Peptide Health Lab

Longevity & cellular

Cartalax

FOR RESEARCH PURPOSES ONLY

Also known as: AED tripeptide, Ala-Glu-Asp

Regulatory status
Research only
Evidence grade
Animal studies only

Last reviewed September 1, 2026 · 15 sources

What Cartalax is and how it works

Cartalax is a synthetic tripeptide, Ala-Glu-Asp, abbreviated AED and also written Kartalax. It comes from the short peptide bioregulator programme at the St Petersburg Institute of Bioregulation and Gerontology, and it is marketed as a cartilage-directed member of that family.

Two identity boundaries have to be stated before anything else, because both are routinely crossed in writing about this compound.

AED is not AEDG. Epithalon is the tetrapeptide Ala-Glu-Asp-Gly. Cartalax is the tripeptide Ala-Glu-Asp — the same first three residues, one glycine shorter. They are different molecules with different reported binding behaviour: the transporter modelling work that includes both docks them separately and returns a different score for each at every transporter site.[13] Epithalon's telomerase and lifespan literature is Epithalon's. None of it transfers here.

AED is not the cartilage polypeptide complex. The chondrocyte and stem cell experiments this compound is best known for compared the tripeptide against a polypeptide complex extracted from cartilage tissue, and reported on both.[2][3] The complex is a different preparation with a different composition, and a result belonging to it is not a result belonging to the tripeptide. The same boundary shows up in the kidney work, where an organotypic explant study reported that the tripeptides stimulated proliferation and reduced apoptosis to a lesser degree than the polypeptide complex they were tested against.[8] Where the two are measured side by side, the complex is repeatedly the stronger agent.

The proposed mechanism is the family mechanism: short peptides are said to enter the cell and the nucleus and bind DNA with sequence preference, altering which genes are transcribed. The support for that is computational. Docking work on nineteen short peptides built spatial models of DNA-peptide complexes and placed this tripeptide at the acct sequence.[12] Molecular modelling of twenty-six ultrashort peptides against the LAT and PEPT transporter families included AED among the twenty-six and placed it among the peptides whose calculated scores at LAT1 were stronger than those of known inhibitors.[13] Label all of that proposed: these are docking scores from a supercomputer, not measurements of a peptide crossing a membrane.

What the research actually shows

The primary literature for this tripeptide is small enough to describe completely: two cartilage-adjacent cell experiments, three other cell-culture experiments, two rat kidney experiments, and no trial.

Chondrocytes and chondrogenesis. Investigators characterized the ageing-associated secretory phenotype of chondrocytes as increased synthesis of the pro-apoptotic proteins p16, p21 and p53 and the pro-inflammatory cytokines TNF-alpha and IL-1alpha, with decreased Sirt1, and reported that the AED peptide and the cartilage polypeptide complex both normalized the synthesis of those molecules.[2] A companion paper in the same journal volume, from the same authors, took human mesenchymal stem cells through replicative ageing and reported that AED at 200 ng/ml activated gene expression and protein synthesis of the chondrogenic differentiation markers SOX9, aggrecan, type II collagen and COMP, with the cartilage polypeptide complex reaching the same effect at 2000 ng/ml.[3] That is the cartilage-specific evidence base: two in-vitro experiments, in Russian-language publication, from the originating institute, neither of them involving a joint.

Skin fibroblasts. In human skin fibroblasts undergoing replicative ageing, this tripeptide activated synthesis of sirtuin-1, sirtuin-6 and collagen I, which the authors described as a geroprotective effect; the comparator dipeptide KE did something different, reducing IL-1, NF-kappaB and TGF-beta.[1] An earlier study in the same model reported that this tripeptide and AEDG both suppressed caspase-dependent apoptosis, and that all the peptides tested inhibited MMP-9 synthesis and raised expression of Ki-67 and CD98hc.[6]

Other ageing cell models. In human embryonic bone-marrow mesenchymal stem cells aged by passaging or by stationary holding, this tripeptide and two companions enhanced IGF1 gene expression 3.5- to 5.6-fold at nanomolar concentrations — and all three also stimulated expression of the NF-kappaB gene, in both ageing models.[5] In an ageing renal cell culture whose species the English abstract does not name, this tripeptide and EDL increased proliferation, decreased p16, p21 and p53, and increased sirtuin-6, with DNA-interaction models constructed to explain it.[7] In human periodontal ligament stem cells, a study co-authored with an Italian laboratory reported raised GAP43 and Nestin expression with a mixture of the four peptides tested and with KED alone, and reported no increase attributable to AED by itself.[15]

Living animals. Two rat experiments are indexed, both from a collaboration between a Ukrainian medical university and the originating institute, and both about the kidney. In rats with cisplatin-induced acute renal failure, AED decreased protein excretion and urinary electrolyte concentration; the kidney polypeptide complex and the peptides EDL and AEDG normalized a longer list of parameters, and EDL was the one the authors singled out as producing the potent nephroprotective effect.[9] In old rats, AED increased diuresis 1.2- to 1.4-fold, reduced urine protein concentration and protein excretion 1.5- to 2.8-fold, and increased distal sodium transport and sodium excretion; the authors reported raised antioxidant-enzyme activity and reduced peroxidation and, with the morphology, read that as evidence of no nephrotoxic effect.[10] A third Russian-language report covers kidney tripeptides under the code names T-31 and T-35 in experimental rhabdomyolysis-induced kidney injury; its English abstract names neither the sequence nor the species, so it is recorded here as the outer edge of the indexed record rather than read for a result.[11]

People. There is one sentence. A Russian-language review states that a polypeptide complex of cartilage and bone tissue from young animals, together with the AED tripeptide — which it names as Kartalax — have shown high efficacy in animal models of osteoarthritis and on oral administration in patients with osteoarthritis of older age groups.[4] That sentence is the whole of the human record. It reports no patient count, no design, no endpoint, no duration and no comparator, it attributes the efficacy to the complex and the tripeptide together, and it does not cite an indexed clinical report behind itself.

Where the evidence is weak

On most pages this section qualifies the evidence. Here it is most of what there is to say.

There is no human trial. There is a clause in a review. The distance between "has shown high efficacy on oral administration in patients" and a published trial is the entire distance this page exists to hold open.[4] A reader who encounters that phrasing second-hand will reasonably assume a study sits behind it. None is indexed.

The animal evidence is real, and it is about the wrong organ. The same review also asserts efficacy in animal models of osteoarthritis. PHL searched PubMed under the compound name, the Kartalax spelling, the Ala-Glu-Asp sequence, the T-31 designation and the originating authors, and found no indexed primary report of an osteoarthritis animal model using this tripeptide.[4] What is indexed is renal: acute renal failure and old-rat kidney function.[9][10] A reader arriving for a joint reason should know that no published in vivo experiment has put this tripeptide near cartilage.

In every in vivo experiment, this tripeptide was one of several agents and was not the leading one. Both rat studies tested AED alongside EDL, AEDG and a kidney polypeptide complex, and in both the complex or EDL carried the stronger result.[9][10] The organotypic explant work says the same thing explicitly — the tripeptides acted in the same direction as the complex, to a lesser degree.[8] A compound that is consistently the weaker arm of its own experiments is being described accurately when that is said out loud.

The cartilage evidence is two in-vitro experiments, and it shares its result with a different preparation. Both reported the tripeptide and the cartilage polypeptide complex producing the same effect, at concentrations an order of magnitude apart.[3] Isolated cells in a dish are several removes from a joint, which is a load-bearing structure with a blood supply, an immune compartment and mechanical demands.[2]

One reported effect is not obviously a benefit. Stimulating NF-kappaB expression in ageing mesenchymal stem cells is reported as a finding, not framed as a problem, in a literature that elsewhere counts reduced NF-kappaB as the desirable direction. Both results come from the same research programme.[5][1]

The proposed mechanism has never been measured. Cell entry, nuclear entry and DNA binding are supported here by docking calculations only.[12][13] That is why the mechanism claim on this page is graded below the cell-culture claims rather than above them: a model of how something might work is weaker evidence than a measurement of it working, not stronger.

Almost every paper comes from one institute and its collaborators, and several are Russian-language. The nearest thing to independent involvement is an Italian laboratory co-authoring a stem cell differentiation study, and that study did not credit an effect to this tripeptide alone.[15] No review published outside that community characterizes this tripeptide specifically. Where an English-language abstract is all that is available, this page has limited itself to what that abstract states.[2][7]

Class-level findings are class-level. Several of the papers here studied a family of short peptides and reported this one as a member. A review listing AED among peptides said to activate neural differentiation is not a result about AED.[14][12]

What the compound-level grade means here. The badge reads "animal studies only" because the rubric this site uses puts animal in vivo and cell-culture evidence in that bucket, and this compound has both: two rat kidney experiments and a set of ageing-cell experiments.[10][3] It does not mean the animal work supports the joint claim — it does not, because none of it involved a joint. The human and articular claims are graded anecdotal individually in the evidence table, and that is where a reader should look before drawing any conclusion about people.

Long-term safety is unknown and unstudied. No carcinogenicity assessment, no repeat-dose toxicology, no human pharmacokinetics. A molecule proposed to suppress apoptosis and lower p16, p21 and p53 in aged cells is acting on the machinery that restrains damaged division, and nobody has published what that does over time.[6][7]

Legal and regulatory status

Cartalax is not approved by the FDA for any indication. A search of approved drug products under the Cartalax and Kartalax spellings and under the Ala-Glu-Asp sequence returns no application with this peptide as an active ingredient and no approved labeling, while a control query of the same shape run in the same session returned approved biologic applications as expected. It does not appear in any category of the FDA's list of bulk drug substances nominated for use in compounding under section 503A, in which other research peptides do appear. There is no approved US drug and no dietary supplement listing under either spelling; material carrying the name is distributed for laboratory research use, which is why every mention of it on this site carries research-only framing.

The published record does describe this compound reaching people, and it does so in one place only: a review from the originating institute names the tripeptide under a product name and refers to oral administration in older patients with osteoarthritis.[4] That is a scientific paper's summary of practice, not a regulatory record, and it should not be read as one. Searching for a marketing authorization behind it — a registration of this tripeptide as a medicine in Russia or anywhere else — produced nothing PHL could name, and this page reports that as the boundary of what was checked rather than as a conclusion in either direction. Being sold somewhere is not being approved anywhere, a status granted in one country is not a status in the United States, and neither substitutes for the review the FDA has not conducted. None of it says anything about what is inside a particular container.

PHL does not sell peptides, does not tell anyone where to obtain anything, and takes no position on how unapproved material reaches anyone. What the regulatory status means for a reader is narrower and more useful: there is no label, no approved manufacturer, no assigned indication, and no regulated quality standard behind anything carrying this name.

Questions to bring to a provider

The productive conversation is not "should I try Cartalax." It is "here is the joint problem I actually have, here is what the standard evidence base offers for it, and where does a tripeptide whose entire in vivo literature is about rat kidneys sit relative to that?" Questions worth raising:

  • What is the actual diagnosis — imaging, examination, inflammatory markers — and what does the guideline-level evidence offer for it before anything investigational is discussed?
  • Given that the only published statement about people taking this compound is a clause inside a review with no study behind it, what would a clinician need to see before treating it as evidence at all?[4]
  • Does it change anything to know that the published animal work on this tripeptide is renal rather than articular, and that in those experiments it was tested alongside agents that outperformed it?[9]
  • Does the reported stimulation of NF-kappaB expression in cell culture raise any question for someone with an inflammatory joint condition rather than a degenerative one?[5]
  • If the proposed mechanism involves lowering p16, p21 and p53 in ageing cells, what would be worth knowing about personal or family cancer history before considering anything?[7][6]
  • What functional measure — range of motion, walking distance, a validated joint score — would make it possible to tell whether anything changed, rather than relying on how a joint feels across a season?

A clinician who answers "the published work here is cell culture and rat kidneys" is describing the literature accurately.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Cartilage and chondrogenic markers in cell culture
Animal studies only in vitro

Two in-vitro experiments from the same institute and the same 2023 journal volume. In isolated chondrocytes, the authors characterized the ageing-associated secretory phenotype as increased p16, p21, p53, TNF-alpha and IL-1alpha with decreased Sirt1, and reported that the AED peptide and a cartilage polypeptide complex both normalized the synthesis of those molecules. In human mesenchymal stem cells undergoing replicative ageing, AED at 200 ng/ml activated gene expression and protein synthesis of the chondrogenic differentiation markers SOX9, aggrecan, type II collagen and COMP, with the polypeptide complex reaching the same effect at 2000 ng/ml. In both, the comparator is a different preparation — a polypeptide complex extracted from cartilage tissue, not a synthetic tripeptide — and results belonging to it are not results belonging to AED. Neither experiment used a joint, an animal, or a person.

[2] [3]

Skin fibroblast ageing markers in culture
Animal studies only in vitro

In human skin fibroblasts undergoing replicative ageing, this tripeptide activated the synthesis of sirtuin-1, sirtuin-6 and collagen I, which the authors read as a geroprotective effect; the comparator dipeptide KE instead reduced IL-1, NF-kappaB and TGF-beta. An earlier experiment in the same model reported that this tripeptide and AEDG both suppressed caspase-dependent apoptosis, and that all peptides tested inhibited MMP-9 synthesis and raised Ki-67 and CD98hc. Confocal immunocytochemistry in cell culture, from the originating institute.

[1] [6]

Gene expression in other ageing cell cultures
Animal studies only in vitro

In human embryonic bone-marrow mesenchymal stem cells aged by passaging or by stationary culture, this tripeptide and two companions enhanced IGF1 expression 3.5- to 5.6-fold and stimulated NF-kappaB expression in both models. In an ageing renal cell culture whose species the English abstract does not state, this tripeptide and EDL increased proliferation, decreased the ageing markers p16, p21 and p53, and increased sirtuin-6. Both are cell-culture results.

[5] [7]

Renal function in living rats
Animal studies only animal

Two indexed in vivo rat experiments exist, both from one collaboration between a Ukrainian medical university and the originating institute, and both about the kidney rather than cartilage. In rats with cisplatin-induced acute renal failure, AED decreased protein excretion and urinary electrolyte concentration, while the kidney polypeptide complex and the peptides EDL and AEDG normalized a longer list of parameters and EDL was singled out as the potent nephroprotective agent. In old rats, AED increased diuresis 1.2- to 1.4-fold, reduced urine protein concentration and protein excretion 1.5- to 2.8-fold, and increased distal sodium transport and sodium excretion. A third Russian-language report describes kidney tripeptides under the code names T-31 and T-35 in experimental rhabdomyolysis-induced kidney injury; its English abstract names neither the sequence nor the species, so this page reports it only as the outer edge of what is indexed. In every one of these, AED was one of several agents tested side by side and was not the strongest.

[9] [10] [11]

Joint or cartilage outcomes in a living animal
Anecdotal reports only review

A Russian-language review asserts that the AED tripeptide and a cartilage-and-bone polypeptide complex have shown high efficacy in animal models of osteoarthritis. PHL searched PubMed under the compound name, the Kartalax spelling, the Ala-Glu-Asp sequence, the T-31 designation and the originating authors, and found no indexed primary report of an osteoarthritis animal model using this tripeptide. The in vivo work that is indexed is renal, not articular. The claim is therefore graded on what supports it — a summary clause in a review — and not on the rat kidney literature, which is about a different organ and a different model.

[4]

Sequence-specific DNA binding and cell entry as the proposed mechanism
Anecdotal reports only in vitro

Both supporting papers are computational and neither reports a laboratory measurement. Docking work on nineteen short peptides constructed spatial models of DNA-peptide complexes and placed this tripeptide at the acct sequence. Separate molecular modelling and computer-assisted docking of twenty-six ultrashort peptides against the LAT and PEPT transporter families included AED among the twenty-six and among the peptides whose calculated LAT1 scores were stronger than those of known inhibitors. This claim is graded below the cell-culture claims deliberately: docking scores are a hypothesis about a mechanism, not evidence that the mechanism operates. No experiment has measured this tripeptide entering a cell or reaching any tissue after administration.

[12] [13]

Neural differentiation attributed to this tripeptide specifically
Anecdotal reports only review · in vitro

A review from the originating programme lists AED among peptides said to activate neural differentiation and among those said to stimulate immune cell differentiation. The primary experiment that tested AED against a neuronal endpoint — in human periodontal ligament stem cells, with an Italian laboratory as co-author — reported increased GAP43 and Nestin expression with a mixture of all four peptides studied and with KED alone, and attributed no increase to AED on its own. A review sentence listing a peptide is not a result belonging to that peptide.

[14] [15]

Osteoarthritis or joint outcomes in people
Anecdotal reports only review

A Russian-language review states that a cartilage-and-bone polypeptide complex and the AED tripeptide, which it names as Kartalax, have shown high efficacy in animal models of osteoarthritis and on oral administration in patients with osteoarthritis of older age groups. That sentence attributes the efficacy to the complex and the tripeptide jointly, and it is a summary assertion inside a review rather than a trial this page can point at: no patient count, no design, no endpoint, no duration, no comparator and no citation to an indexed clinical report. It is the only published statement that this compound has been given to people, and it is graded here for exactly what it is.

[4]

FOR RESEARCH PURPOSES ONLY

Typical protocol range in the research

  • Human mesenchymal stem cell cultures undergoing replicative ageing, in the experiment that measured chondrogenic differentiation markers

    200 ng/ml of the AED tripeptide added to the culture medium; the cartilage polypeptide complex used as the comparator in the same experiment reached the same effect at 2000 ng/ml [3]

  • Human embryonic bone-marrow mesenchymal stem cell cultures aged by passaging or by stationary holding, in the gene-expression experiment that measured this tripeptide alongside two others

    Nanomolar concentrations added to the culture medium; the authors report the peptides as modulating gene expression at that order of concentration rather than at a single stated figure [5]

  • Rats, administered the AED tripeptide, in the two indexed in vivo experiments — cisplatin-induced acute renal failure and renal function in old animals

    No amount, route or schedule is recoverable. Both experiments report what AED did to renal parameters without stating a dose in the English abstract that is the only text available to this page [9] [10]

  • Humans, administered the AED tripeptide, any indication

    No dose is established. The only published statement that this tripeptide has reached patients is a sentence inside a Russian-language review asserting oral administration in older people with osteoarthritis, with no amount, no schedule, no sample size and no study design given [4]

The concentration figures above are culture-medium concentrations, not doses, and the two rat experiments that did administer this tripeptide to living animals cannot be read for an amount. Community-circulated human amounts have no published source behind them and therefore do not appear here.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

  • No human safety data of any kind

    Not established · Unknown, and that is an absence of data rather than a finding of safety. The single published assertion that this tripeptide has been given to patients appears in a review that reports efficacy in a summary clause and reports no adverse events, no tolerability assessment, and no monitoring. A claim of use with no accompanying safety reporting is not the same thing as a clean safety record.

    [4]

  • Absence of nephrotoxicity in old rats, reported as a secondary observation

    Reported in one rat experiment · The one safety-adjacent statement anywhere in this literature is narrow: in old rats given a kidney polypeptide complex or one of three short peptides including AED, the authors reported raised antioxidant-enzyme activity and reduced lipid peroxidation which, together with the morphological findings, they read as evidence of no nephrotoxic effect. That is one organ, one species, one experiment, and a conclusion the authors drew about the group of agents they tested. It is not a toxicology programme and it says nothing about any other tissue or any duration.

    [10]

  • Stimulation of NF-kappaB expression in ageing cell cultures

    Reported in both stem cell ageing models tested · In human embryonic bone-marrow mesenchymal stem cells aged by two different methods, this tripeptide and two companions stimulated expression of the NF-kappaB gene in both models, alongside a 3.5- to 5.6-fold enhancement of IGF1 expression. NF-kappaB is a central inflammatory transcription factor and its upregulation is not straightforwardly a benefit — the same research programme elsewhere counts reduced NF-kappaB as the desirable direction for a different peptide in skin fibroblasts. The finding is reported here as the authors reported it, without interpretation this page cannot support.

    [5] [1]

  • Suppression of apoptosis and senescence markers in aged cells

    Described as the proposed geroprotective mechanism · The effect this compound is built on is keeping aged cells alive and dividing: suppressed caspase-dependent apoptosis in replicatively aged skin fibroblasts, and reduced p16, p21 and p53 with increased sirtuin-6 in aged renal cell cultures. Whatever else that is, it is not obviously a low-consequence intervention, because those markers are also the brakes a cell applies to damaged division. No published experiment has followed that effect over time in an organism, and no carcinogenicity assessment of this tripeptide has been published.

    [6] [7]

  • Unverified identity and purity of unapproved material

    Not quantified · With no approved manufacturer, nothing about the sequence fidelity, concentration, or contaminant profile of material carrying this name is regulated or independently guaranteed. The risk is unusually pointed here: this tripeptide is one amino-acid residue shorter than the tetrapeptide AEDG from the same research programme, the two are routinely discussed in the same papers, and the modelling literature that includes both handles them as separate ligands with separate binding behaviour.

    [13] [4]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage
Lyophilized short peptides are conventionally kept refrigerated at 2–8 °C and protected from light, with freezing used for longer holding. No published stability study exists for this tripeptide. Its published literature is cell-culture work, a small rat kidney literature, and computational modelling, all of it concerned with what the molecule does rather than how long it lasts, so the conventions here come from general lyophilized-peptide practice rather than from data about this compound.
Reconstituted storage
Once in solution, short peptides are conventionally refrigerated at 2–8 °C, protected from light, and treated as short-dated rather than indefinitely stable. No published study establishes a solution shelf life for this tripeptide.
Reconstitution diluent
Bacteriostatic water — sterile water preserved with 0.9% benzyl alcohol — is the conventional diluent for lyophilized research peptides, including short peptides of this family. Preservative-free sterile water is used where a preservative is contraindicated and is treated as single-use.
Reconstitution & handling
Conventional handling only: sanitize the stopper before piercing it, add the diluent slowly down the inside wall of the vial rather than directly onto the powder, and let the powder dissolve on its own. Swirl gently if needed; never shake. A properly prepared solution is clear, and anything cloudy, discolored, or carrying visible particulate is discarded. PHL publishes no volume or unit calculations, because those are dosing decisions and dosing decisions belong with a licensed clinician.
Handling notes
There is no FDA-approved manufacturer, so there is no label, no assigned beyond-use date, and no lot-level stability testing behind any storage claim. The one review that describes this tripeptide reaching patients describes it being given orally, which is a different dosage form again and a form this page has no published handling data for.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

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Citations

15 sources · every identifier checked against PubMed

Before you act on any of this

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