation, vigor, happiness or elation, euphoria, feelings of well-being, reduced anger, enhanced sociability and friendliness, increased reactivity to negative emotional stimuli, decreased ability to recognize expressions of happiness, augmented emotionality in speech, tenseness, confusion, and mild sympathomimetic effects such as pressor effects, among others. Findings on the entactogen-like effects of 2C-B have been mixed, with some studies reporting that it produces such effects but other studies finding no such effects similarly to psilocybin. However, in other research, both psilocybin and MDMA have been found to increase emotional empathy.
Sources: en.wikipedia.org
It is a synthetic tetrapeptide with the sequence alanine-glutamate-aspartate-glycine, often abbreviated AEDG. The molecule is linear and contains no modified residues, so it is fully described by its sequence.
The compound came out of work on epithalamin, a peptide preparation derived from pineal tissue, conducted largely in Russian laboratories. Later studies in other countries examined it mainly in cell cultures and animal models.
The tetrapeptide sequence is a synthetic construct rather than a described circulating peptide. It was derived by analogy to peptide fractions obtained from tissue extracts, not isolated from blood or tissue as such.
Reversed-phase high-performance liquid chromatography is run alongside mass spectrometry. The chromatogram separates components and gives a purity figure, while the mass spectrum confirms that the measured molecular mass matches the expected sequence. Neither measurement on its own is treated as sufficient.