Cartalax, Thymalin and Peptide Bioregulators: The Research Explained

Cartalax is a synthetic tripeptide with the sequence Ala-Glu-Asp. In the peer-reviewed papers that use it, the molecule is labelled AED or by the internal code T-31; a 2020 study of human bone-marrow mesenchymal stem cells and a 2015 study of kidney tissue culture both confirm the same three-residue sequence.^[3][4]

The trade name "Cartalax" itself is almost absent from the searchable peer-reviewed record: it appears in no PubMed title or abstract we could find, which indexes the compound only as AED or T-31. The one primary source where we located the name is a table inside the developers' own 2021 systematic review, written there as "AED, Cartalax".^[1]

Every study of AED we located was carried out by, or with, the St Petersburg institute. Two papers add outside co-authors — a stem-cell laboratory in Chieti-Pescara, Italy, and a molecular-biology group at Lomonosov Moscow State University — but a St Petersburg author is still listed on both, so this is closer to an extended network than independent replication.^[5][3]

In kidney tissue cultured from young and old rats, AED (with a related peptide, EDL) raised the proliferation marker Ki-67 and lowered the pro-apoptotic marker p53, though less than the natural polypeptide complex the tripeptides were derived to resemble. A related 2014 paper from the same group reported the same pair lowering the ageing markers p16, p21 and p53 and raising SIRT-6 in renal cell culture.^[4][6]

In a 2016 study of skin fibroblasts aged in culture, AED — together with three related short peptides — suppressed the caspase-3-dependent apoptosis that increases as fibroblasts age, and increased markers linked to proliferation and cell renewal.^[7]

Not every tissue responded. In a 2011 study of aged thymus-cell culture, T-31 (AED) was tested alongside two other short peptides; the paper reported that only one of them, AB-9, produced the geroprotective pattern — more proliferation, less apoptosis — the authors were looking for.^[8]

The trade name implies a cartilage focus, and the developers' own 2021 systematic review credits "AED, Cartalax" with "regulation of cartilage and skin fibroblast functions, neuronal cell differentiation", citing six of the group's own papers for that line.^[1]

Tracing those six sources shows kidney cell culture, mesenchymal stem cell gene expression, neuronal differentiation of periodontal-ligament stem cells, and one mouse-heart microarray study of two different peptides (Vilon and Epitalon, not AED) — not a cartilage or chondrocyte experiment.^[1][4][3][5]

The same institute later published a dedicated 2023 review of the molecules known to steer stem cells into cartilage-forming chondrocytes. It names several growth-factor-derived and extracellular-matrix peptides — none of them AED or Cartalax. We found no chondrocyte-culture, joint-tissue or osteoarthritis study of AED published under either name.^[9]

Thymalin is a natural low-molecular-weight polypeptide complex, isolated from calf thymus by mild acid extraction. Vladimir Morozov and Vladimir Khavinson developed it at what is now the St Petersburg Institute of Bioregulation and Gerontology, describing it as a pharmaceutical "put into practice as immunocorrector". Two dipeptides isolated from the mixture, EW (Glu-Trp) and KE (Lys-Glu), are named as its active substances; EW was later sold separately under its own name, Thymogen.^[2][10]

The 1997 paper describing thymalin reports that it activates T-cell differentiation and changes the cytokine output (interleukin-2, interferon) of blood lymphocytes. A 2020 study of human haematopoietic stem cells found thymalin reduced two early-differentiation markers, CD44 and CD117, two- to three-fold, and raised CD28 — a mature-T-lymphocyte marker — 6.8-fold, read by the authors as thymalin pushing stem cells toward mature T cells.^[2][11]

A 2023 laboratory study exposed white blood cells from four donors to thymalin and its two active dipeptides after triggering inflammation with bacterial lipopolysaccharide. All three reduced the inflammatory cytokines IL-1β, IL-6 and TNF-α by 1.4- to 6.0-fold, which the authors propose as a mechanism for thymalin's reported anti-inflammatory effect.^[10]

In mice, a Kyiv-based group — distinct from the St Petersburg institute but part of the same Soviet-era bioregulator tradition — reported that a thymalin injection raised serum melatonin at 3 hours in adult CBA mice and lowered it by 24 hours, season-dependent and absent in old mice. A second paper from the same group found thymalin changed bone-marrow progenitor cell counts and restored a disrupted CD4+-cell rhythm in old mice.^[12][13]

The main human evidence is a cohort of 266 elderly people followed for 6–8 years, split between thymalin, epithalamin (pineal peptide), combined, and control groups. The paper reports 2.0–2.1-fold lower mortality with thymalin and fewer respiratory infections versus control; a separate group given both preparations annually for 6 years had 4.1-fold lower mortality. The abstract describes no randomisation or blinding, and the work comes from the same St Petersburg–Kyiv collaboration that developed the compounds.^[14]

More recent evidence comes from Russian hospitals treating severe COVID-19. A 2021 paper reported that adding thymalin to standard therapy sped up the fall in IL-6, C-reactive protein and D-dimer, without stating group sizes. A 2022 paper divided severe COVID-19 patients into three groups (standard therapy alone, plus tocilizumab, plus thymalin) and reported the lowest hospital mortality with thymalin. Its English and Russian abstracts give different figures for that group (20.6% and 16.2%, against 40.9% on standard therapy), and neither states group sizes or describes randomisation.^[15][16]

Multiple peer-reviewed papers describe thymalin as a pharmaceutical already "put into practice" by the late 1990s and still used inside Russian hospital treatment protocols as recently as 2022, but none of the papers we could access states a registration number, an issuing authority or an approval date. We could not verify thymalin's formal registration status from a primary source.^[2][16]

For cartalax (AED) we found no hospital or clinical use reported anywhere in the literature, only the cell-culture experiments described above, which gives even less basis to assess a registration status. We likewise could not verify any registration record for cartalax from a primary source.^[4][3]

Neither compound has an entry in the EMA's medicines database or in Drugs@FDA (both checked September 2026), and neither appears on the FDA's list of bulk substances nominated for compounding-risk review. A ClinicalTrials.gov search for thymalin returned no studies; the one hit for "cartalax" was an unrelated nutrition study, not a trial of the peptide.^{[17][18][19][20][21]}

Claims that cartalax repairs or protects cartilage rest on the product's name, not on a chondrocyte or joint study: the evidence under either name, AED or Cartalax, is limited to kidney, skin, stem-cell and thymus cell cultures. Claims that either compound is a registered medicine anywhere should be treated as unverified until a primary regulatory source is produced.^[4][9]

Peptyds does not sell cartalax or thymalin. The one compound from this same research program that Peptyds does sell is epitalon (Ala-Glu-Asp-Gly), covered in full in its own complete guide with the same evidence-first treatment: cell and animal data, thin human evidence, and no EU or US authorisation.

A third short peptide from the same cluster, pinealon (Glu-Asp-Arg), targets brain tissue and has its own Peptyds research guide; its evidence is mostly cell and animal work from the same research network, plus two small uncontrolled human reports, and Peptyds does not sell it either.