Description
Cartalax, or AED or T-31 peptide, is a synthetic peptide designed to target specific biological pathways that may have implications in cellular aging. The peptide is based on the sequence of amino acids derived from the alpha-1 chain of type XI collagen (hence AED, standing for the amino acid sequence Alanine-Glutamate-Aspartate). It has also been isolated from kidney extracts containing polypeptides. Peptides like Cartalax are often investigated for their potential to modulate biological processes, including inflammation and cartilage repair, which are significant factors in osteoarthritis. More specifically, it is classified among the Khavinson peptides and has been suggested by researchers to act as a bioregulator.
Chemical Makeup
Molecular formula: C12H19N3O8
Molecular weight: 333.29 g/mol
Sequence: Ala-Glu-Asp
Other known titles: AED, T-31, SCHEMBL5324601
Research and Clinical Studies
The data presented here distils the most recent findings from preclinical studies on the potential of Cartalax across a spectrum of experimental frameworks.
Cartalax and Fibroblasts
The peptide Cartalax, when explored for its impacts on skin fibroblasts, appears to hold properties that may potentially influence the aging process of these cells in culture. Cartalax has been suggested to potentially play a role in several critical cellular processes that are pivotal for fibroblast function and longevity. Firstly, Cartalax may contribute to the proliferation of fibroblasts, as suggested by its potential enhancement of Ki-67 expression. Ki-67 is a marker associated with cell proliferation, and its level typically decreases during aging fibroblast cultures. The apparent promotion of Ki-67 by Cartalax implies that this peptide may encourage fibroblast growth or increase their replicative lifespan, potentially offsetting the natural decline in cell division over time.
Additionally, Cartalax’s action on CD98hc is noteworthy. CD98hc is implicated in regeneration and aging processes of cells. The increased expression of CD98hc in the presence of Cartalax may suggest a role in enhancing regenerative capacity or sustaining cell vitality. The study also indicates Cartalax may suppress caspase-3 activity, which could reduce apoptosis (programmed cell death). As apoptosis commonly increases in aging cell cultures, its apparent suppression by Cartalax may allow fibroblasts to avoid the increased cell death typically associated with aging, potentially contributing to an extended cellular lifespan. Cartalax also appears to inhibit MMP-9 synthesis. MMP-9 is involved in extracellular matrix remodelling, and its elevated activity is often linked with aging fibroblasts. By inhibiting MMP-9, Cartalax might help preserve matrix integrity and mitigate degenerative changes associated with aging.
Cartalax and Kidney Cells
Cartalax may carry the potential to favourably influence kidney cell regeneration. Observations in kidney tissue cultures from young and older murine models suggest the presence of Cartalax is associated with increased cell proliferation indicated by elevated Ki-67 expression. Moreover, Cartalax may contribute to decreased apoptosis in kidney cells by reducing expression of the pro-apoptotic peptide p53. This down-regulation of p53 suggests that Cartalax might help sustain cellular integrity and prolong survival. Other studies indicate Cartalax may potentially decrease aging markers such as p16, p21, and p53, which are linked with cellular senescence. Additionally, the peptide may increase SIRT-6 expression, a protein involved in DNA repair and genomic stability, whose levels typically decline with age. These interactions suggest Cartalax might help preserve kidney cell function and potentially slow aging processes.
