Cartalax

Overview

Cartalax is a synthetic tripeptide — Ala-Glu-Asp (L-Alanyl-L-glutamyl-L-aspartic acid, "AED") — from Vladimir Khavinson's "short peptide bioregulator" school (St. Petersburg Institute of Bioregulation and Gerontology). It is marketed toward cartilage, musculoskeletal and connective-tissue "repair."

The honest evidence picture is thin, old, and largely Russian/preclinical. The only peer-reviewed, English-language study that could be verified as studying AED specifically is an in-vitro review/study (Linkova, Khavinson et al., Int. J. Mol. Sci., 2023) reporting gene-expression changes in cell-culture models of mesenchymal stem-cell aging and rat skin fibroblasts — not chondrocyte, animal, or human joint-disease trials. The widely-repeated claims of an "18–38% increase in cartilage area index" and "reduced p53 / increased PCNA in young and old rat chondrocytes" appear only on vendor/marketing sites; the primary source behind them could not be located or verified. There is no human clinical trial evidence, no FDA/EMA approval, and no verifiable CAS number.

Chemistry and structure

The IUPAC name for the confirmed structure is (2S)-2-[[(2S)-2-[[(2S)-2-aminopropanoyl]amino]-4-carboxybutanoyl]amino]butanedioic acid. Values above are drawn from PubChem CID 87815447, whose synonyms include "Cartalax" and "T-31 peptide." PubChem lists no CAS number; a "205640-90-0" seen on some retail sites is unverified against any primary registry and should not be treated as confirmed.

Mechanism of action

• Modulates gene expression in in-vitro MSC-aging models — reported to stimulate NFκB and IGF1 gene expression in replicative and stationary mesenchymal stem-cell (MSC) aging models and to affect TNKS2 expression in the replicative model; also studied in rat skin fibroblasts. [In vitro] (Linkova, Khavinson et al., Int J Mol Sci 2023, PMC10179481 — cell-culture models)
• Proposed "peptide bioregulator" transcriptional mechanism — the short 3-mer peptide is said to enter cells/nucleus and bind DNA/chromatin to modulate transcription of cartilage-matrix genes (e.g. type II collagen, aggrecan) and chondrocyte proliferation/apoptosis. This is the general Khavinson-school hypothesis applied to AED, not a demonstrated cartilage-specific molecular mechanism. [Hypothesis] (Khavinson-school bioregulator literature; restated on secondary/vendor pages)
• Increases chondrocyte proliferation — e.g. a claimed ~18–38% rise in "cartilage area index," increased PCNA and decreased p53 in cultures from young and old rats. [Animal] (Appears only on vendor/marketing sites; the primary Khavinson tissue-culture source could not be located — treat as unconfirmed)

Research and evidence

Human evidence. No human clinical trial evidence was located. There are no FDA/EMA-registered studies, and the only verifiable peer-reviewed data on AED is in-vitro cell-culture work (MSC-aging models, rat fibroblasts). Human efficacy and safety for cartilage/joint indications are unestablished. In short: no well-established human clinical trials. Human dosing, pharmacokinetics (including for oral capsule "bioregulator" formats), and safety profile are not established in verifiable sources.

Status and regulation

Cartalax is not FDA-approved and not an EMA-authorised medicine; no marketing authorisation was located in any Western jurisdiction. It is sold only as a research chemical / research reagent by peptide vendors, without pharmaceutical quality assurance. In Russia, short-peptide bioregulators of this school are distributed within the Cytomed / "Cytogen" product lines, but no verified regulatory-approval document for Cartalax specifically could be found. It should be treated as an unapproved investigational substance: it becomes an unauthorised medicine the moment it is intended for human use, and "no specific ban" is not affirmative permission to take it.

WADA status: no primary WADA source was located, so no class code (S0/S2) is stated here and prohibition cannot be confirmed either way. WADA sport-prohibition is a separate axis from legality.

Safety

• Human safety profile is not established in verifiable sources — no toxicology, pharmacokinetics, or adverse-event data (in any species) were found.
• The only verifiable biological data are from in-vitro cell culture, which does not establish safety in humans; the cartilage/chondrocyte animal claims are unverified.
• Material sold as a research reagent is not a quality-controlled medicine and may vary in identity, purity, and sterility — especially given the frequent structural mislabeling (tetrapeptide vs the correct tripeptide) in the market.
• No human dosing has been established; any human use is experimental and unsupervised by design.

Legal status

Cartalax's regulatory classification is a research reagent ("research use only") — it is not approved for human use in the US or EU. "No specific ban" is not affirmative permission: a compound becomes an unauthorised medicine the moment it is intended for human use, regardless of how it is labeled at point of sale. Regulatory status differs by country and can change. This is not legal advice — verify the status in your own jurisdiction. (Dated 2026-07-08.)

How it compares

• Epitalon — another Khavinson "short peptide bioregulator" (a synthetic tetrapeptide, AEDG). Its acronym is routinely confused with Cartalax in vendor marketing; the two are different molecules. They share the pattern of bold claims resting on limited, single-lineage evidence.
• Thymalin — a peptide preparation from the same St. Petersburg research school; like Cartalax it carries the pattern of older, mostly-Russian, preclinical evidence with limited independent Western replication.
• BPC-157 and TB-500 — other peptides marketed for tissue "repair." They are frequently grouped with Cartalax in recovery marketing, but each has its own separate (and also largely preclinical) evidence base — grouping does not transfer evidence between them.

Common misconceptions

• "Cartalax is a tetrapeptide (AEDL / AEDG / Ala-Glu-Asp-Lys)." The authoritative PubChem record (CID 87815447) lists the tripeptide Ala-Glu-Asp. Tetrapeptide descriptions are marketing errors; "AEDG" is actually Epitalon.
• "Cartilage area index rises 18–38% with PCNA up and p53 down." These numbers appear only on vendor/marketing sites [Animal — unverified]; the primary source could not be located and they should not be treated as established.
• "Its CAS number is 205640-90-0." PubChem lists no CAS for this compound; the retail-cited number is unverified and must not be treated as confirmed.
• "It's proven to repair cartilage." The only verifiable data is a single in-vitro gene-expression study [In vitro] on stem-cell aging models — not a chondrocyte, animal joint, or human trial. There is no well-established human evidence.
• "Not banned means legal to take." No specific ban is not affirmative permission; Cartalax is a research reagent and becomes an unauthorised medicine the moment it is intended for human use.

Russian research

Much of the evidence for cartalax (its active short peptide AED, Ala-Glu-Asp) comes from a single Russian research lineage — Khavinson's St. Petersburg Institute of Bioregulation and Gerontology and its collaborators (Linkova, Ryzhak, Polyakova, Ashapkin recur across the work). It is surfaced here for completeness and framed conservatively; the verifiable data are in-vitro cell-culture studies on aging, not in-vivo joint-disease or human trials.

• AED and chondrocyte proliferation [Animal / In vitro]. This is the primary Russian source behind the cartilage/chondrocyte claim the existing article said "could not be located." In primary chondrocyte cultures from young (3-month) and old (20-month) rats, AED at a reported minimal effective concentration of 200 ng/ml increased chondrocyte numbers roughly 1.4–1.8-fold in young-rat cultures and 1.6–2.1-fold in old-rat cultures versus control. This is cell-culture proliferation counting, not a joint-disease or in-vivo cartilage-repair experiment. Myakisheva S.N., Linkova N.S., Polyakova V.O., Ryzhak G.A. "Peptides of Cartilage Tissue: Regulation of Chondrocyte Proliferation, Geroprotection and Prospects for Use in Osteoarthrosis." Vrach, 2023;34(10):46–49 (DOI 10.29296/25877305-2023-10-08). Note: this is a short (4-page) domestic-journal report; the locatable abstract states only "chondrocyte primary culture" and does not itself specify the anatomical source (e.g. intervertebral disc) or report the PCNA-up / p53-down data — those cartilage-marker details rest on internal references, so they should be read as single-lineage, unreplicated Khavinson-school figures rather than an independently confirmed result.

• AED and skin-fibroblast aging [In vitro]. In a replicative-aging model of cultured skin fibroblasts, KE, KED, AED and AEDG all inhibited MMP-9 (which rises with fibroblast aging) and enhanced Ki-67 (proliferation) and CD98hc; AED and AEDG additionally suppressed caspase-dependent apoptosis. This is a fibroblast study, not a cartilage/chondrocyte experiment. Lin'kova N.S. et al. Bulletin of Experimental Biology and Medicine, 2016;161(1):175–178 (PMID 27259496; DOI 10.1007/s10517-016-3370-x).

• AED and mesenchymal stem-cell aging [In vitro]. In human bone-marrow mesenchymal stem cells (FetMSC line) under "passage" and "stationary" aging models, short peptides including AED modulated aging-related gene expression, with IGF1 expression rising ~3.5–5.6-fold on peptide addition. Ashapkin V. et al. Molecular Biology Reports, 2020;47(6):4323–4329 (PMID 32399807; DOI 10.1007/s11033-020-05506-3).

• Review context [In vitro]. The 2023 review already cited in the article summarizes AED's cell-culture work; on close reading its AED-specific statements point to the two studies above (fibroblast Ki-67/CD98hc and MSC-aging genes such as NFκB, IGF1, TNKS2) and do not attribute direct effects on chondrocyte/cartilage matrix genes such as SOX9, aggrecan (ACAN) or type II collagen to AED — in the review those matrix-gene effects are attributed to other peptides (e.g. SPPEPS, LPP, KLD-12), not AED. Linkova N. et al. International Journal of Molecular Sciences, 2023;24(9):8415 (PMID 37176122; PMC10179481; DOI 10.3390/ijms24098415).

Several commonly repeated claims remain unverified and are flagged rather than cited: the specific "18–38% increase in cartilage area index" figure was not found in any located primary source (the verifiable numbers are the 1.4–2.1-fold proliferation values above); the CAS number "205640-90-0" is widely used on vendor listings but is unverified against an authoritative chemical registry (PubChem CID 87815447, Alanyl-glutamyl-aspartic acid, C12H19N3O8, lists no CAS number); and vendor claims of demonstrated "clinical efficacy in osteochondrosis, osteoarthrosis, osteoporosis, and post-trauma/post-fracture recovery" in humans have no located controlled clinical-trial citation — Russian-language retail pages assert this efficacy, but no independently verifiable human-trial reference was found. Human dosing, half-life and pharmacokinetics are likewise not established in any verifiable source.

On regulatory status, two separate facts should be kept apart. In the West, cartalax is not FDA/EMA-approved and is sold only as a research reagent. In Russia, the retail "Карталакс" (Kartalaks) is part of the Cytogen short-peptide line from NPCRIZ/"Peptides" (Khavinson lineage) and is sold as a БАД — a biologically active dietary supplement subject to state registration (SGR) via Rospotrebnadzor — not as a registered medicine (лекарственный препарат); no verifiable medicines-registry authorisation or controlled clinical-trial citation was located. On quality: the evidence is small, single-group, and under-replicated — every study traces to one research school, all data are in-vitro cell or organotypic culture with no in-vivo animal joint-disease model and no human trial, and the chondrocyte study is a single small dose-response report. Being registered as a supplement in Russia is a regulatory and commercial fact, not proof that the compound works.