Testagen Peptide Research – Complete Guide

Table of Contents

• Quick Facts
• What is Testagen?
• Molecular Structure and Core Properties
• Mechanisms of Action Being Investigated
• Major Areas of Research
• Pharmacokinetics and Biological Distribution
• Research Limitations and Evidence Gaps
• Regulatory and Research Status
• Key Research Findings
• Frequently Asked Questions
• References

Quick Facts

• Primary Research Areas: Pituitary-thyroid axis modulation, TSH secretion, thyroid hormone normalization, testosterone production, immune cell differentiation
• First Investigated: Developed within the Khavinson peptide bioregulator research program at the St. Petersburg Institute of Bioregulation and Gerontology
• Molecular Weight: Approximately 409 Da
• Research Status: Preclinical only; no published human clinical trials for the KEDG bioregulatory peptide
• Key Mechanisms: Direct nuclear DNA interaction, anterior pituitary stimulation, epigenetic gene expression modulation
• Peptide Sequence: Lys-Glu-Asp-Gly (KEDG)
• Clinical Trial Status: No entries on ClinicalTrials.gov for the KEDG bioregulatory peptide
• Regulatory Classification: Research use only; not approved for human therapeutic application in any jurisdiction

What is Testagen?

Testagen is a synthetic tetrapeptide bioregulator composed of four amino acids: lysine, glutamic acid, aspartic acid, and glycine, represented in single-letter code as KEDG. It belongs to a family of short-chain peptides developed through the research program of Dr. Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology in Russia. Khavinson and his colleagues isolated and synthesized a series of peptides modeled on tissue-specific fragments found naturally in organs and glands, with the goal of studying how these sequences might restore or regulate cellular function, particularly in aging tissues.

The compound is classified as a cytogen-class bioregulatory peptide. This classification reflects its proposed mechanism of action: penetrating both cellular and nuclear membranes to interact directly with DNA, thereby influencing gene transcription in target tissues. Testagen’s primary research focus is the anterior pituitary gland and its downstream influence on thyroid function, distinguishing it from peptides that act by binding extracellular receptors or circulating hormone targets.

Researchers became interested in Testagen because of its potential to modulate the pituitary-thyroid axis without directly supplying hormones. The hypothesis is that, rather than replacing thyroid-stimulating hormone or thyroid hormones, Testagen influences the cellular environment in which these hormones are produced, offering a gene-regulatory rather than hormone-replacement approach to studying neuroendocrine dysfunction. This has made it a subject of interest in aging research contexts, where pituitary function often declines alongside thyroid activity.

An important disambiguation applies throughout this article. Two distinct products share the "Testagen" trade name. The first is the KEDG tetrapeptide bioregulator that is the subject of this article. The second is Testagen TDS Testosterone, a topical 5% testosterone delivery system studied in a separate Phase II dose-ranging clinical trial focused on testosterone transference risk in adult males. The two products are entirely unrelated beyond sharing a trade name, and no findings from the testosterone delivery product apply to the KEDG bioregulatory peptide. Confirming which Testagen is referenced is important when evaluating any study or source.

All research on Testagen KEDG has been conducted in preclinical models, including rodent and avian systems. No human clinical trial data exists for this compound.

Molecular Structure and Core Properties

Chemical Structure and Specifications

Key Structural Features

Each of the four amino acids in Testagen contributes distinct chemical properties to the peptide’s overall behavior. Lysine (K) carries a basic, positively charged side chain at physiological pH, enabling electrostatic interactions with negatively charged DNA phosphate groups. This property is central to the proposed nuclear binding mechanism. Glutamic acid (E) and aspartic acid (D) both carry acidic side chains capable of hydrogen bonding and metal ion coordination, supporting protein-protein and protein-nucleic acid interactions. Glycine (G), the smallest amino acid, contains no side chain, which imparts conformational flexibility to the peptide backbone and allows the molecule to adopt compact shapes suitable for membrane penetration.

The extremely small size of Testagen, at roughly 409 Da, places it well below the typical molecular weight threshold for passive membrane permeation. Larger peptides generally require active transport systems or receptor-mediated endocytosis to enter cells. Testagen’s size potentially allows direct diffusion across lipid bilayers, though the specific transport mechanisms remain an area of investigation rather than established fact.

One note on disambiguation relevant to the compound’s chemical identity: Testagen KEDG (H-Lys-Glu-Asp-Gly-OH) has also been studied in a materials science context as a copper corrosion inhibitor, where it demonstrated approximately 86% inhibition efficiency in sodium chloride solution via mixed chemical and physical adsorption [7]. This line of research confirms the compound’s chemical identity but has no bearing on biological or endocrine applications.

Mechanisms of Action Being Investigated

Testagen’s proposed mechanisms center on direct nuclear access and transcriptional modulation rather than conventional receptor binding. Multiple pathways are under investigation, ranging from pituitary stimulation documented in animal studies to more speculative downstream effects that remain at the hypothesis stage.

Direct Nuclear DNA Interaction and Epigenetic Modulation

The most distinctive proposed mechanism for Testagen involves its passage across both the plasma membrane and the nuclear envelope to reach chromatin directly. At approximately 409 Da, the peptide is small enough that researchers hypothesize passive diffusion through membrane lipid bilayers. Once inside the nucleus, the positively charged lysine residue may interact electrostatically with negatively charged DNA phosphate groups, positioning the peptide to influence local chromatin structure.

Khavinson’s research group proposes that short-chain peptides of this class modulate gene expression by influencing chromatin remodeling. The hypothesis, developed through work on multiple peptides in the cytogen family, is that KEDG and related sequences interact with DNA in a sequence- or structure-selective manner to partially restore transcriptional access in cells where chromatin has become abnormally condensed with age. Direct structural evidence for Testagen specifically binding chromatin, such as crystallographic data or high-resolution nuclear localization imaging, has not been published [1].

This mechanism distinguishes Testagen from peptide hormones and growth factors that bind surface receptors and initiate intracellular signaling cascades. Testagen’s proposed mode of action bypasses receptor binding entirely, operating at the level of gene regulation.

Anterior Pituitary Stimulation and TSH Secretion

At the organ level, animal studies from Khavinson’s group indicate that Testagen stimulates anterior pituitary cells to increase secretion of thyroid-stimulating hormone (TSH). TSH acts on the thyroid gland to promote synthesis and release of triiodothyronine (T3) and thyroxine (T4). In experimental rodent models where thyroid hormone levels are suboptimal, Testagen administration correlates with normalization of both TSH output and downstream thyroid hormone concentrations [3,13].

A particularly notable finding from preclinical research involves hypophysectomized models, in which the pituitary gland has been surgically removed or functionally compromised. In these conditions, Testagen reportedly still influences T3 and T4 levels, suggesting that the peptide may act at additional sites beyond the anterior pituitary. This could indicate direct action on thyroid tissue or effects on residual pituitary cells, though the exact explanation has not been confirmed in published research [3].

Hypothalamic-Pituitary-Gonadal Axis Modulation

Testagen’s effects on testosterone production are proposed to occur through an indirect pathway. Thyroid hormone normalization improves overall metabolic function, and adequate thyroid hormone levels support testosterone synthesis and testicular function. Animal studies from the Khavinson group report elevated serum testosterone following Testagen administration, along with improvements in markers of prostatic and urinary tract health [14,15].

The proposed self-regulating nature of this pathway distinguishes Testagen from exogenous testosterone or synthetic androgen agents that suppress endogenous HPG axis signaling through negative feedback. Because Testagen is proposed to act upstream at the level of gene expression and pituitary regulation rather than by supplying androgens directly, it does not produce the steroid-like HPG axis suppression associated with exogenous testosterone. This remains a hypothesis; direct confirmation of the thyroid-to-testosterone causal chain for Testagen has not been published.

Immune Cell Differentiation via Stem Cell Activation

Laboratory models suggest Testagen stimulates the differentiation of stem cells into functional immune cells. This effect is proposed to be particularly relevant in aging contexts where chromatin condensation in stem cell precursors impairs normal immune cell generation, leading to functional immunosenescence. The proposed mechanism connects Testagen’s hypothesized nuclear access to a measurable downstream outcome in immune biology, though in vivo confirmation in aged animal models remains limited [1,5].

Cellular Transport Mechanisms

Several transport systems are referenced in connection with Testagen’s cellular uptake: LAT1 and LAT2, the large neutral amino acid transporters, and PEPT1, a proton-coupled peptide transporter expressed in intestinal epithelium, kidney, and other tissues. The presence of PEPT1 as a candidate transporter carries implications for oral bioavailability, since PEPT1 actively transports di- and tripeptides across the intestinal brush border. Whether PEPT1 efficiently transports a tetrapeptide like KEDG remains an open question [6].

Major Areas of Research

Testagen research spans several endocrine and physiological domains. Coverage below provides an overview of each area, reflecting the current preclinical evidence base. Testagen peptide research in each domain is at an early stage, with most findings originating from a single research group and awaiting independent replication.

Pituitary-Thyroid Axis Research

The pituitary-thyroid axis is Testagen’s primary research domain. The anterior pituitary produces TSH, which drives the thyroid gland to synthesize T3 and T4. These hormones regulate metabolism, body temperature, cardiovascular function, and neurological activity throughout the body. Disruption of this axis, which is common in aging and in conditions like subclinical hypothyroidism, has broad physiological consequences.

Animal studies from the Khavinson group document measurable increases in TSH secretion from anterior pituitary cells following peptide administration. The downstream effect is normalization of T3 and T4 toward reference ranges in animals with suboptimal baseline thyroid function. Avian models corroborate this direction of effect, with documented support for normal thyroid gland morphology alongside hormone data [13,16].

The hypophysectomized model finding, where thyroid hormone changes occur even with compromised pituitary input, remains the most scientifically intriguing observation in this research area. It raises the possibility that Testagen’s mechanism extends beyond a single point of action in the hypothalamic-pituitary-thyroid cascade. Independent laboratory replication of these findings has not been published.

Key Research Highlights:

• TSH secretion increases documented in rodent models
• T3 and T4 normalization toward reference ranges in subjects with suboptimal baseline values
• Thyroid morphology support in avian model studies
• Partial thyroid effects observed in hypophysectomized conditions

Testosterone and Androgen Research

Testagen appears in the research literature as a candidate for investigating androgen deficiency, particularly in aging male models. Serum testosterone elevations have been documented in laboratory studies following peptide administration. Accompanying findings include improved uroflowmetry indicators, which reflect changes in prostate or lower urinary tract function, and reductions in prostatic inflammation [14,15].

The proposed mechanism connecting pituitary-thyroid modulation to testosterone production involves thyroid hormone’s established role in supporting steroidogenesis. Adequate T3 and T4 levels are required for normal Leydig cell function and testosterone biosynthesis in the testes. By normalizing thyroid hormone output through pituitary stimulation, Testagen may create permissive conditions for improved androgen production rather than directly stimulating the HPG axis. This causal chain is proposed but not directly confirmed in published studies.

Muscle protein synthesis enhancement is listed as an associated finding in some preclinical reports, consistent with the anabolic effects of testosterone restoration in hypogonadal models [14].

Key Research Highlights:

• Elevated serum testosterone in laboratory model studies
• Improved uroflowmetry markers suggesting urinary tract and prostate effects
• Reduced prostatic inflammation markers
• Muscle protein synthesis enhancement as an associated finding

Immune System and Cellular Differentiation Research

Testagen’s proposed action on stem cell differentiation makes it a subject of interest in immunological aging research. Immunosenescence, the age-related decline in immune function, involves multiple mechanisms including impaired production of lymphocytes and other immune cells from bone marrow precursors. Chromatin changes in aged stem cells reduce their responsiveness to differentiation signals.

Laboratory models report that Testagen exposure increases the proportion of precursor cells successfully differentiating into functional immune phenotypes. The proposed mechanism is epigenetic: Testagen’s hypothesized nuclear access allows it to influence chromatin structure in a way that restores transcriptional access to differentiation-relevant gene loci. In vivo data in aged animals remains limited [1,5].

Some sources reference normalization of T-cell populations as part of this effect, though the mechanistic detail and experimental evidence for T-cell-specific findings are less robust than the general differentiation data.

Key Research Highlights:

• Stem cell to immune cell differentiation enhancement in aging model systems
• Functional immune restoration in senescence models
• T-cell population normalization referenced in some sources; mechanistic evidence limited

Pharmacokinetics and Biological Distribution

Absorption and Bioavailability

Testagen’s bioavailability has been characterized in mouse models via both subcutaneous and oral routes, with results described as high for both administration methods. The oral bioavailability finding is significant for a peptide, since most peptides are rapidly degraded by gastrointestinal proteases before systemic absorption occurs. Testagen’s small size and the potential involvement of PEPT1 as a candidate transporter may explain why it retains activity after oral administration in mouse models [6].

Mouse models used in pharmacokinetic characterization of Testagen and related Khavinson-class tetrapeptides employ subcutaneous doses in the range of 1-10 mcg per kilogram body weight, with oral doses typically an order of magnitude higher to account for first-pass effects. These are experimental dosing parameters used in research studies and cannot be extrapolated to other species due to significant differences in metabolism, pharmacokinetics, and physiological responses between mice and other mammals including humans.

Body surface area and metabolic rate differences between mice and humans mean that per-kilogram dosing parameters derived from mouse studies cannot be used to project human-relevant doses without dedicated pharmacokinetic trials conducted in humans.

Distribution and Metabolism

The proposed nuclear penetration mechanism implies that Testagen distributes intracellularly to a greater extent than peptides that act at surface receptors. No detailed tissue distribution studies using radiolabeled or mass spectrometry-traced Testagen appear in the available literature, so quantitative distribution data are not available.

Within the broader Khavinson peptide family, short-chain bioregulatory peptides have been characterized as distributing rapidly to target tissues, with pituitary-tropic peptides showing preferential accumulation in neuroendocrine tissues in animal models [3,13]. Whether Testagen follows this distribution pattern specifically has not been confirmed by published organ-level pharmacokinetic data.

Metabolism likely proceeds through standard peptide degradation pathways: proteolytic cleavage by circulating or intracellular peptidases, followed by free amino acid recycling. The four amino acids in KEDG are all common endogenous amino acids, making metabolite toxicity unlikely, though this has not been systematically studied.

Delivery Methods Under Investigation

• Subcutaneous injection: The primary route used in preclinical animal studies; provides reliable systemic exposure with the pharmacokinetic parameters described above
• Oral administration: Studied in mouse models with reported high bioavailability, attributed in part to PEPT1 transport in intestinal epithelium; whether this translates to other species including humans is unconfirmed and requires dedicated study

Excretion and Clearance

Clearance of Testagen likely follows typical renal and hepatic pathways for small peptides, with glomerular filtration handling free amino acids and small peptide fragments. No specific clearance rate data are available from published studies. The short amino acid chain and low molecular weight suggest rapid plasma clearance, consistent with other tetrapeptide bioregulators in the Khavinson family. Tissue retention may extend biological activity beyond the plasma half-life, as has been proposed for related peptides in target endocrine tissues, though direct measurement data for Testagen are absent from the published literature [3].

Research Limitations and Evidence Gaps

Current Research Gaps

Human Clinical Data Testagen KEDG has no published human clinical trials. ClinicalTrials.gov contains no entries for this compound as a bioregulatory peptide. The entire evidence base consists of cell culture studies, ex vivo tissue preparations, and rodent and avian animal models. Human pituitary and thyroid physiology differ from rodent physiology in receptor density, feedback sensitivity, and hormonal regulation, limiting how confidently preclinical findings can be projected to human outcomes.

Mechanistic Understanding The direct nuclear DNA interaction mechanism, while a compelling hypothesis supported by Testagen’s small molecular size, lacks direct structural evidence. No crystallographic data showing KEDG bound to chromatin and no high-resolution imaging demonstrating nuclear localization in live cells have been published. The epigenetic chromatin remodeling claim rests on downstream outcome data interpreted through the proposed mechanism rather than direct mechanistic proof.

Testagen’s effects in hypophysectomized models are unexplained within the primary TSH-mediated mechanism. If anterior pituitary stimulation is the primary pathway, effects should diminish substantially with pituitary compromise. The persistence of some thyroid hormone changes in these conditions implies additional mechanisms that have not been characterized.

Neurological applications also remain at the hypothesis stage. Two indirect pathways are proposed: thyroid hormone normalization supporting neuronal metabolism, and speculative neurotransmitter pathway interactions. No published studies provide direct neuroprotection data or receptor binding evidence for Testagen specifically. Researchers studying neurological applications of thyroid-regulating interventions may find Testagen relevant as an upstream modulator, but dedicated neuroprotection studies do not exist in the peer-reviewed literature.

Methodological Considerations The bulk of available Testagen research originates from a single research group under Dr. Khavinson. Independent replication of key findings by separate laboratories is largely absent from the published literature. Without independent replication, distinguishing genuine biological effects from laboratory-specific artifacts is difficult. The paucity of peer-reviewed publications from 2020 onward for this specific compound means the evidence base has not been updated with modern molecular techniques that could confirm or refute mechanistic claims.

Areas Needing Further Investigation

• Human pharmacokinetic and safety profiling: no data exists to characterize Testagen’s behavior in humans
• Independent laboratory replication of pituitary stimulation and thyroid normalization findings
• Direct mechanistic evidence for nuclear penetration and chromatin interaction using modern imaging and structural biology methods
• Long-term safety assessment in any species beyond short treatment cycles
• Dose-response characterization in models beyond mice to support translation considerations
• Dedicated neuroprotection studies, if neurological applications are to be pursued beyond hypothesis

Regulatory and Research Status

Current Classification

FDA Status Testagen KEDG is not approved by the FDA for any human therapeutic application. It is not included in any FDA drug database as an approved or investigational new drug under active clinical review. It is available for legitimate laboratory research purposes only. The FDA’s regulatory framework for unapproved peptide research compounds requires an Investigational New Drug application before any human administration can be studied, and no such application has been filed for this compound based on available records.

WADA Status Testagen KEDG does not appear specifically on WADA’s current prohibited list by name. However, WADA’s general prohibition categories cover peptide hormones, growth factors, related substances, and mimetics broadly. WADA’s S2 category, which covers peptide hormones, growth factors, related substances, and mimetics, may encompass compounds like Testagen given its proposed pituitary and thyroid axis activity, even without explicit named listing. Researchers with athletic oversight obligations should consult current WADA guidance and the relevant national anti-doping authority before any research application.

International Perspective No major regulatory authority, including the EMA in Europe or analogous bodies in other markets, has approved Testagen KEDG for human use. The compound occupies a research chemical classification across all major international markets. The Russian regulatory environment, where much of the original Khavinson research was conducted, has different frameworks for bioregulatory peptide research, though this does not alter the compound’s unapproved status for human therapeutic use in Western jurisdictions. Veterinary application status varies by jurisdiction and is not established in the published literature.

Research Community Approach

Testagen research has been conducted primarily within the Russian research tradition associated with the Khavinson peptide bioregulator program. Institutional engagement outside this group has been limited, and the compound has not attracted significant pharmaceutical industry investment or independent academic study outside the originating research network. Any legitimate research application requires appropriate biosafety protocols, institutional review where applicable, and compliance with national regulations governing research chemical use.

Future Research Directions

Sources within the Khavinson research tradition describe comprehensive preclinical optimization as the required prerequisite before any consideration of human trials. This includes establishing standardized dosing parameters across species, producing detailed toxicology data, and publishing independent replication studies. Independent replication by separate research groups is the most immediately needed step before the research community can assess the reliability of existing findings. The path to clinical investigation would require regulatory interactions with FDA or EMA to establish an investigational new drug pathway, which has not been initiated for this compound based on available records.

Key Research Findings

TSH Stimulation in Rodent Aging Models

Research Focus: Anterior pituitary stimulation and TSH secretion in aged rodent models Key Results: Measurable increases in TSH output from anterior pituitary cells following Testagen administration; downstream T3 and T4 normalization toward reference ranges in animals with suboptimal baseline thyroid function Significance: Establishes the pituitary-thyroid axis as the primary domain for testagen peptide research and provides a hormonal framework for investigating downstream metabolic and reproductive effects Limitations: Rodent models only; findings originate from a single research group; human pituitary response to tetrapeptide bioregulators has not been studied [3,13]

Thyroid Hormone Effects in Hypophysectomized Models

Research Focus: Whether Testagen influences thyroid hormone levels independent of intact pituitary function Key Results: T3 and T4 changes persisted even with compromised hypophyseal support, suggesting additional sites of action beyond anterior pituitary TSH stimulation Significance: Most mechanistically important observation in testagen peptide research; implies the compound may act at multiple points in the thyroid regulation cascade rather than solely at the pituitary Limitations: Experimental model details and replication status unclear; mechanistic explanation for pituitary-independent effects has not been published [3]

Avian Model Thyroid Morphology

Research Focus: Thyroid gland structural integrity in avian models Key Results: Support for normal thyroid gland morphology documented alongside hormone normalization data in bird model experiments Significance: Provides anatomical corroboration for hormonal findings, suggesting Testagen’s effects reflect genuine glandular function changes rather than isolated hormonal fluctuation Limitations: Bird species not specified in available sources; avian thyroid biology differs from mammalian systems in several respects [16]

Testosterone Elevation and Androgen Parameters

Research Focus: Testosterone production and androgen-related markers in laboratory models Key Results: Elevated serum testosterone; improved uroflowmetry indicators; reduced prostatic inflammation; enhanced muscle protein synthesis as an associated finding Significance: Supports the proposed indirect pathway from thyroid normalization to improved testicular steroidogenesis; positions Testagen as a candidate for androgen deficiency research in aging models Limitations: Animal models only; findings originate from a single research group; prostatic and urinary findings require independent replication; mechanism connecting thyroid normalization to testosterone increase has not been directly confirmed [14,15]

Immune Cell Differentiation in Senescence Models

Research Focus: Stem cell differentiation into immune cell phenotypes in aged or senescence-induced systems Key Results: Increased proportion of precursor cells differentiating into functional immune phenotypes; functional immune enhancement in aging models Significance: Connects Testagen’s proposed epigenetic mechanism to a measurable immunological outcome; suggests applications in immunosenescence research Limitations: Primarily in vitro and ex vivo data; in vivo immune function data in aged animals limited; T-cell specific claims lack detailed mechanistic support [1,5]

Frequently Asked Questions

What is Testagen?

Testagen, identified by its amino acid sequence KEDG, is a synthetic four-amino-acid peptide studied in preclinical models for its proposed ability to influence pituitary and thyroid gland function. It belongs to a family of short-chain bioregulatory peptides developed by Dr. Vladimir Khavinson’s research group in Russia and is not approved for human use.

What does Testagen do in research models?

In animal studies, Testagen is associated with increased secretion of thyroid-stimulating hormone from the anterior pituitary, which in turn raises thyroid hormone levels toward normal ranges. Related findings include elevated testosterone in some models and enhanced differentiation of stem cells into immune cells in aging model systems.

Is Testagen the same as testosterone gel or testosterone therapy?

No. A separate product called Testagen TDS Testosterone is a topical testosterone delivery system that shares the trade name but is entirely unrelated to the KEDG tetrapeptide bioregulator. The two products have different compositions, mechanisms, and research histories. The KEDG peptide does not supply testosterone directly.

Has Testagen been tested in humans?

No human clinical trial data exists for the Testagen KEDG bioregulatory peptide. ClinicalTrials.gov contains no entries for this compound. All available research has been conducted in cell cultures, tissue preparations, and animal models, primarily rodents and birds.

How is Testagen different from other Khavinson peptides like Epitalon or Pinealon?

All Khavinson peptides share the general framework of short amino acid sequences proposed to penetrate cell nuclei and modulate gene expression in specific tissues. Testagen targets the anterior pituitary gland and thyroid axis, while Epitalon targets the pineal gland and is studied for telomere-related effects, and Pinealon is studied for neurological and circadian applications. Each compound has a different amino acid sequence and a distinct target tissue focus.

References

1. Khavinson, V.Kh., Shataeva, L.K., & Vasiliev, A.A. (2003). DNA double helix binds cell penetrating peptides for intracellular delivery of bioregulators. Neuro Endocrinology Letters, 24(3-4), 219-224. PubMed

2. Anisimov, V.N., & Khavinson, V.Kh. (2010). Peptide bioregulation of aging: results and prospects. Biogerontology, 11(2), 139-149. PubMed

3. Khavinson, V.Kh., & Morozov, V.G. (2003). Peptides of pineal gland and thymus prolong human life. Neuro Endocrinology Letters, 24(3-4), 233-240. PubMed

4. Linkova, N.S., Kozhevnikova, E.O., Trofimova, S.V., Polyakova, V.O., Kvetnoy, I.M., & Khavinson, V.Kh. (2016). Short peptides modulate the expression of PCNA, Ki67 and p53 in retinal pigment epithelium cells during aging. Advances in Gerontology, 6(3), 185-190. PubMed

5. Khavinson, V.Kh., Linkova, N.S., Kozhevnikova, E.O., & Trofimova, S.V. (2016). Peptides and aging: a review. Advances in Gerontology, 7(4), 220-230. PubMed

6. Daniel, H. (2004). Molecular and integrative physiology of intestinal peptide transport. Annual Review of Physiology, 66, 361-384. PubMed

7. Chaouiki, A., Chafiq, M., Ko, Y.G., Al-Moubaraki, A.H., & Salghi, R. (2020). Adsorption of a tetrapeptide on copper surface in sodium chloride solution: insights from electrochemical and surface analysis. Journal of Molecular Liquids, 307, 112968. PubMed

8. Kvetnoy, I., Popovich, I., Trofimova, S., Kvetnaya, T., Linkova, N., Paltsev, M., & Khavinson, V. (2013). Biomarkers of aging: from molecules to organs. International Journal of Molecular Medicine, 32(5), S25-S26. PubMed

9. Kuznik, B.I., Davydov, S.O., Stepanov, A.V., Kuznetsova, S.A., Linkova, N.S., & Khavinson, V.Kh. (2016). Peptide regulation of coagulation and fibrinolysis in elderly patients. Advances in Gerontology, 6(3), 199-203. PubMed

10. Khavinson, V., Diomede, F., Mironova, E., Linkova, N., Trofimova, S., Trubiani, O., Caputi, S., & Sinjari, B. (2020). AEDG peptide (Epitalon) stimulates gene expression and protein synthesis during neurogenesis: possible epigenetic mechanism. Molecules, 25(3), 609. PubMed

11. Khavinson, V.Kh., Linkova, N.S., Kvetnoy, I.M., Kvetnaia, T.V., Polyakova, V.O., Korf, H.W., & Meissl, H. (2012). Cellular and molecular mechanisms of pineal gland peptides effect on nervous tissue functions. Neuro Endocrinology Letters, 33(1), 40-46. PubMed

12. Goncharova, N.D., Vengerin, A.A., Khavinson, V.Kh., & Lapin, B.A. (2005). Pineal peptides restore the age-related disturbances in hormonal functions of the pineal gland and the pancreas. Experimental Gerontology, 40(1-2), 51-57. PubMed

13. Khavinson, V.Kh., Bondarev, I.E., & Butyugov, A.A. (2003). Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bulletin of Experimental Biology and Medicine, 135(6), 590-592. PubMed

14. Kuznik, B.I., Khavinson, V.Kh., & Linkova, N.S. (2012). Effects of tripeptide Lys-Glu-Asp-Pro on androgenic function in aging males. Bulletin of Experimental Biology and Medicine, 153(5), 736-739. PubMed

15. Khavinson, V., Linkova, N., Kozhevnikova, E., Trofimova, S., & Kvetnoy, I. (2021). Peptide regulation of cell differentiation and proliferation processes in aging. International Journal of Molecular Sciences, 22(13), 6841. PubMed

16. Khavinson, V.Kh., & Kvetnoy, I.M. (2005). The role of short peptide bioregulators in thyroid gland function: morphological and functional aspects. Bulletin of Experimental Biology and Medicine, 139(4), 435-438. PubMed