Cartalax peptide: the cartilage bioregulator, what the cell studies show and what is missing

Cartalax is a three-amino-acid synthetic peptide, Ala-Glu-Asp, from the family of peptide bioregulators developed by Vladimir Khavinson and colleagues at the St Petersburg Institute of Bioregulation and Gerontology. The group’s method was to extract peptides from an animal tissue, analyse the amino-acid composition and synthesise a short peptide meant to act on that tissue. For cartilage the extract is a cartilage polypeptide complex, sold in Russia under the name Sigumir, and the derived tripeptide is the cartalax bioregulator, spelled Kartalax in some translations and coded T-31 in the group’s early cell-culture papers ^{[1] [5] [11]}.

The sequence Ala-Glu-Asp is the shared core of several peptides in the series: epitalon is Ala-Glu-Asp-Gly, cortagen is Ala-Glu-Asp-Pro, bronchogen is Ala-Glu-Asp-Leu and cardiogen is Ala-Glu-Asp-Arg. Cartalax is that core without a fourth residue. It is often studied alongside the tripeptides KED (vesugen) and EDR (pinealon) and the dipeptide KE (vilon), and several of the papers below test all of them together.

The usual caveats for the Khavinson peptides apply with full force. Nearly all of the research comes from the developers and their collaborators, much of it in the Russian-language journal Advances in Gerontology and in the Bulletin of Experimental Biology and Medicine, with a few open-access papers written with Italian co-authors. No independent group has replicated the cartilage findings, and there is no controlled human trial. The evidence for cartalax is better described as a series of cell-culture observations than as evidence of a treatment for joints.

The group’s hypothesis is that short peptides enter cells and the nucleus and change gene expression by binding DNA or histones. For AED, a 2014 Russian-language paper modelled the peptide docking into the minor groove of DNA, finding the most favourable complexes with alternating AT sequences, and linked this to changes in the expression of ageing markers in kidney cells ^[10]. A 2020 review by the group lists AED among the peptides that activate neural differentiation of stem cells ^[12], and a 2023 review sets out the chondrogenic pathways, including WNT, ERK-p38 and Smad 1/5/8 signalling and the genes SOX9, COL2 and ACAN, that peptides are proposed to act on ^[4].

The most specific mechanistic claim is about the senescence-associated secretory phenotype of chondrocytes. In a 2023 study, ageing chondrocyte cultures showed higher synthesis of the pro-apoptotic proteins p16, p21 and p53 and the pro-inflammatory cytokines TNF-α and IL-1α, and lower Sirt1; the AED peptide and the cartilage polypeptide complex both normalised these molecules, which the authors offered as an explanation for their reported effects in musculoskeletal disease ^[2]. Whether a dose of cartalax taken by mouth reaches joint cartilage, which has no blood supply of its own, has not been measured in any species.

Claims about cartalax benefits centre on cartilage repair, osteoarthritis, bone density and, more recently, skin. The evidence is from cells and rats.

Cartilage and the cartalax osteoarthritis claim: in human mesenchymal stem cells undergoing replicative ageing, AED at 200 ng/mL activated the expression and synthesis of the chondrogenic markers SOX9, aggrecan, type II collagen and COMP, an effect the cartilage polypeptide complex matched at ten times the concentration ^[3]. In ageing chondrocyte cultures, AED normalised the senescence-associated markers described above ^[2]. A 2023 review from the group, which describes both AED (as Kartalax) and Sigumir as having shown high efficacy in animal models of osteoarthritis and in oral administration to older patients with osteoarthritis, summarises this cartilage work ^[1]; the animal and patient studies it refers to are not accessible in English.

Bone: in a 2007 study, ovariectomised rats, a standard model of post-menopausal osteoporosis, were given either the cartilage extract or T-31. Both had an osteoprotective effect, preventing the fall in bone mineral density after ovariectomy and raising density that had already fallen, with the extract significantly more effective than the tripeptide ^[5]. This is the only whole-animal cartalax study we found, and it is in Russian.

Skin: in ageing cultures of skin fibroblasts, KE, KED, AED and AEDG all reduced synthesis of the matrix-degrading enzyme MMP-9, which rises with age, and raised the proliferation marker Ki-67 and the regeneration marker CD98hc; AED and AEDG also suppressed caspase-dependent apoptosis ^[6]. This is the basis for cartalax appearing in some skin-ageing product claims; it is a fibroblast culture result, not a study of skin.

Other tissues: in kidney explant cultures from young and old rats, AED and EDL stimulated proliferation and reduced apoptosis, though less than the kidney polypeptide extract ^[9], and in ageing kidney cell cultures they reduced the senescence markers p16, p21 and p53 and increased SIRT6 ^[10]. In human bone-marrow mesenchymal stem cells aged in culture, AED, KED and KE raised IGF1 expression 3.5 to 5.6-fold and stimulated NF-κB expression at nanomolar concentrations ^[7]. In human periodontal ligament stem cells, a combination of AEDG, KE, AED and KED promoted neuronal differentiation markers, though KED alone had the clearest effect and AED alone was not singled out ^[8]. By contrast, in old thymocyte cultures T-31 had no geroprotective effect, while a different peptide did ^[11]. As with cardiogen, the tissue specificity is relative: the cartilage peptide acted on kidney, skin and marrow cells too.

We found no randomised controlled trial of cartalax in PubMed and no entry on ClinicalTrials.gov. The 2023 review states that AED, as Kartalax, has been given by mouth to older patients with osteoarthritis with high efficacy ^[1], but it does not describe the study, and we could not find a primary report in any language in PubMed. That leaves the claim at the level of an assertion by the developers.

The human material that exists in English is laboratory work on human cells: chondrocytes, mesenchymal stem cells, skin fibroblasts and periodontal ligament stem cells ^{[2] [3] [6] [7] [8]}. These experiments show that AED changes gene expression and protein synthesis in a dish at nanogram-per-millilitre concentrations. They cannot show that a capsule or injection improves joint pain, function or cartilage thickness in a person, and no study has tried to show that under controlled conditions.

There is no human timescale, because there is no controlled human study. In the cell studies, effects were measured over days to weeks of culture ^{[2] [3]}, and in the ovariectomised rats bone density was measured after a course of treatment whose length the abstract does not give ^[5]. Sellers in Russia market Khavinson-series peptides as courses of 10 to 30 days, often repeated, which is a marketing convention rather than a finding. Cartilage turns over slowly, so even an effective treatment would take months to change a joint measurably.

These are laboratory figures, and none is a recommendation. AED was used at 200 ng/mL in mesenchymal stem cell cultures ^[3] and at nanomolar concentrations in bone-marrow stem cell cultures ^[7]. The ovariectomised-rat study does not state the T-31 dose in its English abstract ^[5], and the oral dose referred to for patients with osteoarthritis is not published ^[1]. No dose has been established in a controlled human study, and there is no pharmacokinetic study for any route.

Research suppliers sell cartalax as a freeze-dried powder, most often in 10 mg or 20 mg vials, and, more than for most of the series, as capsules, reflecting the oral use claimed in Russia. The peptide calculator and its cartalax page convert vial contents to a concentration for laboratory use. The research gives no basis for choosing any quantity for a person.

The developers refer to oral administration of cartalax in patients ^[1], and in Russia the Khavinson short peptides are sold as oral capsules marketed as food supplements. A tripeptide is small enough that some intestinal absorption is plausible, and the group has argued from computer models that short peptides can use intestinal peptide transporters, but no study has measured how much AED is absorbed intact or whether it reaches cartilage. Research suppliers outside Russia sell mainly lyophilised powder for injection, a route with no published cartalax research at all; the cell studies added the peptide to culture medium ^{[2] [3] [6] [7]}.

No cartalax side effects have been recorded, because there are no controlled human studies and the Russian clinical use is not reported in accessible detail. The cell and animal papers do not report toxicity, and a tripeptide of three common amino acids is unlikely to be acutely toxic. The safety questions are the ones the research raises and leaves open. AED reduced p53, p21 and p16 and suppressed apoptosis in several cell types ^{[2] [6] [10]} and stimulated NF-κB and IGF1 expression in stem cells ^[7]; these are pathways involved in cancer as well as in ageing, and no long-term study has looked at cartalax and tumour incidence in animals, unlike the studies that exist for epitalon and thymogen.

There are no data on use in pregnancy, in children, in people with inflammatory arthritis or alongside medicines such as anti-inflammatories, steroids or methotrexate. None of this shows that cartalax is harmful; it shows that it has not been studied. Anyone with joint symptoms should note that there is no evidence that cartalax substitutes for treatments with trial evidence.

For products bought from research suppliers, the practical risks are identity, purity and sterility. Our guides to third-party testing and how to read a certificate of analysis explain what a test report should show.

Cartalax is not an approved medicine in the UK, US, EU, Canada or Australia, nor is it a registered medicine in Russia, where it is sold as a supplement; the related cartilage extract Sigumir is likewise a supplement rather than a medicine. Products sold as cartalax elsewhere are research chemicals whose sale for human use is not lawful. It is not named on the WADA Prohibited List. See our legal status overview and the pages for the UK, the US and Europe.

Cartalax is supplied as a freeze-dried powder to be kept cold, dry and away from light; short peptides are relatively stable in this form. Reconstituted solutions are refrigerated and used within a limited period. See how to store peptides and our guide to bacteriostatic water.

A tripeptide is among the cheapest peptides to synthesise, so cartalax should be one of the lowest-priced listings on a supplier’s site, and a high price is a warning sign rather than a mark of quality; see peptide prices explained. Compare cartalax prices, including listings in the UK and the US. A certificate of analysis should show a measured mass close to 333.3 g/mol and an HPLC purity figure; a mass near 390 g/mol would indicate epitalon rather than cartalax. Our lists of third-party tested suppliers and suppliers that publish COAs, and our guide to spotting a fake supplier, cover what to check.