Overview
Overview
Cartalax is a synthetic tripeptide bioregulator (Ala‑Glu‑Asp; sequence “AED”) developed by Prof. Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology[1]. Preclinical studies indicate it may modulate fibroblast proliferation markers (Ki‑67), reduce pro‑apoptotic signaling (p53, caspase‑3), and support extracellular matrix homeostasis[2][3]. Note: Published human posology for subcutaneous Cartalax is limited; this framework extrapolates from available preclinical and
- Category
- Longevity
- Routes
- subcutaneous
Mechanism
Cartalax
Mechanism of action
Mechanism of action
Cartalax (Ala‑Glu‑Asp) is classified among the Khavinson bioregulatory peptides—ultrashort peptides that may interact with DNA and modulate gene expression at nanomolar concentrations [1] [4] . The peptide sequence corresponds to a motif found in the alpha‑1 chain of type XI collagen, a structural protein important for cartilage integrity [5] . In preclinical fibroblast and chondrocyte culture models, Cartalax has been reported to upregulate Ki‑67 (a proliferation marker), increase SIRT‑1/SIRT‑6 expression, reduce p53 and caspase‑3 activity (pro‑apoptotic signals), and inhibit MMP‑9 synthesis (an enzyme linked to extracellular matrix degradation) [2] [3] [6] .
Key research findings
- 01
In vitro (human cells, cartilage/chondrogenesis): In a replicatively aged human mesenchymal stem cell model, the AED tripeptide (200 ng/mL) increased expression of chondrogenic differentiation markers SOX9, aggrecan, type II collagen, and COMP, comparable to a cartilage polypeptide complex used at 2000 ng/mL (According to PubMed: PMID 37782646, Adv Gerontol 2023; no DOI). This is the central finding behind Cartalax's joint/cartilage research positioning.
- 02
In vitro (human chondrocytes, cellular aging): In an aging chondrocyte model, AED reduced markers of the aging-associated secretory phenotype (p16, p21, p53, and the pro-inflammatory mediators TNF-alpha and IL-1alpha) and restored Sirt1, an observed effect in research framed as chondrocyte geroprotection (According to PubMed: PMID 37356100, Adv Gerontol 2023; no DOI).
- 03
In vitro (human mesenchymal stem cells, aging gene expression): At nanomolar concentrations, AED (alongside KED and KE) modulated genes implicated in cellular aging, increasing IGF1 expression roughly 3.5-5.6-fold and stimulating NF-kappaB gene expression across two stem-cell aging models (According to PubMed: PMID 32399807, Mol Biol Rep 2020, [DOI](https://doi.org/10.1007/s11033-020-05506-3)).
- 04
In vitro (fibroblasts, skin aging model): During fibroblast aging in culture, AED suppressed MMP-9 (a matrix-degrading enzyme that rises with aging), increased the proliferation marker Ki-67 and CD98hc, and (together with the tetrapeptide AEDG) reduced caspase-3-dependent apoptosis (According to PubMed: PMID 27259496, Bull Exp Biol Med 2016, [DOI](https://doi.org/10.1007/s10517-016-3370-x)).
- 05
In vitro (rodent renal cells/tissue) + in silico: In aging renal cell and organotypic kidney cultures, AED (lab code T-31) increased proliferation and lowered p16/p21/p53 while raising SIRT-6, though less potently than the parent polypeptide complex; molecular docking modeled AED binding in the DNA minor groove, the basis for the proposed epigenetic/gene-regulatory mechanism (According to PubMed: PMID 25946838, Adv Gerontol 2014, no DOI; PMID 26033601, Bull Exp Biol Med 2015, [DOI](https://doi.org/10.1007/s10517-015-2906-9)).
- 06
Research maturity / honest limits: Effects are tissue- and context-dependent, not universal - in a thymocyte aging model AED (T-31) was tested but a related peptide (AB-9) showed the more complete geroprotective profile (According to PubMed: PMID 22238759, [DOI](https://doi.org/10.1007/s10517-011-1298-8)). A 2023 review asserts AED ('Kartalax') has been used in animal osteoarthritis models and given orally to older osteoarthritis patients (PMID 37782637), but no controlled human trial is indexed in PubMed and ClinicalTrials.gov lists no registered trials, so those clinical claims are not independently verifiable.
Primary source: Limited peer-reviewed data. According to PubMed, the research base specific to Cartalax (the synthetic tripeptide Ala-Glu-Asp / AED, also transliterated Kartalax and coded T-31) is small and early-stage: roughly eight AED-specific primary papers, essentially all in vitro cell-culture or in silico molecular-docking studies, produced almost entirely by the St. Petersburg Institute of Bioregulation and Gerontology (Khavinson group) and a few collaborators, with the cartilage/chondrocyte-focused work appearing only in 2023. There are genuine indexed citations, but no independently replicated controlled human trials, no accessible primary whole-animal in vivo data, and several key cartilage papers are Russian-language abstracts in a low-impact specialty journal (Advances in Gerontology) without DOIs.
Researched Effects
Researched benefits
Areas of active research and investigation. Results may vary and are based on preclinical or early clinical data.
May support fibroblast proliferation and reduce markers of cellular senescence in aged cell cultures[2][3].
Preclinical data suggest modulation of extracellular matrix homeostasis via MMP‑9 inhibition and collagen‑related gene expression[6].
Protocol Reference
Protocol reference
Commonly cited research range: 2–5 mg, daily.
Reference figures reported in the research literature — not a dosing recommendation. For interactive vial math and scheduling, see the Calculator and Schedule tabs.
Cited protocol & reconstitution guide
Source-backed reference fields by phase, including any volume fields authored in the cited guide.
Weeks 1–2
2 mg
Weeks 3–4
3 mg
Weeks 5–8
4 mg
Weeks 9–12
5 mg
Days 1–20 (separate non-validated schedule)
10 mg
| Phase | Reference amount | Units / volume |
|---|---|---|
| Weeks 1–2 | 2 mg | 20 units (0.20 mL) |
| Weeks 3–4 | 3 mg | 30 units (0.30 mL) |
| Weeks 5–8 | 4 mg | 40 units (0.40 mL) |
| Weeks 9–12 | 5 mg | 50 units (0.50 mL) |
| Days 1–20 (separate non-validated schedule) | 10 mg | 100 units (1.00 mL) |
Titration protocol
- Weeks 1–2Start2 mg once daily
0.30 mL = 30 units on a U-100 syringe at 20 mg vial + 3 mL. Phase total 28 mg; running total 28 mg.
- Weeks 3–4Build3 mg once daily
0.45 mL = 45 units at 20 mg + 3 mL. Phase total 42 mg; running total 70 mg.
- Weeks 5–8Build4 mg once daily
0.60 mL = 60 units at 20 mg + 3 mL. Phase total 112 mg; running total 182 mg.
- Weeks 9–12Build5 mg once daily
0.75 mL = 75 units at 20 mg + 3 mL. Phase total 140 mg; running total 322 mg.
- Days 1–20 (separate non-validated schedule)Maintenance10 mg once daily
1.50 mL = 150 units at 20 mg + 3 mL exceeds one full 100-unit syringe — split into two equal draws of 75 units (0.75 mL). Weekly total 70 mg; a 20 mg vial lasts 2 days.
Storage & Handling
Storage requirements(typical for most peptides)
Can be stored for extended periods. Protect from moisture.
Store in refrigerator door. Never freeze after reconstitution.
Label vials with reconstitution date. Discard if cloudy.
Reconstitution steps
- 01🌡️Confirm the vial amount — use the total milligrams printed on the vial. This vial contains 20 mg.
- 02🧴Draw 2 mL bacteriostatic water into a sterile syringe — this 20 mg vial yields 10 mg/mL.
- 03💉Important: This guide is for educational purposes only and is not medical advice. For research use only. Not for human consumption.
Additional storage notes
Store at 2–8 °C (35.6–46.4 °F) or freeze at −20 °C (−4 °F) for long‑term stability; protect from light and moisture [11] .
Refrigerate at 2–8 °C (35.6–46.4 °F); avoid freeze–thaw cycles .
Allow vials to reach room temperature before opening to reduce condensation uptake.
Clinical Evidence
Clinical evidence
Preclinical Khavinson-program research reports tissue-specific peptide regulation; human data are absent.
Limited peer-reviewed data. According to PubMed, the research base specific to Cartalax (the synthetic tripeptide Ala-Glu-Asp / AED, also transliterated Kartalax and coded T-31) is small and early-stage: roughly eight AED-specific primary papers, essentially all in vitro cell-culture or in silico molecular-docking studies, produced almost entirely by the St. Petersburg Institute of Bioregulation and Gerontology (Khavinson group) and a few collaborators, with the cartilage/chondrocyte-focused work appearing only in 2023. There are genuine indexed citations, but no independently replicated controlled human trials, no accessible primary whole-animal in vivo data, and several key cartilage papers are Russian-language abstracts in a low-impact specialty journal (Advances in Gerontology) without DOIs.
- 01In vitro (human cells, cartilage/chondrogenesis): In a replicatively aged human mesenchymal stem cell model, the AED tripeptide (200 ng/mL) increased expression of chondrogenic differentiation markers SOX9, aggrecan, type II collagen, and COMP, comparable to a cartilage polypeptide complex used at 2000 ng/mL (According to PubMed: PMID 37782646, Adv Gerontol 2023; no DOI). This is the central finding behind Cartalax's joint/cartilage research positioning.
- 02In vitro (human chondrocytes, cellular aging): In an aging chondrocyte model, AED reduced markers of the aging-associated secretory phenotype (p16, p21, p53, and the pro-inflammatory mediators TNF-alpha and IL-1alpha) and restored Sirt1, an observed effect in research framed as chondrocyte geroprotection (According to PubMed: PMID 37356100, Adv Gerontol 2023; no DOI).
- 03In vitro (human mesenchymal stem cells, aging gene expression): At nanomolar concentrations, AED (alongside KED and KE) modulated genes implicated in cellular aging, increasing IGF1 expression roughly 3.5-5.6-fold and stimulating NF-kappaB gene expression across two stem-cell aging models (According to PubMed: PMID 32399807, Mol Biol Rep 2020, [DOI](https://doi.org/10.1007/s11033-020-05506-3)).
- 04In vitro (fibroblasts, skin aging model): During fibroblast aging in culture, AED suppressed MMP-9 (a matrix-degrading enzyme that rises with aging), increased the proliferation marker Ki-67 and CD98hc, and (together with the tetrapeptide AEDG) reduced caspase-3-dependent apoptosis (According to PubMed: PMID 27259496, Bull Exp Biol Med 2016, [DOI](https://doi.org/10.1007/s10517-016-3370-x)).
- 05In vitro (rodent renal cells/tissue) + in silico: In aging renal cell and organotypic kidney cultures, AED (lab code T-31) increased proliferation and lowered p16/p21/p53 while raising SIRT-6, though less potently than the parent polypeptide complex; molecular docking modeled AED binding in the DNA minor groove, the basis for the proposed epigenetic/gene-regulatory mechanism (According to PubMed: PMID 25946838, Adv Gerontol 2014, no DOI; PMID 26033601, Bull Exp Biol Med 2015, [DOI](https://doi.org/10.1007/s10517-015-2906-9)).
- 06Research maturity / honest limits: Effects are tissue- and context-dependent, not universal - in a thymocyte aging model AED (T-31) was tested but a related peptide (AB-9) showed the more complete geroprotective profile (According to PubMed: PMID 22238759, [DOI](https://doi.org/10.1007/s10517-011-1298-8)). A 2023 review asserts AED ('Kartalax') has been used in animal osteoarthritis models and given orally to older osteoarthritis patients (PMID 37782637), but no controlled human trial is indexed in PubMed and ClinicalTrials.gov lists no registered trials, so those clinical claims are not independently verifiable.
Evidence maturity varies by compound; much peptide research is preclinical (in vitro or animal-model). Where human data are limited, findings should be read as research observations, not clinical conclusions.
References
Literature references
Published research articles and sources related to Cartalax.
- 01Neuroendocrinology Letters (2002) — Khavinson VK. Peptides and Ageing. Overview of bioregulatory peptide development and geroprotective mechanisms. View Sourceet al. (2002)
- 02Bulletin of Experimental Biology and Medicine (2016) — Lin’kova NS et al. Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro. AED peptide effects on Ki‑67, CD98hc, caspase‑3, and MMP‑9. View Sourceet al. (2016)
- 03Bulletin of Experimental Biology and Medicine (2014) — Khavinson VK et al. Peptides regulate the expression of signaling molecules in kidney cell cultures during in vitro aging (p53, p16, SIRT‑6). View Sourceet al. (2014)
- 04Molecular Biology Reports (2020) — Ashapkin V, Khavinson V et al. Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides. View Sourceet al. (2020)
- 05International Journal of Molecular Sciences (2023) — Linkova N, Khavinson V et al. Peptide Regulation of Chondrogenic Stem Cell Differentiation. View Sourceet al. (2023)
- 06Advances in Gerontology (2020) — Khavinson VK, Linkova NS et al. Short peptides: regulation of skin function during aging (collagen, SIRT‑1/‑6, MMP regulation). View Sourceet al. (2020)
- 07PubChem — Compound summary for Cartalax (AED peptide; CID 87815447): molecular formula C₁₂H₁₉N₃O₈, MW 333.29. View Source
- 08CDC — Vaccine administration: subcutaneous route (angle/site; no aspiration). View Source
- 09Advances in Therapy (PubMed) — Subcutaneous injection factors and tolerability; practical volume considerations. View Source
- 10StatPearls (NCBI Bookshelf) — Medication routes of administration; cautions for large single‑site SC volumes. View Source
- 11Bachem — Handling and Storage Guidelines for Peptides (lyophilized and reconstituted stability). View Source
- 12NCBI Bookshelf — Best practices for injection (asepsis, preparation, and administration). View Source
- 13Pure Lab Peptides — Cartalax (20 mg) product page (quality and batch documentation). View Source
Observed Effects
Observed effects in cited research
Reported
- General tolerability: Khavinson bioregulator peptides have been described as well tolerated in observational settings; occasional mild injection‑site reactions (redness, itch) may occur with subcutaneous
Research Considerations
Research considerations
Research Use Only - not for human or veterinary therapeutic use. Current evidence is limited to in vitro and/or animal-model research; human data are minimal or absent. Consult a licensed healthcare professional for any clinical decisions.
Factors noted in the research literature; not patient-specific medical advice.
Regulatory Status
Regulatory status
RUO
Comparisons
Comparisons
| Compound | Mechanism | Route | Status |
|---|---|---|---|
| Cartalaxthis | A synthetic tripeptide bioregulator (Ala-Glu-Asp) studied for gene-regulatory activity in connective and cartilage tissue, with proposed anti-inflammatory and regenerative effects. | subcutaneous | Investigational / RUO |
| Chonluten | A short tripeptide bioregulator (Glu-Asp-Gly) studied for effects on bronchopulmonary tissue and modulation of inflammatory signaling in monocyte/macrophage models. | subcutaneous | Investigational / RUO |
| Cortagen | A synthetic tetrapeptide (Ala-Glu-Asp-Pro) of the Khavinson bioregulator class studied for neuroprotective and neuroregenerative activity, including peripheral nerve repair. | subcutaneous | Investigational / RUO |
| Epitalon (Epithalon) | A synthetic tetrapeptide (Ala-Glu-Asp-Gly) studied for activation of telomerase and modulation of pineal/melatonin and circadian pathways, of interest in geroprotection research. | subcutaneous | Investigational / RUO |
| FOXO4-DRI | A D-retro-inverso peptide designed to disrupt the FOXO4-p53 interaction in senescent cells, releasing p53 to selectively induce apoptosis of senescent cells (a senolytic mechanism). | subcutaneous | Investigational / RUO |
| Cerebrolysin | A porcine brain-derived preparation of low-molecular-weight neuropeptides and free amino acids studied for neurotrophic activity supporting neuronal survival, synaptic plasticity, and modulation of neuroinflammation. | subcutaneous | Investigational / RUO |
| CJC-1295 | Binds to GHRH receptors to stimulate GH release. Modified structure provides extended duration of action (up to 7 days). | subcutaneous | Investigational / RUO |
Attributes shown for research comparison only; not a statement of efficacy or therapeutic equivalence.
FAQ
Frequently asked questions
Cartalax (also transliterated Kartalax) is a synthetic short-peptide bioregulator - the tripeptide Ala-Glu-Asp (AED, lab code T-31) - developed by the St. Petersburg Institute of Bioregulation and Gerontology. It is a Research Use Only material, not an approved medicine. Note that it is a distinct molecule from Epitalon (AEDG, a tetrapeptide); some non-scientific vendor pages incorrectly list Cartalax as AEDG, but the peer-reviewed literature consistently defines it as the AED tripeptide.
According to PubMed, the indexed evidence is limited and almost entirely in vitro or in silico. Studies report increased chondrogenic markers (SOX9, aggrecan, type II collagen, COMP), reduced senescence/SASP markers in aging chondrocytes, modulation of aging-associated genes in stem cells, and proliferation and anti-apoptotic signals in cultured fibroblasts and renal cells. These are mechanistic, cell-level observations in research, not demonstrated clinical outcomes.
Most AED studies use cellular-aging models - replicatively aged stem cells, chondrocytes, fibroblasts, and renal cells - and the 2023 cartilage work frames it as a candidate for studying age-related cartilage and chondrocyte biology and osteoarthritis models. The longevity/joint association comes from these laboratory aging contexts, not from established effects in people.
No controlled human trials specific to Cartalax/AED are indexed in PubMed, and ClinicalTrials.gov returns no registered trials. A 2023 Russian-language review (PMID 37782637) asserts oral use in older osteoarthritis patients and use in animal osteoarthritis models, but the underlying primary data are not accessible in indexed English-language literature, so human efficacy and safety remain unestablished. Pain-reduction percentages circulating on commercial sites are not traceable to verifiable peer-reviewed sources.
The proposed mechanism is epigenetic/gene-regulatory: short peptides are hypothesized to interact with DNA and chromatin to influence transcription. For AED specifically, in silico molecular docking modeled binding within the DNA minor groove (PMID 25946838), and related tetrapeptide work modeled histone binding. This remains a working hypothesis supported mainly by computational modeling and cell-culture gene-expression changes rather than by definitive target validation.
This is a Research Use Only material and the following is not medical advice. Research-reported handling and concentrations vary by experimental model - for example, cell-culture studies used nanomolar concentrations or about 200 ng/mL - and no validated human dosing is established. For any protocol parameters, consult the specific protocol reference for the study in question rather than generalized figures, and treat dosing numbers found on vendor pages as unverified.
The body of work is small, largely from a single research network, concentrated in low-impact and partly non-English journals (some without DOIs), and dominated by in vitro and in silico methods with no independent replication and no controlled human data. Findings should be read as preliminary research signals warranting further study, not as established effects.
Research-use notice
Research Use Only. This educational content and calculation support is intended for private research documentation. It does not provide medical advice, human-use directions, or claims of safety or effectiveness.