Cartalax

What it is

Cartalax belongs to the cytogens, the short synthetic peptides of the Khavinson school. In the scientific literature, it is usually just called AED or referred to by the laboratory code T-31. The 2007 patent describes it as a peptide that normalizes metabolism in bone and cartilage tissue and is intended for use in degenerative diseases of the joints and spine.

Cartalax must be distinguished from Sigumir. Sigumir is a polypeptide complex from the cartilage and bone of young animals, that is, an extract with many components. Cartalax is a single, precisely defined molecule. The link between the two: according to the developer group, AED is one of the building blocks of the cartilage polypeptide complex. According to a 2023 review, this complex was in a phase 2 trial for osteoarthritis in Russia; Cartalax itself was not.

How it is supposed to work

The basic idea of the school: ultrashort peptides enter the cell nucleus, attach to DNA and histones and change which genes are read. In the case of Cartalax, this is supposed to affect the genes of cartilage formation and the signals with which aging cartilage cells damage their surroundings.

Precisely these two points have been measured in cell culture. In replicatively aged human mesenchymal stem cells, AED activated genes and proteins of cartilage differentiation: SOX9, aggrecan, type II collagen and COMP. In aged cartilage cells, it normalized the senescence-associated secretory phenotype, in which the cells produce more p16, p21, p53, TNF-α and IL-1α and less Sirt1. Osteoarthritis is considered a disease in which precisely this phenotype wears down the cartilage.

Findings from other tissues fit with this. In aging human skin fibroblasts, AED increased sirtuin-1, sirtuin-6 and collagen I, and in stem cell cultures, the short peptides tested, including AED, raised the expression of the growth factor IGF1 3.5- to 5.6-fold.

What AED does outside cartilage

The group has also studied AED in kidney tissue. In aging kidney cell cultures, the peptide increased cell proliferation, lowered the aging markers p16, p21 and p53 and raised sirtuin-6. In old rats, it reduced protein excretion in the urine, and in a model of cisplatin-induced acute kidney failure, it reduced protein and electrolyte losses. For joints, these findings are only indirectly relevant, but they show a recurring pattern: in several aging tissues, AED acts in the direction of renewal and less cellular stress.

The clinical report in the patent

The patent contains an example with 29 patients aged between 52 and 72 who had suffered from knee osteoarthritis for 5 to 20 years and had taken pain and anti-inflammatory drugs for a long time. According to the patent, they were randomized into 2 groups; 12 patients formed the control group and received saline injections on the same schedule. Treatment ran for 20 days with daily intramuscular injections.

The result: less pain and better mobility in 54.5 to 62.7 percent of cases, depending on severity, most clearly in early stages. According to the patent, the X-ray findings did not change substantially during the observation period.

What the studies show

Osteoarthritis patients in the patent

According to the 2007 patent, 29 patients with knee osteoarthritis were randomized, 12 of whom received saline. After 20 days of intramuscular administration, pain and mobility improved in 54.5 to 62.7 percent of cases; X-rays showed no substantial change. The result of the control group, rating scales, blinding and side effects are not reported.

Cartilage differentiation in aged stem cells

Myakisheva and colleagues added AED and the cartilage polypeptide complex to replicatively aged human mesenchymal stem cells (Adv Gerontol 2023). Both activated genes and proteins of cartilage formation: SOX9, aggrecan, type II collagen and COMP.

Aging phenotype of cartilage cells

In a second paper by the same group (Adv Gerontol 2023), aged cartilage cells produced more p16, p21, p53, TNF-α and IL-1α and less Sirt1. AED and the cartilage complex normalized this signature.

Rat cartilage explants

In the patent, 28 cartilage fragments from the femoral head of rats were cultured. Under AED, the area index, as a measure of cell outgrowth, was 26 percent above the control on day 3, and the same effect was seen after 7 days.

Where the data stop

There is no peer-reviewed study in humans, and no public trial registry lists one. The only clinical report is the patent example, and it lacks crucial information: how the control group fared is not stated, nor are scales, blinding and statistics. An effect versus placebo cannot be read from it. The developers’ review, which speaks of efficacy with oral administration, cites no study that can be found in PubMed. According to the patent, nothing visibly changed structurally in the cartilage within 20 days.

Two further points belong to the assessment. In the patent, the peptide was injected, but mostly capsules are sold; whether a swallowed tripeptide reaches the joint has not been measured. And the effect is not limited to cartilage: in studies by the same group, AED also acted on kidney cells, on the kidney function of old rats and on skin fibroblasts. This does not make the peptide ineffective, but it puts the idea of a pure joint bioregulator into perspective.

Status, approval and legal

Cartalax is not an approved medicine in Germany or the EU. Authorization under the Novel Food Regulation (EU) 2015/2283, which would be required for sale as a dietary supplement, is lacking. In Russian-speaking countries and online, it is offered for joint complaints; in Germany, as a research peptide. In sport, a non-approved substance falls under group S0 of the World Anti-Doping Agency.

Safety

There are no systematic safety data in humans. The toxicology in the patent comes from the developers and only from animals: 66 mice in acute testing, 64 rats over 90 days, 90 guinea pigs over 6 months, each without pathological findings. The patient report does not document side effects, neither their occurrence nor their absence. Interactions with painkillers, anticoagulants or osteoarthritis therapies have not been studied. There are no data for pregnancy and breastfeeding, and with research-grade products, content and purity are unverified. A suddenly swollen, hot or reddened joint should be checked by a doctor.

Sources

• Khavinson et al., Patent RU 2299741 (2007) – peptide for normalizing bone and cartilage metabolism
• Myakisheva et al., Adv Gerontol 2023 – AED and cartilage differentiation of aged stem cells
• Myakisheva et al., Adv Gerontol 2023 – peptides against the aging phenotype of chondrocytes
• Myakisheva et al., Adv Gerontol 2023 – chondrocyte SASP and peptide bioregulation (review)
• Linkova et al., Int J Mol Sci 2023 – Peptide Regulation of Chondrogenic Stem Cell Differentiation
• Ashapkin et al., Mol Biol Rep 2020 – AED, KED and KE in aging stem cell cultures
• Fridman et al., Bull Exp Biol Med 2020 – KE and AED in aging skin fibroblasts
• Khavinson et al., Adv Gerontol 2014 – tripeptides AED and EDL in aging kidney cell cultures
• Zamorskii et al., Adv Gerontol 2018 – peptides and kidney function in old rats
• WADA – Prohibited List (group S0)