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Signalling peptide

Cartalax

Also known as Ala-Glu-Asp

A short peptide from the Khavinson bioregulator tradition, associated with cartilage and connective tissue.

InsufficientHealthy Aging
Human studies
0
Trials tracked
0
Preclinical
1
Safety signals
2
Last reviewed
27 Sept 2026
Reviewed by
Not yet reviewed

Part of a genuine, decades-long Russian research programme in short peptide bioregulators, associated with the St Petersburg Institute of Bioregulation and Gerontology. The grade reflects one specific gap and not the tradition's origin: we could locate no substantive independent replication outside the originating group. A body of work that has not been tested by people with no stake in the outcome is hard to weigh however large it is, and that would be equally true of a Western programme. We found no human study of the synthetic Ala-Glu-Asp tripeptide in PubMed, Europe PMC or ClinicalTrials.gov. The nearest human-facing items all fall short. The originating group's 2023 Russian-language review asserts efficacy with oral administration in older patients with osteoarthritis, but its abstract gives no data and cites no trial (PMID 37782637). The group's 2023 review in the International Journal of Molecular Sciences states that a polypeptide complex isolated from animal cartilage tissue, which it says contains AED among its short peptides, is currently in the second phase of clinical trials in Russia. It gives no results, and that complex is an extract, not the tripeptide (PMID 37176122). A temporomandibular-joint report tested Sigumir (PMID 22708467), which the group describes as a polypeptide complex of cartilage and bone tissues of young animals (PMID 37782637). None of these is evidence for Cartalax. Every located experiment that administered AED is in cell culture or rodents, and all of it comes from the St Petersburg Institute of Bioregulation and Gerontology or collaborators co-authoring with Khavinson, Linkova or Ryzhak. We found no independent replication.

This dossier has not been reviewed yet. Our editorial board is not appointed. Every page is supposed to carry a named scientific and medical reviewer with declared conflicts, and until that is true this page has had no expert check — treat it accordingly. We would rather say so than print a name-shaped placeholder where a person should be.
Cartalax is not an approved medicine for human use in the jurisdictions listed below. This page summarises research. It is not a recommendation, and it contains no dosing or administration guidance. If you are considering anything described here, discuss it with a qualified clinician.
On this page

What it is

A 3-amino-acid peptide (Ala-Glu-Asp) from the Khavinson short peptide series, in which each sequence is proposed to act on a specific tissue — here cartilage and connective. Epitalon is the best-known member of the same family.

How it is proposed to work

The programme's central hypothesis is that very short peptides can enter cells, reach the nucleus and interact with DNA in a sequence-specific way, modulating gene expression in the tissue each peptide is matched to. This is a strong and specific claim. It is also testable, and independent testing is what the literature most lacks.

Approved medical uses

None. Cartalax has no approved human medical indication in the jurisdictions we track. Any use is outside an approved label.

Human research

Each entry states what the study found and, separately, what it cannot show.

No adequate published human research. This absence is the reason for the evidence grade above — it is not a gap we can fill with animal data.

Preclinical research

Animal and laboratory work. Useful for generating hypotheses; it cannot establish that something works in people.

  • In vitro2023

    Chondrogenic markers in replicatively aged human stem cells exposed to the AED tripeptide: cell culture from the originating group

    Finding. A cell-culture study in human mesenchymal stem cells undergoing replicative aging. It studied the AED peptide and a cartilage polypeptide complex (CPC). The outcomes were gene expression and protein synthesis of four chondrogenic-differentiation markers: SOX9, aggrecan, type II collagen and COMP. The authors report that AED "activates gene expression and protein synthesis during aging of MSCs" and that CPC "has the same effect". They conclude that the data indicate "the stimulating effect of studied peptides on regulation of chondrogenesis", and they say effectiveness in osteoarthritis models still needs to be investigated. The abstract gives no effect sizes, no replicate numbers and no statistics.

    Limitation. The work comes from the originating St Petersburg group. All five authors (Myakisheva, Linkova, Diatlova, Polyakova, Ryzhak) list the Saint-Petersburg Institute of Bioregulation and Gerontology, and some also list the St Petersburg Research Institute of Phthisiopulmonology and Belgorod State National Research University. We found no independent replication, which is the central reason for the grade. This is a cell-culture experiment and says nothing about cartilage, joints or outcomes in a living person. The second agent studied, CPC, is not the AED tripeptide: the same group's 2023 review describes it as a polypeptide complex isolated from animal cartilage tissue that contains AED among its short peptides (PMID 37176122). Only the AED results bear on Cartalax. The abstract does not itself say the AED used was synthesised; treating the AED arm as the Cartalax tripeptide is our inference from the group's other publications. The abstract reports the direction of effect without magnitudes, control details, replicate counts or p-values. The article is in Russian, and we read only the English and Russian abstracts, not the full text. The authors describe testing in osteoarthritis models as a prospect still to come.

Potential safety concerns

  • CautionInsufficient

    No systematic human safety dataset we could inspect. Very short peptides are often assumed benign on the basis of size alone, which is an assumption rather than a finding.

  • CautionInsufficient

    If the nuclear gene-expression mechanism is real, its long-term consequences would need study. If it is not real, the compound does nothing. Both possibilities argue for evidence before use, and neither has been resolved.

Known interactions and contraindication considerations

  • Uncharacterised in accessible literature.

This list is not exhaustive and is not a substitute for a clinician reviewing your full medication history.

Regulatory status

Status is shown per jurisdiction and is accurate only as of the date stated. Where a compound is approved, the approval is bound to a specific formulation, manufacturer and indication — shown in the detail column.

Russian Federation
Ministry of Health / Roszdravnadzor
Listed
as of 11 Aug 2026

Marketed in Russia, generally in a supplement or parapharmaceutical category rather than as a registered medicine. Certificate details in circulation could not be verified: the same number appears against different products on the manufacturer's own materials, and they follow a format from a registration regime since superseded.

United States
FDA
Unapproved / investigational
as of 11 Aug 2026

No marketing authorisation. The FDA has not evaluated this compound — that is an absence of any opinion, not a negative finding.

European Union
EMA
Unapproved / investigational
as of 11 Aug 2026

No marketing authorisation.

India
CDSCO
Unapproved / investigational
as of 11 Aug 2026

Not approved for human use. A first-time synthetically manufactured peptide falls under the new-drug pathway.

How it is being used

What the grey community actually runs, the reasoning they give, and our read on whether it follows from known biology. This is observation, not evidence, and not a recommendation.

No community use documented for this compound yet. Absence here means our editorial team has not reviewed and verified a pattern — not that none exists.

Active clinical trials

No registered trials currently tracked for Cartalax.

Search all tracked trials

What remains unknown

The questions that would change our assessment if they were answered.

  • Can any of the central findings be replicated by a group with no connection to the originating institute?
  • Does a peptide this short reach the nucleus intact in a human?
  • Is tissue specificity demonstrated, or inferred from the tissue each peptide was derived from?

References

  1. 1.Myakisheva SN, Linkova NS, Diatlova AS, Polyakova VO, Ryzhak GA. [The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging]. Adv Gerontol. 2023;36(3):383-390.PMID 37782646

Editorial change history

When we change a grade or a regulatory note, we log it here rather than editing quietly.

  • Dossier created. All registration certificate numbers and all trial figures excluded as unverifiable. Graded on absence of independent replication, not on country of origin.

  • Corrected the sequence from Ala-Glu-Asp-Gly to Ala-Glu-Asp. The old sequence belongs to Epitalon and came in through the shared Khavinson generator. The originating group's own publications name Cartalax as the AED tripeptide (PMIDs 37782637, 37176122), so whatItIs now describes a 3-amino-acid peptide, and the aliases are Ala-Glu-Asp and AED. Removed the generic human placeholder (cartalax-h1) and its placeholder reference. We found no human study that gave the AED tripeptide itself, so humanResearch is now empty. The human-facing reports we did find concern tissue extracts: a cartilage polypeptide complex described as in phase II trials, with no results reported, and Sigumir. Added one in-vitro study from the originating group (PMID 37782646) on chondrogenic markers in aged human mesenchymal stem cells. The grade stays "insufficient" because we still found no independent replication.

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