Cartalax
Cartalax — Ala-Glu-Asp (AED) Khavinson Cartilage Cytogen
Cartalax is a synthetic tripeptide (Ala-Glu-Asp / AED, MW 333.29 g/mol) developed at the St. Petersburg Institute of Bioregulation and Gerontology under Vladimir Khavinson. The sequence matches a motif in the alpha-1 chain of type XI collagen, providing the structural rationale for cartilage-tissue targeting. Cell culture studies have documented chondrocyte proliferation effects and modulation of senescence markers including p16, p21, and p53. No human clinical trial has been published. The compound has no FDA or EMA approval.
Evidence
Effects
Routes
Also known as
Educational content only
This information is provided for research and educational purposes. It is not medical advice, diagnosis, or treatment. Many peptides described are not approved for human use outside clinical trials. Always consult a qualified healthcare professional before using any compound.
Research summary
Cartalax is a synthetic tripeptide composed of alanine, glutamic acid, and aspartic acid (Ala-Glu-Asp, single-letter code AED). Molecular weight is 333.29 g/mol. The sequence corresponds to a motif found in the alpha-1 chain of type XI collagen, a structural protein important for cartilage extracellular matrix organization. Cartalax was originally identified from kidney peptide extract analysis at the St. Petersburg Institute of Bioregulation and Gerontology and subsequently characterized for cartilage-related effects.
The Khavinson bioregulator program produced two parallel compound classes. Cytomaxes are organ-specific peptide extracts containing heterogeneous mixtures. Cytogens are short synthetic peptides designed to reproduce single defined active sequences. Cartalax is positioned as the cartilage Cytogen.
The AED tripeptide is the shortest of the Khavinson Cytogens at three residues. It shares the AED core with Cardiogen (AEDR tetrapeptide for cardiac tissue), Epitalon (AEDG tetrapeptide for pineal), and Cortagen (AEDP tetrapeptide for cortex). The shared AED core suggests common upstream chromatin-binding chemistry, with the C-terminal extensions claimed to direct tissue specificity. The plausibility of strict tissue-selective targeting from such minimal sequence differences remains debatable in independent reviews.
The Evidence
The compound-specific evidence base consists of:
Chondrocyte and fibroblast proliferation work. Cell culture studies have reported that Cartalax stimulates proliferation of chondrocytes and fibroblasts in both young and aged rat tissue cultures. The effect is observed at picomolar to nanomolar concentrations consistent with the broader Khavinson framework.
Aging marker modulation. Cartalax exposure in cell culture has been associated with:
- Reduction in pro-apoptotic p53 expression
- Reduction in senescence-associated p16 and p21 expression
- Increase in SIRT6 expression (associated with longevity in animal models)
- Reduction in MMP-9 activity (matrix-degrading enzyme)
- Modulation of Ki-67 proliferation marker
Skin fibroblast studies (Linkova et al., 2016). Cartalax effects on skin fibroblasts during in vitro aging documented restoration of proliferation rates and matrix protein synthesis patterns characteristic of younger cells.
Kidney cell renewal (Khavinson 2014). Studies in organotypic kidney tissue cultures from young and aged rats reported that Cartalax promotes cellular proliferation, extending the proposed mechanism beyond cartilage tissue.
Independent Western confirmation is sparse. PubMed indexing returns predominantly Khavinson-affiliated publications. No registered ClinicalTrials.gov trial exists for Cartalax as of May 2026.
Regulatory and Legal Status
FDA. No approval. Not on bulk drug substances list.
EMA. No approval.
Russia. Sold as a biologically active dietary supplement.
WADA. Not on 2026 Prohibited List.
Mechanism of action
The proposed mechanism is consistent with the broader Khavinson short-peptide bioregulation framework, with claimed cartilage-tissue specificity through structural similarity to type XI collagen.
Type XI collagen connection. The AED sequence corresponds to a motif in the alpha-1 chain of type XI collagen, providing the structural rationale for cartilage-targeting. Type XI collagen plays a key role in regulating type II collagen fibril diameter and overall cartilage extracellular matrix organization. The proposed model is that the AED tripeptide acts as a signaling mimetic of this collagen motif, providing feedback signaling to chondrocytes about extracellular matrix status.
Cellular entry and nuclear localization. AED is hypothesized to enter chondrocytes and other cells through peptide transporters, reach the nucleus, and modulate gene expression. The two acidic residues (Glu, Asp) and one neutral residue (Ala) provide a net negative charge under physiological conditions, supporting hypothesized interactions with histone proteins and nucleic acids.
Senescence pathway modulation. Cartalax exposure has been associated with reduction in pro-apoptotic p53 expression and senescence markers p16 and p21, alongside increase in SIRT6 expression. The combined effect pattern is positioned as "anti-senescence" cellular reprogramming, though independent confirmation in transcriptomic studies is limited.
Cartilage-specific effects. In chondrocyte cultures, Cartalax has been reported to:
- Stimulate proliferation in both young and aged cells
- Reduce apoptosis under stress
- Modulate extracellular matrix gene expression
- Affect inflammatory cytokine production
- Inhibit matrix metalloproteinase activity (MMP-9 specifically)
Pharmacokinetics. Tripeptides face significant gut hydrolysis after oral administration. The Khavinson framework proposes signaling at the gut-mucosa interface propagated systemically. Direct measurement of intact Cartalax in plasma after administration has not been published.
Human pharmacokinetic data is not published.
Reported effects
Cell culture and animal model data report:
- Stimulation of chondrocyte proliferation in young and aged rat models
- Stimulation of skin and other fibroblast proliferation
- Reduction in senescence-associated markers (p16, p21)
- Reduction in pro-apoptotic p53 expression
- Increase in SIRT6 expression
- Inhibition of cartilage-degrading MMP-9
- Effects on kidney epithelial cell renewal
- Possible chondroprotective effects in animal osteoarthritis models
Research-chemical user reports describe subjective improvements in joint comfort and recovery from athletic training. Reports are uncontrolled, unverified for vial identity, and confounded by simultaneous lifestyle modifications. The osteoarthritis-treatment positioning that some vendors emphasize is not supported by any controlled human trial.
Dosing in research
No standardized human dosing protocol supported by independent pharmacokinetic data exists for Cartalax.
Russian retail Cartalax is dosed as 1 to 2 capsules once or twice daily before meals for a 30-day course, repeated 2 to 3 times per year. Each capsule contains approximately 20 mg of active peptide.
Research-chemical Cartalax is sold as lyophilized powder in 20 mg vials. Subcutaneous protocols in user communities typically use 200 to 500 mcg per day over 10 to 20 day cycles. Some user protocols use higher doses of 1 to 5 mg per day. These doses are extrapolated from generic Khavinson recommendations and lack Cartalax-specific human pharmacokinetic support.
The course-and-cycle pattern is standard Khavinson protocol. Optimal cycle spacing for Cartalax has not been independently validated.
Side effects & safety
The Khavinson bioregulator class has a benign published adverse-event profile. Russian manufacturer documentation for Cartalax lists individual intolerance, pregnancy, and lactation as contraindications. No serious adverse events have been reported in Russian-language publications.
The constituent amino acids (alanine, glutamic acid, aspartic acid) are common dietary amino acids. Tripeptide doses at the microgram-to-milligram level fall within typical dietary peptide exposure. Acute toxicity is mechanistically unlikely.
Long-term human safety data with controlled endpoints does not exist. Theoretical concerns specific to chronic use:
- Effects on chondrocyte proliferation with chronic high-dose exposure are uncharacterized
- The reported effects on senescence pathways (p16, p21, p53 reduction; SIRT6 elevation) could in principle affect tumor surveillance; this concern has not been formally evaluated
- Drug-drug interactions with NSAIDs, intra-articular corticosteroids, hyaluronic acid injections, and disease-modifying osteoarthritis drugs have not been studied
- Effects in patients with rheumatoid arthritis, gout, or other inflammatory arthropathies have not been evaluated
The compound's claimed effects on cellular senescence markers, if accurate, would warrant more careful long-term safety evaluation than has been performed.
Stacks & combinations
Within the Khavinson system, Cartalax is the synthetic cartilage Cytogen. The standard Cytogen-then-Cytomax sequence does not have a widely marketed cartilage-specific Cytomax counterpart, so Cartalax is typically used as a standalone Cytogen or paired with other tissue-specific compounds.
For musculoskeletal-focused stacks, Cartalax combines with research-chemical peptides like BPC-157 and TB-500 (broader tissue-healing claims), though the combination has not been studied in any controlled setting. For broader Khavinson geroprotective protocols, Cartalax joins Epitalon, Cardiogen, and other organ-specific bioregulators.
External pharmaceutical comparators for osteoarthritis and cartilage health have varied evidence bases:
- NSAIDs (oral and topical) for symptomatic relief, substantial Phase 3 evidence
- Intra-articular corticosteroid injections for acute flares, established short-term efficacy
- Intra-articular hyaluronic acid for knee osteoarthritis, mixed evidence base
- Glucosamine and chondroitin sulfate as widely used supplements with mixed evidence
- Surgical interventions (arthroscopy, osteotomy, joint replacement) for advanced disease
- Weight management and exercise therapy as first-line evidence-based interventions
Cartalax has no comparable evidence base for any specific musculoskeletal indication and is not a substitute for evidence-based osteoarthritis care.
For informational and educational purposes only. Not medical advice. Not for human consumption unless prescribed by a licensed physician for an FDA-approved indication. Consult a qualified healthcare provider before using any peptide or pharmaceutical product.
Frequently asked questions
What is Cartalax?
Cartalax is a synthetic tripeptide with the amino acid sequence Ala-Glu-Asp (AED), molecular weight 333.29 g/mol. It belongs to the Khavinson Cytogen class and is positioned as the cartilage and connective tissue bioregulator. The AED sequence is reported to correspond to a motif found in the alpha-1 chain of type XI collagen, a structural protein important for cartilage integrity.
Is Cartalax FDA-approved?
No. Cartalax has no FDA or EMA approval. It is sold as a research chemical and is not authorized for human consumption.
Does Cartalax repair cartilage?
Cell culture studies have reported that Cartalax stimulates chondrocyte (cartilage cell) proliferation in both young and aged rat models, and modulates markers including Ki-67 (proliferation), caspase-3 (apoptosis), and MMP-9 (matrix degradation). Animal studies have suggested potential for chondroprotection in osteoarthritis models. No human clinical trial has been published, and translation to clinically meaningful cartilage repair in humans is unproven.
How is Cartalax different from BPC-157 or TB-500?
Different mechanisms and tissue targets. BPC-157 and TB-500 are 15-amino-acid and longer peptides with broader tissue healing claims operating through different pathways (BPC-157 through nitric oxide and angiogenesis; TB-500 through actin-binding and progenitor cell mobilization). Cartalax is a Khavinson Cytogen tripeptide claimed to operate through chromatin and gene-expression effects in chondrocytes specifically. The compounds are not interchangeable, and head-to-head comparative evidence does not exist.
Is Cartalax banned by WADA?
Cartalax is not on the 2026 WADA Prohibited List. Athletes should verify status with their sport governing body before use of any tissue-repair-positioned compound.
How is Cartalax administered?
Russian retail Cartalax is sold as oral capsules containing approximately 20 mg of active peptide. Standard Russian-protocol dosing is 1 to 2 capsules once or twice daily before meals for a 30-day course, repeated 2 to 3 times per year. Research-chemical subcutaneous protocols typically use 200 to 500 mcg per day.
Can Cartalax treat osteoarthritis?
No. Diagnosed osteoarthritis requires evidence-based management under physician supervision. Established approaches include weight management, exercise therapy, physical therapy, NSAIDs, intra-articular injections (corticosteroids, hyaluronic acid in some contexts), and joint replacement for severe disease. Cartalax has no comparable evidence base and is not a substitute for these established interventions.
References
- [1] Khavinson VK et al., 2014 — Tripeptides slow aging in renal cell culture
- [2] Linkova NS et al., 2016 — Peptide regulation of skin fibroblast functions during aging
- [3] Khavinson VK et al., 2020 — Short peptides skin regulation during aging
- [4] Khavinson VK et al., 2020 — Short peptides interaction with DNA
- [5] WADA 2026 Prohibited List
- [6] FDA Drug Approvals Database
Educational content only
This information is provided for research and educational purposes. It is not medical advice, diagnosis, or treatment. Many peptides described are not approved for human use outside clinical trials. Always consult a qualified healthcare professional before using any compound.
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