Cartalax
Also known as: AED, Ala-Glu-Asp, T-31, T-31 peptide, alanyl-glutamyl-aspartic acid
3 notable studies · 4 references
TLDR
Cartalax is the synthetic tripeptide Ala-Glu-Asp (AED/T-31), studied primarily in preclinical models of gene expression, cellular aging, bone metabolism, and tissue renewal, but its popular characterization as a cartilage-regenerating peptide is considerably stronger than the direct evidence and controlled human efficacy has not been established.
Research Supports
- Studied for associations with cartilage and bone biology
- Investigated for effects on mesenchymal stem-cell aging and gene expression
- Examined for effects on kidney-tissue cell renewal
Observations Reported in Research
- Increased IGF1 expression roughly 3.5-5.6-fold in aging human mesenchymal stem-cell cultures (Ashapkin et al., 2020)
- Produced an osteoprotective effect on bone mineral density in ovariectomized rats, though a cartilage-derived peptide complex was more effective (Povorozniuk et al., 2007)
- Increased Ki-67 and decreased p53 in rat kidney organ-culture explants, with weaker effects than a complete kidney-derived peptide complex (Chalisova et al., 2015)
- No direct human administration evidence has been identified
These are brief summaries of what the referenced research examined or reported — not conclusions about safety or effectiveness, and not medical advice. See Notable Studies and Sources & References below for the full context and citations.
At a Glance
Classification: Synthetic tripeptide; short peptide bioregulator; experimental cartilage/bone-associated peptide
Cartalax is an extremely short synthetic peptide consisting of only three amino acids: Ala-Glu-Asp, or AED. The U.S. National Library of Medicine's MeSH database recognizes cartalax and T-31 peptide as names associated with alanyl-glutamyl-aspartic acid. It comes from the Khavinson short-peptide bioregulator research program and is generally positioned as the family's cartilage-associated peptide. Research involving AED has examined bone metabolism, cellular aging, mesenchymal stem cells, gene expression, kidney tissue, and cell proliferation and apoptosis. But there is an important surprise: the published evidence directly supporting Cartalax as a cartilage-regenerating therapy is remarkably thin. Much of the modern research-market description is considerably more specific than the underlying literature.
What Is Cartalax?
Cartalax is the tripeptide Ala-Glu-Asp (AED). PubChem lists it as a three-amino-acid peptide with molecular weight approximately 333.29 g/mol. It belongs to the same broad short-peptide research tradition as Epitalon (AEDG), Vesugen (KED), Pinealon (EDR), Vilon (KE), and Cortagen (AEDP). These compounds are sometimes collectively described as peptide bioregulators. The proposed concept is that extremely short peptide sequences can influence tissue-associated cellular and gene-expression processes. That remains a research framework rather than a clinically established general mechanism.
What Are Researchers Studying?
Cartilage and bone biology
Cartalax is most commonly associated with cartilage. However, one of the clearest in-vivo studies of T-31/AED actually examined bone mineral density in ovariectomized rats rather than regeneration of damaged cartilage. Researchers compared T-31 with a peptide preparation derived from cartilage tissue. Both produced osteoprotective effects, but the complex cartilage-derived preparation was significantly more effective than T-31. That's considerably more nuanced than: “Cartalax regenerates cartilage.” The experiment supports biological activity in an animal bone-loss model. It does not establish cartilage regeneration in humans.
Mesenchymal stem-cell aging
A 2020 study exposed aging cultures of human embryonic bone-marrow mesenchymal stem cells to AED, KED, and KE. Researchers measured genes involved in aging-related biology, including IGF1, FOXO1, TERT, TNKS2, and NFκB. AED, KED and KE increased IGF1 expression approximately 3.5–5.6-fold under the experimental conditions and altered other gene-expression patterns. This is direct evidence that AED can affect cultured human cells. But: Human cells in a dish ≠ human treatment. And increased expression of a gene does not automatically imply rejuvenation.
Cellular aging
Short-peptide researchers have investigated whether AED modifies molecular changes occurring during cellular senescence. The mesenchymal stem-cell work found that AED altered expression of genes associated with aging biology. This supports the narrower statement: AED can modulate gene expression in experimental aging cell cultures. It does not establish: AED reverses human biological aging.
Kidney-cell renewal
Interestingly, some of the clearest AED experiments aren't in cartilage at all. A 2015 organ-culture study examined kidney tissue from young and old rats. T-31/AED increased the proliferation marker Ki-67, decreased p53, and promoted cellular-renewal-associated changes. However, the complete peptide complex isolated from calf kidney produced stronger effects than AED. This tells us something important about Cartalax: Its experimentally observed effects may not be nearly as cartilage-specific as the commercial name implies.
Gene-expression regulation
Gene-expression modulation is one of the recurring themes across the Khavinson peptide literature. AED has altered expression of several genes in cultured human mesenchymal stem cells. Researchers in this field propose that very short peptides may interact with chromatin or DNA-associated regulatory systems. That remains substantially different from having a well-defined classical receptor mechanism. For Cartalax, there is no established Cartalax receptor.
How Does It Work?
The mechanism remains uncertain. The broad proposed model is: AED → cellular uptake → interaction with gene-regulatory/chromatin-associated processes → changes in transcription → altered proliferation, differentiation or cellular-aging pathways. Experiments demonstrate that gene expression can change following AED exposure. What they do not establish is a simple pathway such as: Cartalax → cartilage receptor → cartilage regeneration. That mechanism has not been demonstrated.
What Does the Research Show?
Human research
Direct human therapeutic evidence for Cartalax/AED is not established in the literature located for this profile. There are experiments using human-derived cells, particularly mesenchymal stem-cell cultures. That's useful mechanistic evidence. It is not a clinical trial. So Aminodex should classify Cartalax as: Human administration evidence: insufficient / not established, rather than allowing human-cell experiments to populate the “human evidence” bucket.
Animal research
Limited but real. T-31/AED has been investigated in ovariectomized rat bone-loss models, rat kidney organ cultures, and aging-related experimental systems. In the osteoporosis model, T-31 showed an osteoprotective effect, although the cartilage-derived peptide complex was significantly more effective.
In-vitro research
This is the strongest category. AED has demonstrated measurable effects in human mesenchymal stem cells, rat organotypic kidney cultures, and other experimental cell-aging systems. These findings establish biological activity. They do not establish a clinically meaningful effect on human joints.
Notable Studies
Gene Expression in Human Mesenchymal Stem Cell Aging Cultures: Modulation by Short Peptides
in-vitroResearchers studied AED, KED and KE in two models of aging human embryonic bone-marrow mesenchymal stem cells. The peptides altered expression of genes associated with cellular aging. AED, KED and KE increased IGF1 expression approximately 3.5–5.6-fold under the experimental conditions, while effects on other genes differed by peptide and aging model.
Limitations: Cultured cells only. Multiple peptides were studied simultaneously, and changes in gene expression don't establish improved cartilage, joint function, longevity or clinical outcomes.
View publication →Effect of Peptide Regulators on the Structural and Functional Status of Bone Tissue in Ageing Rats
animalResearchers compared a cartilage-derived peptide preparation with T-31/AED in an experimental osteoporosis model. Both interventions produced osteoprotective effects involving bone mineral density, but the complex cartilage preparation was significantly more effective than T-31.
Limitations: Rat study focused substantially on bone density rather than a human cartilage disorder. It does not demonstrate regeneration of human cartilage or treatment of osteoarthritis.
View publication →Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals
in-vitroResearchers examined a calf-kidney polypeptide complex and short peptides T-31/AED and T-35/EDL. AED increased Ki-67 and reduced p53 expression in kidney explants, although its effects were weaker than those of the complete kidney-derived peptide complex.
Limitations: Ex-vivo rat kidney tissue—not cartilage and not human treatment. This study supports general biological activity rather than Cartalax's marketed tissue-specific identity.
View publication →What We Still Don't Know
Whether Cartalax improves human cartilage; whether it treats osteoarthritis; whether it increases human cartilage thickness; human pharmacokinetics; human bioavailability; human safety; primary molecular target; whether proposed tissue specificity actually exists in vivo; whether gene-expression changes produce meaningful physiological effects; whether effects replicate independently; whether it alters human joint pain or function; long-term consequences of repeated exposure; whether research-market Cartalax corresponds to experimental T-31/AED material.
Related Compounds
Recent publications
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Sources & References
- Citation: Ashapkin V, Khavinson V, Shilovsky G, Linkova N, Vanyushin B. Gene Expression in Human Mesenchymal Stem Cell Aging Cultures: Modulation by Short Peptides. Molecular Biology Reports. 2020. Link: https://pubmed.ncbi.nlm.nih.gov/32399807/
- Citation: Povorozniuk VV, et al. Effect of Peptide Regulators on the Structural and Functional Status of Bone Tissue in Ageing Rats. 2007. Link: https://pubmed.ncbi.nlm.nih.gov/18306703/
- Citation: Chalisova NI, et al. Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals. 2015. Link: https://pubmed.ncbi.nlm.nih.gov/26033601/
- Citation: NLM MeSH Supplementary Concept — alanyl-glutamyl-aspartic acid / Cartalax / T-31. Link: NLM MeSH record (https://www.ncbi.nlm.nih.gov/mesh/).
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