Cartalax
Anti-AgingAla-Glu-Asp — Synthetic Peptide
Overview
Cartalax (Ala-Glu-Asp) is a synthetic tripeptide developed by Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology as part of the bioregulator peptide program. It belongs to a class of ultra-short peptides (2-4 amino acids) that Khavinson's group has investigated for tissue-specific regulatory effects over several decades. Cartalax was designed to target cartilage and musculoskeletal tissue, with the aim of preserving cartilage integrity and promoting chondrocyte function during aging.
The bioregulator peptide concept posits that short peptides can interact directly with DNA through sequence-specific binding to the minor groove, influencing gene expression without requiring membrane receptor activation. This is a non-conventional mechanism for peptide action and remains an area of active research, primarily within Russian academic institutions. Cartalax is part of a larger family of Khavinson peptides that includes Epitalon (AEDG), Pinealon (EDR), and others, each claimed to have tissue-specific tropism.
Mechanism of Action
Cartalax's proposed mechanism of action involves direct interaction with DNA in chondrocytes and cartilage progenitor cells. According to the bioregulator peptide model, the Ala-Glu-Asp sequence binds to complementary nucleotide sequences in gene promoter regions, modulating transcription of cartilage-specific genes. In vitro studies have shown that Cartalax increases expression of collagen type II and aggrecan — the major structural components of hyaline cartilage — while reducing expression of matrix metalloproteinase-13 (MMP-13), a collagenase responsible for cartilage degradation in osteoarthritis.
The peptide also influences cell cycle regulators, affecting Ki-67 (proliferation marker) and p53 (apoptosis/senescence regulator) expression in ways that favor cellular renewal over senescence. Whether these effects result from direct DNA interaction or from more conventional signaling mechanisms (such as interaction with cell surface peptide transporters or intracellular targets) has not been definitively resolved. The extremely small size of Cartalax (319 Da) allows it to cross cell membranes readily, which is consistent with either mechanism.
Research Dosing
Courses typically repeated every 3-6 months. Part of the Khavinson bioregulator peptide family. No standardized clinical dosing. Often used in combination with other short peptides (Epitalon, Pinealon).
Oral route studied for cartilage and musculoskeletal applications. Small molecular size may permit intestinal absorption. Available as capsule formulations in some markets.
Research data only. These dosing ranges are derived from published studies, primarily in animal models. This is not medical advice. No peptide discussed on this site is approved for human therapeutic use unless otherwise noted.
Published Studies
Peptide regulation of gene expression and protein synthesis in bronchial epithelium
Khavinson VKh, Tendler SM, Vanyushin BF — Lung, 2014
Demonstrated that short peptides including Cartalax modulate gene expression in bronchial epithelial cells, affecting proliferation, differentiation, and apoptosis markers. The tripeptide influenced expression of Ki-67 and p53, suggesting effects on cell cycle regulation.
PMID: 25015171 →Peptide bioregulation of aging: results and prospects
Khavinson VKh — Advances in Gerontology, 2008
Comprehensive review of the bioregulator peptide approach to aging, covering 35+ years of research on short peptides including Cartalax. Summarized evidence for tissue-specific peptide effects on gene expression, protein synthesis, and functional restoration in aging animal models.
Short peptides stimulate cell regeneration and regulate gene expression in chondrocyte cultures
Khavinson VKh, Linkova NS, Polyakova VO, et al. — Bulletin of Experimental Biology and Medicine, 2016
Cartalax stimulated chondrocyte proliferation and increased expression of collagen type II and aggrecan in human cartilage cell cultures. The peptide also reduced expression of matrix metalloproteinase-13 (MMP-13), suggesting a protective effect against cartilage degradation.