Overview
Cartalax is the name under which the synthetic tripeptide L-alanyl-L-glutamyl-L-aspartic acid (Ala-Glu-Asp, AED) is catalogued; the same peptide is designated T-31 in some kidney cell studies6,7. It belongs to the family of short peptides studied by Khavinson and colleagues, and in several papers it is compared with a polypeptide complex extracted from cartilage1,2.
The literature is small and comes almost entirely from that group. It is limited to cell and tissue culture: human mesenchymal stem cells, chondrocytes, skin fibroblasts and kidney cell cultures, mostly in models of replicative or in vitro ageing1,2,3,4,5,6,7. The two chondrocyte studies are published in Russian with English abstracts1,2.
Mechanism of action
As described in the research literature
As described in the research literature, the proposed mechanism follows the group's general model for short peptides: entry into the cell and nucleus, and interaction with DNA or histones that alters the expression of genes, including those involved in cell differentiation8. This model is the originating group's proposal and has not been established independently.
The reported changes are at the level of gene expression and protein synthesis. In human mesenchymal stem cells undergoing replicative ageing, AED was reported to increase expression and synthesis of the chondrogenic markers SOX9, aggrecan, type II collagen and COMP1. In ageing chondrocytes, AED and the cartilage polypeptide complex were reported to normalise markers of the senescence-associated secretory phenotype, including p16, p21, p53, TNF-α, IL-1α and SIRT12. In fetal bone marrow mesenchymal stem cells, AED, KED and KE modulated IGF1 and NF-κB gene expression in two culture ageing models5.
Research areas
What published studies have examined
Chondrogenic differentiation and chondrocyte ageing
Gene expression and protein synthesis of SOX9, aggrecan, type II collagen and COMP were measured in human mesenchymal stem cells during replicative ageing, comparing AED with a cartilage polypeptide complex1. Senescence-associated secretory phenotype markers were characterised in ageing chondrocytes and compared after exposure to AED or the complex2.
Sources [1] [2]
Skin fibroblast ageing
In human skin fibroblasts during replicative ageing, AED was compared with the dipeptide KE for sirtuin-1, sirtuin-6, collagen I, IL-1, TGF-β and NF-κB expression3. An earlier study compared KE, KED, AED and AEDG for Ki-67, CD98hc, caspase-3 and MMP-9 in ageing fibroblast cultures4.
Sources [3] [4]
Mesenchymal stem cell gene expression
Expression of IGF1, FOXO1, TERT, TNKS2 and NF-κB genes was measured in a human fetal bone marrow mesenchymal stem cell line aged by serial passage or by stationary culture, with AED, KED and KE added at nanomolar concentrations5. The group's review places these findings within its wider work on peptide regulation of cell differentiation8.
Sources [5] [8]
Kidney cell cultures
In primary kidney cell cultures during ageing, a calf kidney polypeptide complex and the peptides T-31 (AED) and T-35 (EDL) were compared for Ki-67, p53, MMP-14 and IL-8 expression6. In organotypic kidney tissue cultures from young and old rats, the same peptides were examined for proliferation and apoptosis markers alongside the polypeptide complex7.
Sources [6] [7]
Specifications
- Sequence
- Ala-Glu-Asp (AED)
- Molecular formula
- C12H19N3O8
- Molecular weight
- 333.3 g/mol
- CAS number
- 85806-95-7
- Form
- White to off-white lyophilised powder in a sealed vial
- Storage
- Store lyophilised powder at -20 °C, protected from light and moisture. Once reconstituted, keep refrigerated at 2 to 8 °C and protect from light.
- Solubility and reconstitution
- Reconstitute with bacteriostatic water. Add the diluent slowly down the inside wall of the vial and swirl gently until clear; do not shake.
References
- 1
The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging.
Myakisheva SN, Linkova NS, Diatlova AS, et al. Advances in Gerontology (Uspekhi Gerontologii), 2023.
PubMed 37782646 ↗
- 2
Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging.
Myakisheva SN, Linkova NS, Kozhevnikova EO, et al. Advances in Gerontology (Uspekhi Gerontologii), 2023.
PubMed 37356100 ↗
- 3
Comparison of the Effects of KE and AED Peptides on Functional Activity of Human Skin Fibroblasts during Their Replicative Aging.
Fridman NV, Linkova NS, Kozhevnikova EO, et al. Bulletin of Experimental Biology and Medicine, 2020.
PubMed 33231794 ↗DOI 10.1007/s10517-020-05022-1 ↗
- 4
- 5
- 6
Peptides regulate expression of signaling molecules in kidney cell cultures during in vitro aging.
Khavinson VKh, Lin'kova NS, Polyakova VO, et al. Bulletin of Experimental Biology and Medicine, 2014.
PubMed 24958378 ↗DOI 10.1007/s10517-014-2540-y ↗
- 7
Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals.
Chalisova NI, Lin'kova NS, Nichik TE, et al. Bulletin of Experimental Biology and Medicine, 2015.
PubMed 26033601 ↗DOI 10.1007/s10517-015-2906-9 ↗
- 8