Cartalax

Cartalax is the synthetic tripeptide alanine–glutamic acid–aspartic acid (AED). It belongs to the "peptide bioregulators", a family of two- to four-amino-acid peptides developed by Vladimir Khavinson's group. The developers say these peptides enter cell nuclei and regulate gene expression in specific tissues [1]. Its sister peptides include Epitalon (AEDG) [1]. In older papers it appears under the code T-31 [5].

Cartilage. The case for Cartalax as a joint peptide rests on cell work from the developers' group:

• In human mesenchymal stem cells ageing in culture, 200 ng/mL of AED raised the genes and proteins of cartilage formation (SOX9, aggrecan, type II collagen and COMP). A cartilage extract needed a tenfold higher concentration for the same effect [3].
• In chondrocyte cultures, AED and the same cartilage extract normalised markers of the ageing, inflammatory "secretory phenotype" [4].
• In rats with osteoporosis after ovary removal, T-31 prevented and partly reversed bone loss. A cartilage-extract product worked significantly better [6].

A 2023 review by the same group says AED worked in animal models of osteoarthritis and when taken by mouth by older patients [2]. No such patient trial could be found on PubMed.

Other tissues.

• It slowed signs of ageing in skin fibroblast cultures, where it also reduced cell death [7].
• It raised proliferation and lowered ageing markers in kidney cell cultures [5][8][9].
• It raised IGF1 gene expression in ageing stem cells [10].
• In rats it reduced protein in the urine, both in cisplatin kidney injury and in old age [11][12].

Not every result was positive. In ageing thymus cells, T-31 had no protective effect, while a different peptide did [13]. In human dental stem cells, the western-blot evidence of a shift towards nerve cells held for a peptide mix and for KED, but not for AED on its own [14]. In the cisplatin study, a sister peptide (EDL) protected the kidneys more strongly than AED [11].

Who did the research. Almost every paper includes Khavinson or his close collaborators, and several are published in Russian with short English abstracts [2][3][9]. No independent group has replicated the cartilage findings.

The developers propose that short peptides like AED pass through cell and nuclear membranes and bind DNA or histones directly, switching particular genes on or off [1]. For AED, the evidence for DNA binding comes from computer docking models, not from measurements [9][15].

Downstream, the reported effects in cell culture are more cartilage-forming gene activity in stem cells [3], normalised ageing and inflammation markers (p16, p21, p53, TNF-α, IL-1α, SIRT1) in chondrocytes [4] and higher IGF1 and NF-κB gene expression in ageing stem cells [10].

There are no published human safety data. In old rats, kidney tissue showed no sign of toxicity after AED and related peptides [12]. AED is made of three common dietary amino acids, but that does not show a synthetic product is safe. Products sold online are unregulated.