Longevity: Peptides and Research Compounds in the Context of Ageing

Rapamycin extended the lifespan of mice when treatment began at an age corresponding to a human’s sixties. The result was reproduced at three independent centres, in mice of varied genotype, and to this day it is the benchmark for a rigorous study in the biology of ageing. No compound in our catalogue has data of that class, and most have not a single study in humans. That sentence is worth starting from in any reading about “longevity”.

This guide ties together our articles on compounds studied in the context of ageing. It explains what longevity is as a field of science, which mechanisms of ageing the molecules in the catalogue concern, how to read results from models before anyone translates them to a person, what the legal and anti-doping status of this group is, and finally it leads to five articles on specific compounds. We give no doses in any of them; the FAQ section explains why.

In our catalogue, the compounds discussed in this article are chemical reagents intended solely for laboratory research (Research Use Only). They are not medicinal products, dietary supplements or foods, and they are not intended for use in humans or animals. What this status means is explained in our material on the legal status of research reagents.

What longevity is as a field of research

The biology of ageing acquired a common language in 2013, when five authors described nine “hallmarks of ageing”: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication (López-Otín et al., 2013, PMID 23746838). Ten years later the same group extended the list to twelve, adding disabled macroautophagy, chronic inflammation and dysbiosis, and set out three conditions a hallmark must meet: it must intensify with age, its experimental accentuation must accelerate ageing, and intervening in it must slow ageing down (López-Otín et al., 2023, PMID 36599349).

That third condition is the crux of the whole field. It is not enough to show that a compound changes a marker associated with ageing; one has to show that the change in the marker translates into a longer life or longer health, and in an organism rather than a dish. A 2024 review summarising a decade of citations of the concept shows that the “hallmarks of ageing” have become a framework for health and longevity research too, while the debate over which candidates to add to the list continues (Tartiere et al., 2024, PMID 38292053). The intervention with the strongest human data remains regular exercise: a 2025 review co-authored by the concept’s originators describes its effect on each of the twelve hallmarks (Qiu et al., 2025, PMID 41352451).

Which mechanisms concern the compounds in the catalogue

Telomeres. Telomere attrition is one of the nine original hallmarks. Epitalon, the tetrapeptide AEDG, owes its fame to a 2003 paper in which it induced telomerase activity and lengthened telomeres in cultured human somatic cells (Khavinson et al., 2003, PMID 12937682). Telomere biology, however, is more complex than that observation suggests: telomere length is specific to individual chromosome ends (Karimian et al., 2024, PMID 38603523), and telomerase reactivation is a feature of cancer cells, so telomerase-based interventions carry their own risk (Dunn et al., 2024, PMID 39693017). The details are in our article on Epitalon and telomeres.

Mitochondria. Mitochondrial dysfunction is another hallmark, and two compounds in the catalogue target it from different sides. MOTS-c is a peptide encoded in the mitochondrial genome; in mice it regulated metabolic homeostasis and insulin sensitivity (Lee et al., 2015, PMID 25738459), its levels rose after exercise, and in old mice it delayed the decline in physical performance (Reynolds et al., 2021, PMID 33473109). The role of such “mitokines” in ageing is summarised in a review (Burtscher et al., 2023, PMID 36642986). SLU-PP-332 acts from the side of the ERR receptors that govern mitochondrial biogenesis: in mice it switched on the aerobic-exercise gene programme (Billon et al., 2023, PMID 36988910), and in 21-month-old animals it reversed age-related mitochondrial dysfunction and inflammation in the kidney (Wang et al., 2023, PMID 37717940). We cover both compounds separately: MOTS-c and SLU-PP-332.

NAD⁺ and NNMT. Deregulated nutrient sensing includes the pathways that depend on NAD⁺ and sirtuins. The enzyme NNMT removes nicotinamide from the NAD⁺ pool, and its small-molecule inhibitors, including 5-amino-1MQ, reversed obesity in mice on a high-fat diet (Neelakantan et al., 2018, PMID 29155147); a 2026 review describes their clinical translation as still to come (Puleo et al., 2026, PMID 42067476). On the other side of this pathway stand the NAD⁺ precursors. Nicotinamide mononucleotide (NMN) is the only compound in this guide with randomised trials in humans: in 80 healthy middle-aged people it raised blood NAD⁺ over 60 days (Yi et al., 2023, PMID 36482258), and a comparison of three precursors in 65 people indicated that NMN and nicotinamide riboside raise NAD⁺ through conversion to nicotinic acid with the help of the gut microbiota (Christen et al., 2026, PMID 41540253). A rise in NAD⁺ is a marker, not a health outcome; these trials measured no hard endpoints. The background to the enzyme and its inhibitor is in our article on 5-amino-1MQ.

Peptide bioregulators. The St Petersburg school proposes that short peptides designed from tissue extracts regulate gene expression by binding to DNA. Cortagen, Cardiogen and Bronchogen have data from animal models and cultures, almost all from a single centre; we discuss them in our article on Cortagen and peptide bioregulators.

Exercise mimetics. This is a label rather than a mechanism: compounds that, in a model, trigger part of the molecular response to exercise. Since movement acts on all twelve hallmarks of ageing at once (Qiu et al., 2025), an agonist of a single receptor copies a fraction of them. That is why in our texts the word “mimetic” describes a research direction, not a promise.

How to read anti-ageing promises: from the model to the human being

The 2009 rapamycin study shows what a high standard looks like. The drug was given from day 600 of life, at three independent centres, to genetically heterogeneous mice so as to exclude effects tied to a single strain; the age at which 90% of the population had died rose by 14% in females and 9% in males (Harrison et al., 2009, PMID 19587680). Every paper on an “anti-ageing” compound is worth measuring against that benchmark. How many centres? One strain or many? Lifespan or a marker? Old animals or young? For most compounds in this guide the answers are: one centre, one model, a marker, and no human studies.

The second filter is the road from marker to outcome. A rise in blood NAD⁺, telomerase activity in a culture or the expression of an exercise gene in mouse muscle are intermediate variables. The field has a long list of interventions that improved markers and changed neither the length nor the quality of life. The third filter is the category itself: the promised effect, a longer life, is in practice unverifiable within the time a buyer has at their disposal. That makes longevity claims resistant to falsification, which is a feature of advertising, not of science. The fourth filter is the structure of the literature: when most papers on a compound come from a single centre and the reviews are written by the same authors, the number of citations does not measure the strength of the evidence.

There is also the question of whom the data concern in the first place. A 2026 review of peptides in sports medicine separates approved from unapproved therapies and points out that for the latter the data on efficacy and safety in humans are limited or absent (Mendias and Awan, 2026, PMID 41966639). Preclinical results from rodents do not transfer automatically to humans in direction, in size or in safety; a mouse lives three years and falls ill differently.

Regulatory status of this group

European Union and United States. None of the compounds discussed in the cluster is approved as a medicine in the European Union or in the United States; the Drugs@FDA database and the EU medicines data (Article 57, as of 9 October 2026) contain no entry for Epitalon, MOTS-c, 5-amino-1MQ, SLU-PP-332, Cortagen, Cardiogen or Bronchogen (checked 7 November 2026). No approval in other countries is known to us for any of them; Cortexin, registered in Russia, is a different product from Cortagen. The reagents in the catalogue are material for laboratory research.

NMN is a separate case. In the EU Novel Food Catalogue, nicotinamide mononucleotide has the status “not yet authorised novel food” (NOT_YET_AUTHORISED_NOVEL_FOOD, as of 7 November 2026), so in the EU it cannot lawfully be an ingredient of a food supplement until it passes the authorisation procedure. We discuss it as a compound with human data, not as a product. The identity and purity of a reagent batch are confirmed by an analytical document; how to read it is explained in our article on the certificate of analysis.

Anti-doping note, for the whole group

The WADA 2026 Prohibited List names MOTS-c in class S4.4.1 (metabolic modulators, AMPK activators). The remaining compounds of the cluster are not named, but as substances without approval for human use they fall under class S0, prohibited at all times. The 2027 List, in force from 1 January 2027, keeps MOTS-c in S4.4.1, adds “SLU-PP-332, SLU-PP-915 and related substances” there by name and puts “peptides” among the examples in the description of class S0. Epitalon, Cortagen, Cardiogen, Bronchogen and 5-amino-1MQ fall under S0 in both editions as non-approved substances (2026 and 2027 Lists). Athletes tested in the United States fall under the same List, because USADA is a signatory to the World Anti-Doping Code. The classification rules are set out in our guide to the WADA Prohibited List; the decision rests with WADA and the national agencies.

Map of the cluster: where to find the details

Epitalon and telomeres: why the structure of the literature matters here as much as its content, and what telomere biology does not confirm.

MOTS-c and mitochondrial peptides: mitokines, the 2015 mouse model, the kinase CK2 and what is missing, namely human studies.

5-amino-1MQ, an NNMT inhibitor: an enzyme at the junction of NAD⁺ and methylation, mouse data and the state of clinical translation.

Cortagen and peptide bioregulators: the St Petersburg school, Cardiogen and Bronchogen, the quality of the evidence and the difference between Cortagen and Cortexin.

SLU-PP-332, an ERR agonist: where the exercise-mimetic label came from, model data and two editions of the WADA List.

Frequently asked questions

What is longevity?
The field of research into the biology of ageing, organised since 2013 around the “hallmarks of ageing”, of which there are now twelve. An intervention deserves attention when it acts on a hallmark and at the same time lengthens life or health in an organism, not merely changes a marker.

Does any of these compounds extend life in humans?
There are no such data for any of them. Only NMN has randomised trials in humans, and they measured blood NAD⁺ concentration, not the length or quality of life. The rest are animal models and cultures.

Why does rapamycin appear in the guide when it is not in the catalogue?
Because the 2009 study is the methodological benchmark: three centres, varied genotype, old animals, lifespan as the endpoint. We measure every paper on an “anti-ageing” compound against it.

Can NMN be bought as a supplement in the EU?
In the EU Novel Food Catalogue NMN has the status of a not yet authorised novel food, so it cannot lawfully be an ingredient of a food supplement in the EU. We discuss it here solely as a compound with human data.

Why are there no doses in this guide?
Because the reagents in the catalogue are laboratory material that is not administered to humans or animals outside a study, and figures from mouse and culture work have no translation to a person. None of these compounds has gone through the procedure in which such values are established.

Are longevity compounds prohibited in sport?
MOTS-c is named in class S4.4.1, and from 2027 so is SLU-PP-332. The others, as substances without approval, fall under class S0. All are prohibited at all times.

Summary

Longevity is a field with a sound conceptual framework and a strict criterion: an intervention must change a hallmark of ageing and at the same time lengthen life or health in an organism. The compounds in the catalogue target telomeres, mitochondria, the NAD⁺ pathway and the regulation of gene expression, but their data come from rodents and cultures, often from a single centre, and there are no human studies; the exception is NMN, with trials of the NAD⁺ marker; in the EU it is not authorised as a food. The benchmark of rigour remains the 2009 rapamycin study, and the intervention with the best human data is regular exercise. None of the compounds is a medicine in the EU or the United States; in sport MOTS-c and SLU-PP-332 are named, the rest fall under class S0.

Product documentation

Reagent pages with batch documentation: Epithalon 10 mg, Epithalon 20 mg PEN, MOTS-c, MOTS-c 20 mg PEN and 5-Amino-1MQ. The pages for Cortagen and SLU-PP-332 are given in the articles on those compounds. The identity and purity of each batch are confirmed by a certificate of analysis.

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