Peptides for Anti-Aging & Longevity

Fourteen compounds appear in this ranking, and the distance between the top and bottom of the list is unusually large.

HGH 191AA (recombinant somatropin) stands alone at the top because it carries FDA approval for defined indications — growth hormone deficiency in children and adults, Turner syndrome, chronic renal insufficiency, Prader-Willi syndrome and HIV-associated wasting — supported by decades of controlled trials. Glutathione occupies the next tier: it has genuine human clinical research across several conditions, though many of those trials are small and rely on oxidative-stress biomarkers rather than hard clinical endpoints. NAD+ and thymalin sit below it as early or mixed human evidence — one widely used but under-tested in large trials, the other supported mainly by a single research group's long-term cohorts. The remaining eight entries — Vilon, Livagen, Bronchogen, Cardiogen, Pancragen, Vesilute, Testagen and Prostamax — are short synthetic peptides with animal or tissue-culture data only. Several share a common origin in Khavinson's St Petersburg bioregulation program and a common limitation: little or no independent replication outside that literature.

Rank here reflects the quality of the evidence behind each compound, not its popularity or its proposed potency.

Evidence Rating: A

Category: Growth Hormone

HGH 191AA is recombinant human growth hormone (somatropin): a single-chain, 191-amino-acid polypeptide of roughly 22,124 g/mol whose sequence is identical to growth hormone produced by the human pituitary. The "191AA" label distinguishes it from somatrem, the older 192-amino-acid variant that carried an extra N-terminal methionine and provoked greater immunogenicity.

Regulatory status is the clearest of any compound on this page. Somatropin is FDA-approved for growth hormone deficiency in children and adults, Turner syndrome, chronic renal insufficiency, Prader-Willi syndrome and HIV-associated wasting. That approval attaches to the pharmaceutical product; research-grade material sold for laboratory use falls outside it.

Studies indicate that replacement in GH-deficient adults improves body composition, increasing lean mass and reducing fat mass. Extending the same reasoning to healthy older adults is where the evidence thins. Rudman and colleagues reported gains in lean mass and losses in fat mass in men over 60 (NEJM, 1990), but later reviews found the effects modest and accompanied by a meaningful rate of adverse events — arthralgia, edema, carpal tunnel symptoms and impaired glucose tolerance. The compound's place at the top of this ranking therefore comes with a caveat: a deficiency-treatment evidence base does not automatically generalise to normal aging.

Evidence Rating: B

Category: Antioxidant / Detoxification

Glutathione (Glu-Cys-Gly, MW ~307.3 g/mol) is a tripeptide and the most abundant intracellular antioxidant in mammalian cells, central to Phase II detoxification, free-radical scavenging, immune function and cellular redox homeostasis. Its clinical usefulness is constrained by pharmacokinetics: oral bioavailability is poor, on the order of 3%, which is why human studies have generally used subcutaneous or intravenous routes in order to reach measurable plasma levels.

The list of conditions studied is broad — non-alcoholic fatty liver disease and Parkinson disease among them — and that breadth is both the compound's strength and its weakness. Human data exist, which separates glutathione from most entries on this page, but many trials are small, short in duration, and report changes in oxidative-stress markers rather than clinical outcomes. Reduced oxidative stress and support for hepatic detoxification pathways are the claims most consistently supported; whether normalising a biomarker translates into a disease-modifying or longevity effect has not been established by large randomised trials.

Safety in the reported studies has generally been favourable by injection. The principal gap in this evidence tier is replication across larger, more diverse populations.

Evidence Rating: C

Category: Anti-Aging / Telomere

NAD+ is a coenzyme present in all living cells, serving as an electron carrier in metabolic reactions and as a substrate for enzymes including sirtuins, PARPs and CD38 — proteins involved in DNA repair, cellular stress responses and energy metabolism. Tissue levels decline with age, by roughly 50% between ages 40 and 60 in the studies that have measured them, and that observation drives much of the interest.

Two points of accuracy matter here. First, NAD+ is not a peptide; it and its precursors NMN and NR appear in this ranking because they circulate in the same research and clinic discussion. Second, the causal chain running from declining NAD+ to aging phenotypes is not established in humans.

IV NAD+ infusion is widely offered at anti-aging clinics, yet large-scale human efficacy trials are limited, and infusion studies have focused largely on tolerability and on temporary rises in circulating NAD+. Trials of precursors such as NR have generally shown increased blood NAD+ levels alongside inconsistent functional or clinical benefits. Regulatory status also differs by compound: NAD+ infusion is not FDA-approved for any anti-aging indication, and FDA has stated that NMN is not lawful as a dietary supplement ingredient. The category's central claims remain hypotheses supported mainly by animal models.

Evidence Rating: C

Category: Immune / Anti-Aging

Thymalin is a polypeptide complex extracted from calf thymus glands, developed by Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology. It has been used clinically in Russia since the 1980s for immunodeficiency states and as an anti-aging intervention — a history that predates and outpaces its formal clinical trial record.

The most cited evidence is a six-year study by Khavinson et al. (2003) in which elderly patients receiving thymalin plus epithalamin showed a mortality rate roughly 4.1 times lower than controls. That is a striking effect size, and it deserves to be read alongside the study's design: long follow-up in an elderly cohort, conducted by the peptide's own developers, published outside the mainstream Western literature, and without the large-scale independent replication that would ordinarily accompany a claim of this magnitude.

The proposed mechanism is biologically plausible — age-related thymic involution reduces T-cell output, and thymic peptides are hypothesised to restore some of that capacity — but mechanistic plausibility does not confirm the mortality finding. Thymalin holds no FDA or EMA approval for any indication, which is why it belongs in the early human / mixed evidence tier rather than beside glutathione.

Evidence Rating: D

Category: Immune / Anti-Aging

Vilon (Lys-Glu, KE) is a synthetic dipeptide of about 275.3 g/mol, developed by Khavinson as a simplified synthetic stand-in for the active component of thymalin. At two amino acids, it is among the shortest bioregulatory peptides proposed to have immunomodulatory activity, and that is a large part of its research interest: if a dipeptide can influence gene expression, the proposed signalling mechanism would be unusually direct.

Under Khavinson's bioregulation theory, short peptides interact with specific DNA sequences and thereby modulate transcription — in this case of genes tied to immune function and thymopoiesis. The claims attributed to Vilon follow from that framework: restoration of immune function in aging animals and sequence-specific gene modulation. The evidence base, however, is essentially animal and cell-culture work published predominantly in Russian-language journals, with limited Western validation and no controlled human outcome trials identified.

The mechanism also raises unresolved questions, among them how a dipeptide achieves sequence-specific nuclear effects given its short half-life and limited cellular uptake. Vilon therefore sits in the animal/preclinical tier: mechanistically interesting, biologically speculative, and unproven in humans.

Livagen (Lys-Glu-Asp-Ala, KEDA) belongs to the family of short synthetic bioregulatory peptides developed by Khavinson, and like its relatives it is built around a proposed nuclear mechanism rather than a receptor-mediated one. At roughly 432.5 g/mol, KEDA is small enough that direct interaction with DNA or chromatin-associated proteins is mechanistically conceivable; the working hypothesis holds that it decondenses heterochromatin in hepatocytes, re-exposing gene regions that fall transcriptionally silent during aging and thereby restoring hepatic function. Published studies report effects on chromatin structure and gene expression in aged liver tissue, and these observations form the primary basis for the hepatic-restoration claim.

The limitations are substantial. Supporting evidence rests largely on Russian publications with limited independent replication, and the page classifies Livagen as animal/preclinical only (grade D). No controlled human data appear to connect chromatin changes in aged hepatocytes to measurable liver outcomes, and the causal chain from peptide uptake to gene reactivation to organ-level benefit remains unverified in the Western literature. Livagen is best understood as a hypothesis-generating probe for chromatin-directed geroprotection rather than a compound with established anti-aging activity.

Bronchogen is the tripeptide Ala-Glu-Asp (AED), approximately 333.3 g/mol, and the shortest sequence among the lung-directed Khavinson bioregulators. Three residues leave little structural surface for highly specific target engagement, which makes the reported tissue selectivity for bronchial epithelium both a point of mechanistic interest and a reasonable source of skepticism.

The compound is proposed to regenerate bronchial epithelium and improve respiratory parameters in aging or chronically diseased lung tissue. Claims in the literature include improved respiratory function in elderly subjects and epithelial regeneration, but the primary sources are Russian biogerontology publications, and the evidence grade assigned here is D. Independent Western validation is scarce, and much of the work predates current standards for respiratory endpoint reporting, blinding, and controls. The central research question — whether a three-residue peptide can shift epithelial repair programs in aged lung tissue — has not been examined with modern transcriptomic or imaging methods, so the regeneration claims remain tentative rather than established.

Among the cardiac-directed entries on this page, Cardiogen is defined by the sequence AEDR — Ala-Glu-Asp-Arg, approximately 489.5 g/mol. It differs from Bronchogen (AED) by a single C-terminal arginine, a change that adds a positively charged residue and, within the Khavinson framework, is said to redirect gene-regulatory activity toward cardiomyocytes rather than bronchial epithelium. The proposed mechanism involves modulation of gene expression in cardiac muscle cells, with downstream effects reported on contractile function and age-related cardiac fibrosis.

Published claims include improved cardiac function in elderly subjects and reduced fibrotic change. These originate predominantly in Russian biogerontology literature, and the evidence grade is D, corresponding to animal and preclinical work. The sequence-sensitivity argument is notable but difficult to evaluate without replication: the same core motif is reported to target lung tissue when unmodified, and the structural basis for that apparent tissue switch has not been characterized through binding assays or transcriptomic profiling in independent laboratories. Cardiogen holds no regulatory approval for any indication.

Pancragen (Lys-Glu-Asp-Trp, KEDW) is a pancreatic bioregulator of approximately 562.6 g/mol — the heaviest of the Khavinson tetrapeptides profiled here, a consequence of its C-terminal tryptophan. The rationale is tissue-specific gene regulation in the endocrine pancreas, with restoration of beta-cell function, improved insulin secretion, and normalized glucose metabolism in aging or metabolically compromised models proposed as downstream effects.

Two features shape how the evidence should be read. First, the claims are unusually testable: glucose handling and beta-cell output are measurable with standard assays, which makes the thinness of independent replication more conspicuous than it would be for a purely structural hypothesis. Second, the published record is concentrated in Russian biogerontology literature. Pancragen carries grade D — animal and preclinical only — and no regulatory approval for any indication. Its metabolic endpoints have not been reported in the Western clinical literature at a scale that would support the proposed effects, and the mechanism by which a four-residue peptide would influence insulin secretion remains speculative.

Vesilute is the tripeptide Lys-Glu-Asp (KED), roughly 390.4 g/mol, positioned within the Khavinson framework as a vascular-specific bioregulator. Its sequence is notable for a second reason: KED appears as the N-terminal motif in several longer peptides discussed elsewhere on this page, including Livagen (KEDA), Pancragen (KEDW), and Testagen (KEDG). Whether the tripeptide acts as the shared active core of those compounds or as an independent vascular signal has not been resolved.

Reported activity centres on endothelial function, atherosclerotic change, and vascular elasticity in aging models. The claims — improved vascular function in aging and reduced endothelial dysfunction — derive mainly from Russian-language sources, and the evidence grade is D, animal and preclinical only. No regulatory approval exists for Vesilute in any jurisdiction, and no controlled human trial data appear to establish effects on vascular endpoints. Its relevance to longevity research therefore remains at the level of mechanism generation rather than demonstrated vascular benefit.

Testagen (Lys-Glu-Asp-Gly, KEDG) is a tetrapeptide of approximately 447.4 g/mol, proposed as a testicular-specific bioregulator within the Khavinson family. Its stated mechanism is restoration of Leydig cell function with a consequent rise in testosterone production during aging, and improved spermatogenesis is reported as an additional claim in the same body of work.

Endocrine endpoints of this kind are among the most straightforward to measure in vivo, which makes the current evidence base — grade D, animal and preclinical only — a meaningful limitation rather than a technical one. Sources are again concentrated in Russian biogerontology publications, and the compound holds no regulatory approval for any indication in any jurisdiction. Independent groups have not reported controlled studies replicating the testosterone or spermatogenesis findings, and the pathway linking a four-residue peptide to steroidogenic gene expression in Leydig cells remains a proposal rather than a characterized mechanism. Age-related declines in testosterone also have multiple contributing causes that a single peptide target would not address, which complicates interpretation of any single-mechanism claim.

Prostamax, abbreviated KEDP, is a synthetic tetrapeptide with the sequence Lys-Glu-Asp-Pro and a molecular weight of roughly 487.5 g/mol. It belongs to the Khavinson family of short bioregulatory peptides and is positioned as a prostate-directed agent: the proposed rationale is that such peptides interact sequence-specifically with chromatin and modulate transcription in target tissue, in this case restoring prostate tissue homeostasis during aging. The two claims repeated most often in source material are reduced benign prostatic hyperplasia (BPH) symptoms and normalised prostate function in older men.

Its D rating reflects the evidence base rather than the plausibility of that rationale. Reports appear primarily in Russian urology and gerontology journals, generally as small animal experiments or uncontrolled clinical observations, with limited randomisation, blinding or replication by independent groups and comparatively little presence in English-language or indexed registries. That combination makes reported effect sizes difficult to interpret and leaves questions about dose-response, durability and tissue specificity unresolved. Prostamax holds no FDA or EMA approval for BPH or any other indication, and no approved BPH therapy is pharmacologically equivalent to it. As with other peptides in the preclinical tier, characterisation and purity data for research-grade material originate with the supplier rather than from regulatory review.