Cartalax is the name used for the synthetic tripeptide Ala-Glu-Asp (AED), coded T-31 in parts of the research literature. It belongs to the Khavinson bioregulator family and is associated with cartilage and bone.

Is there human research on Cartalax?

The only human data we found come from a knee osteoarthritis observation of 29 people described in a 2007 Russian patent filed by the developers. It has not been published as a peer-reviewed trial, so it cannot be weighed as clinical evidence.

Has Cartalax been studied in cartilage cells?

Yes, but only recently and only in vitro. Two 2023 Russian language papers report that AED increased markers of cartilage formation in human mesenchymal stem cells and normalised ageing-related markers in chondrocytes. Most of its other published work involves kidney cells, skin fibroblasts and stem cell lines.

Has anyone outside the Khavinson group replicated the findings?

Not that we could find. Some studies involved collaborators in Moscow or Ukraine and appeared in English language journals, but Khavinson or his St Petersburg colleagues are co-authors throughout.

Cartalax (AED): The Cartilage Bioregulator and What the Research Shows

Quick Answer

Cartalax is the synthetic tripeptide Ala-Glu-Asp (AED), developed by Vladimir Khavinson's group and associated with cartilage and bone. Its published record is wider than most bioregulators but almost entirely preclinical and spread across tissues: kidney, skin and stem cell cultures, two recent cartilage cell studies and a rat bone model. The only human data are a small osteoarthritis observation in the developers' patent. Nearly all of the work comes from one research network, and much of it is in Russian.

Cartalax is presented as the cartilage peptide of the bioregulator family. It has more published studies than most of its relatives, which makes it a useful test case: the volume of papers is real, but most of them are not about cartilage.

What Cartalax is

Cartalax is the tripeptide H-Ala-Glu-Asp-OH, abbreviated AED, with the formula C12H19N3O8 and a molecular weight of about 333.3. Papers from the group often call it T-31, and PubMed's indexing vocabulary lists Cartalax, Ala-Glu-Asp and T-31 peptide as synonyms. The group's 2021 systematic review lists AED under the name Cartalax (Khavinson et al., 2021).

The cartilage association has two sources. A 2007 Russian patent from the developers describes AED as a peptide that normalises metabolism in bone and cartilage tissue. The group also reports that AED is one of the short peptides in a polypeptide complex extracted from animal cartilage, which it has developed as a separate product (Linkova et al., 2023).

The proposed mechanism

As with the rest of the class, the hypothesis is that AED enters cells and nuclei and influences gene expression through interactions with DNA and histones. Docking models place AED on a specific four-base DNA sequence (Khavinson et al., 2016) and suggest it could use amino acid and peptide transporters to enter cells (Khavinson et al., 2023). These are computer predictions. The experimental support is gene expression data: in a human embryonic bone marrow stem cell line aged in culture, the three peptides tested, including AED, raised IGF1 expression 3.5 to 5.6 fold and increased NF-κB expression (Ashapkin et al., 2020). Whether changes like these matter in cartilage tissue has not been tested.

What the studies show

Cartilage and bone

Stem cells and cartilage markers: in human mesenchymal stem cells undergoing replicative ageing, AED increased gene expression and protein synthesis of the cartilage-forming markers SOX9, aggrecan, type II collagen and COMP (Myakisheva et al., 2023a).
Ageing chondrocytes: in chondrocytes with an ageing-associated secretory profile, AED normalised levels of p16, p21, p53, TNF-α, IL-1α and SIRT1 (Myakisheva et al., 2023b).
Cartilage explants: the patent reports increased growth of rat femoral cartilage explants in culture.
Bone density: in ovariectomised rats, a model of bone loss after oestrogen withdrawal, AED (as T-31) and a cartilage extract both limited the fall in bone mineral density, with the extract the more effective (Povorozniuk et al., 2007).

The three journal papers are short Russian language reports, and the cell studies measured marker expression rather than tissue structure or function.

Other tissues

Most published AED work concerns other cells. In ageing skin fibroblast cultures it reduced the matrix-degrading enzyme MMP-9, raised proliferation markers and suppressed caspase-dependent apoptosis (Lin'kova et al., 2016), and in human skin fibroblasts it increased SIRT1, SIRT6 and type I collagen (Fridman et al., 2020). In rat kidney tissue cultures it increased proliferation and reduced apoptosis, though less than a kidney extract did (Chalisova et al., 2015), and in rats with cisplatin-induced kidney injury it reduced urinary protein loss (Zamorskii et al., 2015). Not every result was positive: in ageing thymus cell cultures, T-31 did not show the combined effects seen with another test peptide (Lin'kova et al., 2011).

Human data

The only human data we found come from the 2007 patent: 29 people aged 52 to 72 with knee osteoarthritis, described as randomly divided into a peptide group and a control group of 12, with less pain and better joint mobility reported in the peptide group. It was not published as a peer-reviewed trial, we found no registration on ClinicalTrials.gov, and the patent does not describe blinding. A 2023 Russian language review by the group states that AED has been effective in animal osteoarthritis models and in older patients (Myakisheva et al., 2023c), but we could not locate those studies as peer-reviewed papers on PubMed.

How strong is the evidence?

Broad but shallow. More than a dozen papers exist, spread across kidney, skin, thymus, stem cells and cartilage, and most measure marker expression in culture.
Cartilage evidence is recent and thin. The direct cartilage work is two 2023 in vitro reports in Russian, a patent explant experiment and a 2007 rat bone study.
One network. Some papers have co-authors in Moscow or Ukraine, but Khavinson or his St Petersburg colleagues are on all of them. We found no unaffiliated replication.
No peer-reviewed human trial. The osteoarthritis figures quoted for Cartalax trace back to the patent.

Read fairly, Cartalax has early cell data from a single source that point in a consistent direction, and its cartilage label rests more on the patent and the cartilage extract than on cartilage experiments.

For background on the whole class, including where the tissue mapping comes from, see Bioregulator Peptides: What the Khavinson Research Actually Claims. The same approach is applied to Cardiogen and Chonluten.

References

Khavinson VK, et al. 2021. "Peptide Regulation of Gene Expression: A Systematic Review." Molecules 26(22):7053. PMID 34834147
Linkova N, et al. 2023. "Peptide Regulation of Chondrogenic Stem Cell Differentiation." International Journal of Molecular Sciences 24(9):8415. PMID 37176122
Khavinson VK, et al. 2016. "Short Peptides Regulate Gene Expression." Bulletin of Experimental Biology and Medicine 162(2):288-292. PMID 27909961
Khavinson VK, et al. 2023. "Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters." Biomolecules 13(3):552. PMID 36979488
Ashapkin V, et al. 2020. "Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides." Molecular Biology Reports 47(6):4323-4329. PMID 32399807
Myakisheva SN, et al. 2023a. "The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging." Advances in Gerontology 36(3):383-390. In Russian. PMID 37782646
Myakisheva SN, et al. 2023b. "Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging." Advances in Gerontology 36(2):234-238. In Russian. PMID 37356100
Myakisheva SN, et al. 2023c. "Chondrocytes secretory phenotype associated with aging: role in the pathogenesis of osteoarthritis and prospects for peptide bioregulation." Advances in Gerontology 36(3):313-323. In Russian. PMID 37782637
Povorozniuk VV, et al. 2007. "Effect of peptide regulators on the structural and functional status of bone tissue in ageing rats." Advances in Gerontology 20(2):134-137. In Russian. PMID 18306703
Lin'kova NS, et al. 2016. "Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro." Bulletin of Experimental Biology and Medicine 161(1):175-178. PMID 27259496
Fridman NV, et al. 2020. "Comparison of the Effects of KE and AED Peptides on Functional Activity of Human Skin Fibroblasts during Their Replicative Aging." Bulletin of Experimental Biology and Medicine 170(1):154-157. PMID 33231794
Chalisova NI, et al. 2015. "Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals." Bulletin of Experimental Biology and Medicine 159(1):124-127. PMID 26033601
Zamorskii II, et al. 2015. "Peptides Restore Functional State of the Kidneys During Cisplatin-Induced Acute Renal Failure." Bulletin of Experimental Biology and Medicine 159(6):736-739. PMID 26515176
Lin'kova NS, et al. 2011. "Peptidergic regulation of thymocyte differentiation, proliferation, and apoptosis during aging of the thymus." Bulletin of Experimental Biology and Medicine 151(2):239-242. PMID 22238759
Khavinson VKh, et al. 2007. "Peptide normalizing metabolism in osseous and cartilage tissue." Russian patent RU 2299741 C1.