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A specimen of the Repair & Recovery drawer Drawer B · Repair & Recovery

Cartalax

Research Only

A synthetic tripeptide (Ala-Glu-Asp) from Vladimir Khavinson's bioregulator framework, proposed to support cartilage tissue repair and chondrocyte function. All research originates from Russian institutes with no independent Western validation or controlled human clinical trials.

AED peptide · Ala-Glu-Asp · cartilage bioregulator

Research evidence
Very Low

Preclinical evidence only

Preclinical
63%
Clinical
0%

Based on 8 cited sources

Evidence Score27/100
Preliminary
Research Depth17/100
Mechanism32/100
Plausibility56/100
Global Coverage13/100
Community Experience15/100
EffectivenessNot Established

Demonstrated effect magnitude — not a recommendation or safety claim.

Research depth: only single-group in-vitro (MSC/chondrocyte/fibroblast) and a few animal OA models; an unstructured mention of oral use in elderly OA patients lacks any described controlled design, so no creditable human tier. Mechanism: AED modulates Ki-67/CD98hc/MMP9/SASP markers in cell models but target is inferred with no binding/knockout validation. Plausibility: chondrogenic-marker (SOX9, COL2, aggrecan) coherence is decent though mechanism-to-cartilage-outcome links remain unproven. Global coverage: all work originates from the Khavinson/Linkova St. Petersburg group with no independent or non-Russian replication. Community experience: negligible — no meaningful user reports. Effectiveness not-established: no quantified human efficacy estimate and no meaningful community effect signal.

Scored May 2026 How we rate →
!!
Evidence Level
very low
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 3 AA · 333 Da
Also Known As
AED peptide • Ala-Glu-Asp • cartilage bioregulator
Class
Tripeptide
Length
3 amino acids
Mol. weight
333 Da
Sequence
AED
Molecular Structure
A
E
D
Hydrophobic
Polar
Positive
Negative

The proposed mechanisms of Cartalax are based entirely on Russian bioregulator research. No independent Western validation or controlled human clinical trials exist.

How It Works (Simplified)

Cartalax is proposed to target cartilage tissue through peptide bioregulation:

Cell Penetration

Short tripeptide (AED) proposed to penetrate cell membranes and interact with DNA/chromatin in chondrocytes.

Proposed upregulation of ECM synthesis genes (collagen, proteoglycans) and proliferation markers (Ki-67, CD98hc).

Matrix Protection

Proposed inhibition of MMP-9, an enzyme that degrades cartilage extracellular matrix.

Anti-Senescence

Proposed reduction of cellular aging markers (p16, p21, p53) and upregulation of longevity-associated SIRT-6.

Note: These pathways are theoretical and based on in-vitro/animal studies from a single research group. No human pharmacological validation exists.

Key Research: Linkova N et al. IJMS 2023;24(9):8415

Important Limitations

  • 100% of published research originates from Russian institutes (primarily Khavinson’s group at St. Petersburg Institute of Bioregulation and Gerontology)
  • No independent Western replication of any Cartalax-specific findings
  • No controlled human clinical trials — all evidence is preclinical (cell culture and animal models)
  • The bioregulator framework’s proposed mechanism (short peptides interacting with DNA) remains unvalidated by mainstream molecular biology
  • Do not confuse with Epithalon (AEDG) — different peptide with different proposed targets despite similar sequence
  • No human pharmacokinetic, dosing, or safety data exists
i. Chondrocyte Gene Regulation · Proposed
Cartalax (AED tripeptide)Cell membrane penetrationDNA/chromatin interactionGene expression modulation
ECM synthesis genes ↑ (collagen, proteoglycans)
Ki-67, CD98hc ↑ (proliferation/regeneration)
MMP-9 ↓ (matrix degradation)
p16/p21/p53 ↓, SIRT-6 ↑ (anti-senescence)

Net effect.Proposed cartilage tissue maintenance — theoretical, from in-vitro/animal work by a single research group.

Mechanism Chondrocyte gene regulation promoting cartilage matrix synthesis
Emerging 3 direct studies
Benefit may support cartilage tissue repair and chondrocyte function
Evidence Level
Very Low
2 Animal
1 In Vitro
Mechanism MMP-9 inhibition reducing cartilage extracellular matrix degradation
Emerging 2 direct studies
Benefit suggested to preserve cartilage matrix integrity
Evidence Level
Very Low
1 Animal
1 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Week 1-2

Theoretical: Peptide-DNA interactions begin at cellular level. No measurable effects expected. Based on bioregulator framework claims — no human pharmacokinetic data exists.

Phase 02 2
Week 2-4

Theoretical: Gene expression changes in target tissues may begin. Proposed upregulation of ECM synthesis pathways. Based on cell culture studies only.

Phase 03 3
Month 1-3

Theoretical: Accumulated effects on cartilage matrix may become relevant. Russian protocols suggest this timeframe for tissue-level changes. No controlled human data.

Phase 04 4
Month 3-6

Theoretical: Maximal proposed benefit window per Khavinson bioregulator framework. No long-term human safety or efficacy data available.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Good Signs (6 indicators)
Published in indexed Western journals (IJMS, Molecules)
Defined amino acid sequence (AED — Ala-Glu-Asp, 3 amino acids)
Consistent with broader Khavinson bioregulator research framework
Certificate of analysis confirming tripeptide identity
Mass spectrometry confirmation (~333 Da)
HPLC verification of AED sequence
Warning Signs (5 indicators)
All research from a single research group (Khavinson lab)
No independent Western replication
Cell culture and animal models only
No human pharmacokinetic data
Unclear manufacturing source
Bad Signs (6 indicators)
Claims of proven cartilage repair in humans (no human trials exist)
Confusion with Epithalon (AEDG — a different peptide with 4 amino acids)
Vendor marketing claiming clinical validation
Any dosing recommendations (no human dose-finding studies)
No certificate of analysis
Cannot verify sequence identity
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Synergistic
Compatible
Caution
Avoid

Both Khavinson bioregulator peptides with distinct targets — Cartalax for cartilage/chondrocytes, Epithalon for pineal/telomerase. Often referenced together in Russian bioregulator protocols. Note: Cartalax (AED) shares three of four amino acids with Epithalon (AEDG) but targets different tissues.

Different mechanisms for connective tissue support. BPC-157 has broader tissue repair evidence from non-Russian research. No known pharmacological interaction.

Complementary tissue repair mechanisms. TB-500 (thymosin beta-4) promotes cell migration and tissue remodeling. No known interaction with short bioregulator peptides.

Both target cartilage/joint tissue in the bioregulator framework. Sigumir is a cytamin-class complex extract; Cartalax is a defined tripeptide. Often paired in Russian cartilage protocols.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

8 Sources 0 Human 5 Preclinical

Full reference list available on request. All citations link to PubMed for verification.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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