Cartalax 20 mg peptide vial with white lyophilized powder, labeled Batch No.004, dated 14-01-2026, pharmaceutical glass vial with rubber stopper and metal seal.

Cartalax 20mg vial

€40,00 EUR
Přejít na informace o produktu
Cartalax 20 mg peptide vial with white lyophilized powder, labeled Batch No.004, dated 14-01-2026, pharmaceutical glass vial with rubber stopper and metal seal.
Cartalax 20mg vial

Cartalax 20mg vial

€40,00 EUR
Včetně daní.

                                               NOT FOR HUMAN CONSUMPTION

Cartalax (AED / AC-4): synthesized cartilage bioregulator peptide 


Cartalax is commonly described as a short, synthesized “tissue-specific” peptide bioregulator for cartilage, often referenced as the tripeptide AED (Ala-Glu-Asp) and/or peptide complex AC-4 (marketed in some regions as a dietary supplement/BAA, and separately sold by research vendors as a lyophilized peptide).

Core concept
The “bioregulator” framing is that ultrashort peptides like AED may influence gene expression and reparative programs in cartilage-relevant cells (e.g., MSCs/chondrocyte-like systems), potentially supporting cartilage homeostasis and repair pathways relevant to degenerative joint/spine disorders. 

Additional benefits now under investigation (Cartalax/AED-centered)

BENEFIT KEY TAKE-AWAYS
1) Joint/spine symptom improvement signals Vendor/bioregulator materials describe pain and symptom improvement in degenerative spine/joint conditions and report “clinical study” use in osteochondrosis/osteoarthritis contexts, but details are often not presented as full peer-reviewed RCTs.
2) Chondro-/geroprotective gene programs A chondrogenesis review notes AED (Ala-Glu-Asp) within cartilage peptide complexes and summarizes effects on NFκB, IGF1, TNKS2 expression in MSC aging models, positioning it as “chondro/geroprotective.”
3) MSC/chondrocyte support (preclinical) The same review links AED to MSC metabolism/differentiation and fibroblast proliferation/apoptosis markers in aging models—used as mechanistic rationale for cartilage repair interest.
4) Musculoskeletal recovery concept A scientific lecture/source (Institute-affiliated) describes Cartalax (AED) as derived from cartilage complex analysis and positioned for arthrosis/arthritis/osteochondrosis/osteoporosisprevention/adjunct use—again, mostly programmatic + preclinical framing.
5) “Cartilage ECM normalization” hypothesis Commercial and institute-adjacent descriptions repeatedly frame Cartalax as supporting connective tissue/cartilage normalization, consistent with its positioning as a cartilage bioregulator rather than a receptor agonist drug.

Evidence quality note: The most concrete peer-reviewed material you can cite today is mechanistic/biological discussion (e.g., MSC gene expression effects in review context). Claims of broad clinical benefit often come from non-RCT marketing/lecture/vendor documents rather than widely indexed, high-quality multicenter trials.

2) Molecular mechanism of action

2.1 “Pharmacodynamics” framing (how it’s typically described)

Cartalax/AED is discussed as an ultrashort peptide potentially capable of modulating gene expression and cellular programs relevant to cartilage repair and inflammation (as part of the broader peptide bioregulator paradigm).

2.2 Down-stream biology (summarized from the chondrogenesis review)

PATHWAY FUNCTIONAL OUTCOME CONTEXT
NFκB-linked signaling AED reported to affect NFκB gene expression in MSC aging models; review suggests relevance to inflammatory regulation in OA contexts. MSC aging / OA rationale
IGF1 AED reported to stimulate IGF1 gene expression in MSC aging models (review inference: supports synthetic/anabolic processes). MSC aging / tissue repair rationale
TNKS2 / Wnt-related / cell metabolism AED reported to affect TNKS2 expression (tankyrase-related functions include telomere integrity and Wnt activity, among others). Cell growth/metabolism framing
Proliferation/apoptosis markers Review cites AED effects on markers like Ki67, caspase-3, MMP9 in fibroblast aging models—used to argue reparative potential. Supportive mechanistic evidence

3) Pharmacokinetics

There isn’t a single authoritative, drug-label PK profile for “Cartalax” because it’s sold in supplement/bioregulatorformats and research formats. For ultrashort peptides, exposure is typically shaped strongly by route, formulation, and degradation by peptidases.

4) Pre-clinical and clinical evidence

4.1 Mechanistic / preclinical evidence (stronger)

A peer-reviewed chondrogenic differentiation review explicitly discusses cartilage peptide complexes containing AED (Ala-Glu-Asp) and summarizes gene-expression effects in MSC models relevant to aging/OA biology.

4.2 Human evidence (weaker / often non-standardized reporting)

Institute-adjacent and vendor PDF materials state that “clinical study” work supports benefit in osteochondrosis/osteoarthritis/osteoporosis and post-injury contexts, but these sources typically do not provide full RCT-grade details in the document itself (randomization, endpoints, blinding, etc.).

5) Emerging clinical interests

FIELD RATIONALE STATUS
Osteoarthritis / degenerative spine disease Symptom relief + cartilage repair hypothesis mostly mechanistic + adjunct/real-world claims; robust RCT evidence unclear
“Geroprotective” cartilage support MSC aging gene programs (NFκB/IGF1/TNKS2) early biology/translation stage

6) Safety and tolerability

High-certainty statement: there is no FDA/EMA drug label establishing Cartalax safety/contraindications in the way there is for approved medicines.
Some product documents claim good tolerability/no side effects, but those statements aren’t a substitute for regulated pharmacovigilance and controlled trials.

Practical uncertainties to flag:

  • Product quality/sterility/purity variability across non-regulated supply chains (especially for injectable “research” formats).

  • Immunologic reactions are possible with peptide products (risk depends on formulation/route/purity).

7) Regulatory landscape

  • Investigational / supplement-marketed bioregulator positioning rather than an approved pharmaceutical indication set.

8) Future directions (what would make the claims “real”)

  1. Well-designed clinical trials in OA/degenerative spine disease with standardized endpoints (pain/function scores, imaging, biomarkers).

  2. Clear formulation + route standardization (capsule/lingual vs injectable research peptide are not interchangeable).

  3. Mechanism bridging (showing that the MSC gene-expression effects translate into cartilage structural/clinical outcomes in humans).

Selected references

  • Chondrogenesis review summarizing AED (Ala-Glu-Asp) within cartilage peptide complexes and downstream gene effects:

  • Institute-adjacent lecture PDF describing Cartalax (AED) positioning and musculoskeletal pathology context:

  • Cartalax product PDF claiming clinical study usage and listing AC-4 ingredients:

  • General peptide bioregulator gene-expression review (background)