Cartalax

Cartalax (Ala-Glu-Asp-Leu) is a synthetic tetrapeptide bioregulator derived from cartilage tissue, developed by Vladimir Khavinson's group at the Saint Petersburg Institute of Bioregulation and Gerontology. As a four amino acid sequence containing the Ala-Glu-Asp core shared with Epithalon (pineal) and related bioregulators, Cartalax targets cartilage and connective tissue biology through the proposed epigenetic bioregulator mechanism.

The Ala-Glu-Asp-Leu sequence positions Cartalax within the Khavinson bioregulator series targeting musculoskeletal and connective tissue biology. The leucine C-terminal residue distinguishes it from pineal Epithalon (Ala-Glu-Asp-Gly) and cortical Cortagen (Ala-Glu-Asp-Pro), suggesting that the fourth amino acid residue provides tissue-targeting specificity while the Ala-Glu-Asp core maintains the common chromatin-interacting pharmacophore.

Chondrocyte biology research is the primary laboratory application for Cartalax. Primary chondrocyte cultures isolated from articular cartilage (human or bovine) provide the relevant cell model. Research endpoints include: type II collagen gene expression (COL2A1) by RT-PCR and protein by ELISA; aggrecan expression (ACAN) as the primary cartilage proteoglycan; SOX9 transcription factor expression (master regulator of chondrocyte differentiation); MMP-13 and ADAMTS-5 expression as catabolic enzyme markers relevant to cartilage degradation research; and chondrocyte viability under inflammatory challenge (IL-1beta, TNF-alpha stimulation as model of joint inflammation).

Published research from Khavinson's institute has examined Cartalax in aged animal models examining cartilage histology, collagen content, and connective tissue integrity. The anti-ageing research context positions Cartalax within the musculoskeletal longevity research framework alongside SS-31 (mitochondrial), MOTS-c (metabolic), and FOXO4-DRI (senescence) as complementary tools addressing different aspects of age-related tissue decline.

Cartalax research design considerations: for chondrocyte biology research, the inflammatory challenge model is the most research-relevant paradigm. Stimulate primary chondrocytes or ATDC5 cells with IL-1beta (10ng/mL) for 24 hours to establish an inflammatory phenotype characterised by: upregulated MMP-13 (collagenase-3), ADAMTS-5 (aggrecanase-2), COX-2, and iNOS; downregulated type II collagen and aggrecan synthesis. Pre-treatment or co-treatment with Cartalax (1nM-1uM) allows assessment of whether the bioregulator can modulate the inflammatory catabolic response while maintaining or restoring anabolic matrix synthesis.

Comparison with other bioregulators from the Khavinson series provides mechanistic insight: Epithalon (pineal, Ala-Glu-Asp-Gly) and Cartalax (cartilage, Ala-Glu-Asp-Leu) share the Ala-Glu-Asp core. Running both in parallel at matched molar concentrations in chondrocyte versus pinealocyte cell models allows tissue-specificity assessment — if Cartalax preferentially affects chondrocytes and Epithalon preferentially affects pinealocytes at the same concentration, this supports the tissue-targeting specificity hypothesis for the C-terminal amino acid. Gene expression endpoints: COL2A1, ACAN, SOX9, MMP-13, ADAMTS-5 by RT-PCR; type II collagen protein by Western blot and ELISA. MW: 460.51 g/mol. Reconstitute in bacteriostatic water at 1mg/mL. Store lyophilised at -20°C. For laboratory and analytical research purposes only.

Cartalax and osteoarthritis research models: the most clinically relevant in vitro model for Cartalax research uses human osteoarthritic chondrocytes isolated from cartilage obtained during total knee replacement surgery. These cells already exhibit the catabolic phenotype relevant to joint disease — elevated MMP-13, ADAMTS-5, IL-6, and COX-2; reduced type II collagen and aggrecan synthesis — without requiring exogenous IL-1beta stimulation. Cartalax treatment (1nM-10µM) of OA chondrocytes for 48-72 hours allows assessment of whether the bioregulator can modulate the established disease phenotype. Primary endpoints: type II collagen synthesis (PICP ELISA, collagen II Western blot); MMP-13 activity (fluorogenic substrate assay, MMP-13 ELISA); aggrecan content (dimethylmethylene blue colorimetric assay for glycosaminoglycans); and gene expression panel by RT-PCR (COL2A1, ACAN, SOX9, MMP-13, ADAMTS-5, IL-6, COX-2).

For three-dimensional cartilage tissue engineering research: agarose gel (2%) or fibrin hydrogel encapsulation of chondrocytes at 20×10^6 cells/mL creates a three-dimensional culture environment that maintains the chondrocyte rounded morphology and supports type II collagen and aggrecan deposition over 3-6 weeks. Cartalax supplementation in the culture medium throughout the culture period allows assessment of effects on matrix accumulation. Quantify matrix accumulation by biochemical assays (hydroxyproline for total collagen, dimethylmethylene blue for glycosaminoglycans) and histology (Safranin-O staining for proteoglycans, type II collagen immunohistochemistry) at weekly intervals. Compare Cartalax with transforming growth factor-beta 3 (TGF-beta3, the standard chondrogenic differentiation factor) at sub-maximal concentrations to assess whether the bioregulator acts synergistically through Smad2/3-independent pathways. MW: 460.51 g/mol. Molecular formula: C20H32N4O8. Reconstitute in bacteriostatic water at 1mg/mL. Store lyophilised at -20°C. For laboratory and analytical research purposes only.