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epitalon-notes.peptides8425.com › Data › Structure, Naming And Discovery — Complete Guide

Structure, Naming And Discovery — Complete Guide

By Editorial Desk · published 2025-09-18 · last reviewed 2025-10-07 · Data

epitalon 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 2025-10-07 and is reviewed periodically as new material appears.

Structure, Naming and Discovery

Residue composition is the property that most cleanly separates verified material from mislabelled samples. Alanine, glutamate, aspartate and glycine appear in that order from the N-terminus, and the two acidic residues sit in the middle of the chain. Because the peptide is short, it can be produced by solid-phase synthesis and characterised by mass spectrometry without ambiguity. Any reported sample whose measured mass departs substantially from 390 daltons is a different compound or a degraded mixture rather than epitalon.

Epitalon is a synthetic tetrapeptide whose four residues are alanine, glutamate, aspartate and glycine, commonly abbreviated AEDG. Its molecular formula is C14H22N4O9 and its monoisotopic mass is near 390.35 daltons. The peptide carries two acidic side chains, so it is neutral to negatively charged in most aqueous buffers. Published reference summaries usually list it under both spellings, epitalon and epithalon, and treat the two names as the same material.

The compound is generally described as a synthetic analogue of a fragment isolated from a pineal gland extract. Researchers associated with the Saint Petersburg Institute of Bioregulation and Gerontology introduced it during the 1980s and 1990s while studying short peptides from animal tissue. The original extract, called epithalamin, is a heterogeneous mixture, whereas epitalon is a single defined sequence. That distinction matters because findings reported for the extract are not automatically findings about the pure tetrapeptide, and claims about broader biological effects remain a separate question from the chemical identity described here.

Background and Proposed Mechanism

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.

Epitalon at a glance

PropertyValueNotes
Molecular formulaC14H22N4O9Derived from the four constituent residues
Molecular massAbout 390.35 DaMonoisotopic value, confirmed by mass spectrometry
Residue sequenceAla-Glu-Asp-GlyRead from the N-terminus to the C-terminus
Common synonymsEpithalon; AEDGBoth forms appear in reference catalogues
Net charge near neutral pHNegativeTwo acidic side chains give a low isoelectric point

Epitalon Background and Discovery

The peptide emerged from research carried out in Saint Petersburg from the late 1980s onward, where investigators searched for shorter active fragments of a pineal preparation known as epithalamin. The name epitalon was chosen to reflect that parent extract. Early reports described effects on neuroendocrine markers and on the lifespan of laboratory animals. Much of that work appeared in Russian-language journals, with English translations following later, which affects how readily the original protocols can be assessed by outside groups.

Published studies on epitalon are dominated by a small number of research groups, and independent replication in other laboratories remains limited. Proposed mechanisms include activation of telomerase and modulation of melatonin rhythms, but the evidence for either rests mainly on cell cultures and animal models. Whether the peptide produces comparable effects in humans is an open question, and the absence of large controlled trials means the literature is best read as exploratory rather than settled.

Epitalon is a synthetic four-amino-acid peptide with the sequence alanine-glutamate-aspartate-glycine, commonly abbreviated AEDG. Its molecular formula is C14H22N4O9, and its calculated molar mass is approximately 390.35 grams per mole. The compound is a short fragment related to a peptide fraction isolated from bovine pineal gland extracts, and it is normally supplied as a lyophilised powder intended for laboratory research. It is not a registered pharmaceutical product in most countries.

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Identity and Research Background

Epitalon is a synthetic tetrapeptide whose sequence is alanine–glutamate–aspartate–glycine, commonly abbreviated AEDG. It was developed in Russia during the 1980s and 1990s by investigators associated with the St. Petersburg Institute of Bioregulation and Gerontology, who studied short peptides as regulators of gene expression and tissue function. The alternative spelling epithalon appears interchangeably in the literature, and the two names refer to the same molecule. Outside Russia it is encountered chiefly as a research chemical rather than a licensed medicine, and it holds no approval from the United States Food and Drug Administration or the European Medicines Agency.

The peptide is a synthetic analogue of epithalamin, a preparation extracted from bovine pineal glands. Investigators sought a short, chemically defined molecule that would reproduce some of the endocrine and gerontological observations attributed to the glandular extract. Proposed mechanisms centre on induction of telomerase activity, an effect reported in cultured human somatic cells in the early 2000s, together with influences on melatonin secretion and neuroendocrine regulation. Those mechanisms remain incompletely characterised, and the reported telomerase response has not been consistently reproduced by independent groups working in comparable systems.

Further detail

Rec. ITU-R BT.1201-1 (2004) Rec. ITU-R BT.1769 (2006) Rec. ITU-R BT.2020 (2012, revised 2014) Rec. ITU-R BT.2035-0 (07/13) A reference viewing environment for evaluation of HDTV program material or completed programmes Rec. ITU-R BS.2051-0 (02/14) Advanced sound system for programme production Rec. ITU-R BT.2100 (2016) Other documents prepared or being prepared by ITU-R:

Chemical inhibiting BMP signals in chicken embryo caused a disruption of MD invagination and blocked the epithelial thickening of the MD-forming region, indicating that the BMP signals play a role in early MD development. Moreover, BMP signaling is involved in the formation of foregut and hindgut, intestinal villus patterning, and endocardial differentiation. Villi contribute to increase the effective absorption of nutrients by extending the surface area in small intestine. Gain or lose function of BMP signaling altered the patterning of clusters and emergence of villi in mouse intestinal model. BMP signal derived from myocardium is also involved in endocardial differentiation during heart development. Inhibited BMP signal in zebrafish embryonic model caused strong reduction of endocardial differentiation, but only had little effect in myocardial development. In addition, Notch-Wnt-Bmp crosstalk is required for radial patterning during mouse cochlea development via antagonizing manner. Mutations in BMPs and their inhibitors are associated with a number of human disorders which affect the skeleton. Several BMPs are also named 'cartilage-derived morphogenetic proteins' (CDMPs), while others are referred to as 'growth differentiation factors' (GDFs). BMPs are also involved in adipogenesis and functional regulation of adipose tissue. BMP4 favors white adipogenesis, whereas BMP7 activates brown fat functionality; BMP inhibitors are also involved in this regulation

==== Alzheimer's disease ==== mTOR signaling intersects with Alzheimer's disease (AD) pathology in several aspects, suggesting its potential role as a contributor to disease progression. In general, findings demonstrate mTOR signaling hyperactivity in AD brains. For example, postmortem studies of human AD brain reveal dysregulation in PTEN, Akt, S6K, and mTOR. mTOR signaling appears to be closely related to the presence of soluble amyloid beta (Aβ) and tau proteins, which aggregate and form two hallmarks of the disease, Aβ plaques and neurofibrillary tangles, respectively. In vitro studies have shown Aβ to be an activator of the PI3K/AKT pathway, which in turn activates mTOR. In addition, applying Aβ to N2K cells increases the expression of p70S6K, a downstream target of mTOR known to have higher expression in neurons that eventually develop neurofibrillary tangles. Chinese hamster ovary cells transfected with the 7PA2 familial AD mutation also exhibit increased mTOR activity compared to controls, and the hyperactivity is blocked using a gamma-secretase inhibitor. These in vitro studies suggest that increasing Aβ concentrations increases mTOR signaling; however, significantly large, cytotoxic Aβ concentrations are thought to decrease mTOR signaling. Consistent with data observed in vitro, mTOR activity and activated p70S6K have been shown to be significantly increased in the cortex and hippocampus of animal models of AD compared to controls.

Vasoconstriction (vasospasm or vascular spasm): Here, this refers to contraction of smooth muscles in the tunica media layer of endothelium (blood vessel wall). Activation of platelets and platelet plug formation: Platelet activation: Platelet activators, such as platelet activating factor and thromboxane A2, activate platelets in the bloodstream, leading to attachment of platelets' membrane receptors (e.g. glycoprotein IIb/IIIa) to extracellular matrix proteins (e.g. von Willebrand factor) on cell membranes of damaged endothelial cells and exposed collagen at the site of injury. Platelet plug formation: The adhered platelets aggregate and form a temporary plug to stop bleeding. This process is often called "primary hemostasis". Coagulation cascade: It is a series of enzymatic reactions that lead to the formation of a stable blood clot. The endothelial cells release substances like tissue factor, which triggers the extrinsic pathway of the coagulation cascade. This is called as "secondary hemostasis". Fibrin clot formation: Near the end of the extrinsic pathway, after thrombin completes conversion of fibrinogen into fibrin, factor XIIIa (plasma transglutaminase; activated form of fibrin-stabilizing factor) promotes fibrin cross-linking, and subsequent stabilization of fibrin, leading to the formation of a fibrin clot (final blood clot), which temporarily seals the wound to allow wound healing until its inner part is dissolved by fibrinolytic enzymes, while the clot's outer part is shed off.

Carrey reunited with Joel Schumacher, director of Batman Forever, for The Number 23 (2007), a psychological thriller co-starring Virginia Madsen and Danny Huston. In the film, Carrey plays a man who becomes obsessed with the number 23, after finding a book about a man with the same obsession. The film was panned by critics. The following year Carrey provided his voice for Dr. Seuss' Horton Hears a Who! (2008). Carrey voiced Horton the Elephant for the CGI-animated feature, which was a box office success, grossing over $290 million worldwide. Carrey returned to live-action comedy, starring opposite Zooey Deschanel and Bradley Cooper in Yes Man (also 2008). Carrey played a man who signs up for a self-help program that teaches him to say yes to everything. Despite reviews being mixed, Rene Rodriquez of The Miami Herald stated, "Yes Man is fine as far as Jim Carrey comedies go, but it's even better as a love story that just happens to make you laugh." The film earned $225 million at the box office worldwide.

Sources: en.wikipedia.org

Background from the literature

== Market withdrawal == Bayer announced that it ceased the production of lepirudin (Refludan) on May 31, 2012. At the time of the announcement, the company expected that supply from wholesalers was going to be depleted by mid-2013.

=== Centering the Z-Ring === One model of Z-ring formation permits its formation only after a certain spatial signal that tells the cell that it is big enough to divide. The MinCDE system prevents FtsZ polymerization near certain parts of the plasma membrane. MinD localizes to the membrane only at cell poles and contains an ATPase and an ATP-binding domain. MinD is only able to bind to the membrane when in its ATP-bound conformation. Once anchored, the protein polymerizes, resulting in clusters of MinD. These clusters bind and then activate another protein called MinC, which has activity only when bound by MinD. MinC serves as a FtsZ inhibitor that prevents FtsZ polymerization. The high concentration of a FtsZ polymerization inhibitor at the poles prevents FtsZ from initiating division at anywhere but the mid-cell. MinE is involved in preventing the formation of MinCD complexes in the middle of the cell. MinE forms a ring near each cell pole. This ring is not like the Z-ring. Instead, it catalyzes the release of MinD from the membrane by activating MinD's ATPase. This hydrolyzes the MinD's bound ATP, preventing it from anchoring itself to the membrane. MinE prevents the MinD/C complex from forming in the center but allows it to stay at the poles. Once the MinD/C complex is released, MinC becomes inactivated. This prevents MinC from deactivating FtsZ. As a consequence, this activity imparts regional specificity to Min localization. Thus, FtsZ can form only in the center, where the concentration of the inhibitor MinC is minimal.

In 2021, the average annual salary in the private sector was €18,630 for women and €24,640 for men, reflecting a 24.4% gap. This difference is partially attributed to variations in working hours, job types, and the prevalence of part-time work, which accounted for approximately 40% of the wage gap in 2017. When adjusted to full-time equivalents, the average wage gap was 15.5% in 2021, down from 17.5% in 2016. The wage gap tends to increase with age: it was 4.6% at age 25 and rose to 27.5% among those over 60. Differences in working time decrease with age, from 20% under age 25 to 10% between ages 25 and 60. For workers, women earned 14.3% less than men for equivalent hours and worked 23.3% fewer hours. Among employees, women earned 4.7% less for similar hours and had nearly equal working time. The pay gap for equal hours was 16.1% among executives and 12.2% among intermediate professions, with women in these groups also working fewer hours (4.7% and 10.9%, respectively). For equivalent positions and working hours, the wage gap was 4.3%, though occupational segregation—such as differences in sector and employer—affects this figure. In the public sector, the overall gender wage gap was 14%. Among executives, the gap was 23%; among workers, 17%; and among employees, 7%. For full-time salaried positions, the gender wage gap declined from 29.4% in 1976 to 16.3% in 2017. The gap narrowed steadily until 1980, remained largely stable until 2000, and began to decrease again thereafter, though part-time employment among women influenced this trend.

In both meetings, according to him, "the good relations between Brazil and the Holy See and the harmonious collaboration between Church and State in favour of the promotion of moral values and the common good" were highlighted.

Sources: en.wikipedia.org

Frequently asked questions

What is epitalon made of?

It is a four-amino-acid peptide built from alanine, glutamate, aspartate and glycine in that order. Its formula is C14H22N4O9, and it is made by chemical synthesis rather than extracted from tissue. The synthetic peptide is a single defined molecule, unlike the pineal extracts it is often compared with.

Are epitalon and epithalon different compounds?

No. The two spellings refer to the same tetrapeptide, and the difference reflects transliteration from Russian. Laboratories and catalogues use both forms interchangeably. The material is also indexed as AEDG, taken from the one-letter codes of its residues.

How does epitalon differ from epithalamin?

Epithalamin is a mixed preparation derived from animal pineal tissue and contains many peptides. Epitalon is one synthetic sequence chosen for study from that broader mixture. Statements about one do not transfer directly to the other.

Is epitalon the same substance as epithalamin?

No. Epithalamin is a peptide-containing extract of bovine pineal glands, while epitalon is a single synthetic tetrapeptide. The extract contains many peptides and other tissue components, so its composition varies between batches in ways that a synthesised sequence does not.

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