Cartalax Research, Specifications & Scientific Information

Introduction

Cartalax is three residues — Ala-Glu-Asp, 333 daltons — and it is the member of this batch whose literature is still being added to.

Most of the Khavinson series was studied hardest between 2000 and 2015. This tripeptide has primary papers from 2020 and two from 2023, and they are more methodologically specific than the older work: named differentiation genes with protein confirmation, a defined senescence phenotype characterised before it was intervened on, and a concentration comparison against the tissue extract the peptide was designed from ^{[2, 3, 1]}.

It is also published almost entirely under the label AED rather than its trade name, which is why it looks thinner than it is. The trade name appears mainly in review tables; the experiments say "AED peptide" ^[7].

The family's shared limitations still hold and are stated once here. Everything primary comes from the St Petersburg Institute of Bioregulation and Gerontology and its collaborators; the 2023 papers are in a Russian-language gerontology journal; nothing is independently replicated; and the entire record is cell culture apart from one rat study. No clinical report of any design has been identified.

What Is Cartalax?

A synthetic tripeptide with free termini, AED in single-letter code: L-alanyl-L-alpha-glutamyl-L-aspartic acid. PubChem carries Cartalax, Ala-Glu-Asp and the laboratory code T-31 as names for compound identifier 87815447, under CAS registry number 85806-95-7.

One caution belongs on the record rather than in a footnote. That same PubChem entry also lists the synonym H-Asp-Glu-Asp-OH, which is a different sequence with a different composition and is inconsistent with the record's own molecular formula and structure. The formula, the structure and the CAS number all correspond to Ala-Glu-Asp. Register synonym lists are aggregated from many sources and are not curated to the standard of the structure records they sit beside; this page uses the structure.

Within the series the tripeptide is assigned to cartilage, and the assignment is supported more directly than most: the compound is repeatedly tested against the cartilage polypeptide complex it was designed from, which is the comparison that matters for a series built on the premise that a short sequence reproduces an extract's activity ^{[2, 3]}.

Cartalax has not been approved by the U.S. Food and Drug Administration for any indication. No marketing application is on record in the United States, and no study of it appears on ClinicalTrials.gov.

Cartalax Specifications

PubChem carries the free tripeptide as compound identifier 87815447 with CAS registry number 85806-95-7, formula C12H19N3O8 and an average mass of 333.29 g/mol; the record lists Cartalax, Ala-Glu-Asp and the laboratory code T-31 as names for the same substance. No unique ingredient identifier resolves in the FDA/NCATS Global Substance Registration System. One caution belongs on the record: the same PubChem entry also carries the synonym H-Asp-Glu-Asp-OH, which is a different sequence of different composition, and appears to be an error in that synonym list rather than a statement about the compound. The structure, formula and CAS number on the record are consistent with Ala-Glu-Asp. Most of the primary literature refers to this compound as the AED peptide rather than by trade name, so searching the sequence label returns considerably more than searching the name.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Cartalax Work?

Not established. No receptor has been identified, none is proposed, and the specification table shows primary target, receptor family and agonist status as not publicly characterised.

What the literature offers instead is a transcriptional pattern that holds across three different cell types — and the consistency deserves attention, with the proviso set out below about what it is.

In mesenchymal stem cells the tripeptide raised gene expression and protein synthesis of four chondrogenic differentiation markers ^[2]. In chondrocytes it normalised the six molecules that had been shown to define the senescence-associated secretory phenotype in those cells ^[3]. In dermal fibroblasts it raised sirtuin-1, sirtuin-6 and type I collagen ^[1]. Sirtuin-1 appears in two of the three, moving in the same direction.

That is a pattern. It is not a mechanism, for a specific reason: every measurement is of a gene or a protein whose level changed, which places all of them downstream of whatever the peptide did first. No binding partner, no transporter, no signalling intermediate and no structural work connects the molecule to any of these endpoints.

The concentration comparison is the most informative datum on this page. In ageing mesenchymal stem cells the tripeptide produced its effect at 200 ng/ml, while the cartilage polypeptide complex required 2000 ng/ml for the same effect ^[2]. The series' founding claim is that a short sequence carries the activity of its parent extract. A tenfold difference in effective concentration by mass is at least the right shape for that claim — a purified active component should be more potent by mass than the mixture it came from. It is a single comparison in one system, both arms were run by the same group, and mass-based potency comparisons between a defined tripeptide and an undefined complex are crude. But it is the closest thing to a test of the premise found anywhere in this batch.

No pharmacokinetic dataset exists for this tripeptide in any species.

Cartalax Mechanism of Action

In vitro research

Chondrogenic differentiation in ageing stem cells. Human mesenchymal stem cells aged by serial passage were exposed to the tripeptide or to the cartilage polypeptide complex, and four markers of chondrogenic differentiation were measured at both gene and protein level: SOX9, the master transcription factor of the chondrocyte lineage; aggrecan, the principal proteoglycan of cartilage matrix; type II collagen; and cartilage oligomeric matrix protein. The tripeptide at 200 ng/ml activated all four; the complex did the same at 2000 ng/ml ^[2].

Measuring both messenger RNA and protein for the same four markers is a real methodological strength — transcript changes that do not reach protein are a common and easily overstated result. The indexed abstract gives no replicate counts and no statistics.

The chondrocyte senescence phenotype. The senescence-associated secretory phenotype of chondrocytes was first characterised: raised p16, p21 and p53 — the proteins of cell-cycle arrest — raised tumour necrosis factor alpha and interleukin-1 alpha, and lowered sirtuin-1. Both the tripeptide and the complex were then reported to normalise the synthesis of those molecules ^[3].

Characterising a phenotype before intervening on it is the right order of operations and is not what most papers in this literature do.

Dermal fibroblasts, against a dipeptide. In human dermal fibroblasts during replicative ageing, this tripeptide and Vilon were compared by immunocytochemistry and confocal microscopy. Vilon reduced interleukin-1, NF-kB and transforming growth factor beta and raised sirtuin-6, which the authors describe as normalising the cells' immunological function. This tripeptide raised sirtuin-1, sirtuin-6 and type I collagen, which they describe as a geroprotective effect ^[1]. The two peptides separated within one experiment — different proteins, different described role.

Fibroblasts in a four-peptide comparison. With three siblings, the tripeptide reduced MMP-9 synthesis and raised Ki-67 and CD98hc in ageing fibroblasts; it and Epitalon also suppressed caspase-dependent apoptosis, where the other two did not ^[5].

Gene expression in ageing stem cells. With Vesugen and Vilon, at nanomolar concentrations, the tripeptide stimulated expression of the NFkB gene in two different models of cell ageing, and IGF1 expression rose three-and-a-half to five-and-a-half-fold with the peptides added ^[6].

Everything in this section was observed in cultured human cells. None of it establishes anything about an intact animal, and none of it about a person.

Preclinical Research on Cartalax

Animal research

Cisplatin-induced acute renal failure in rats

Rats with acute renal failure induced by cisplatin received a kidney polypeptide complex or one of three short peptides: this tripeptide, EDL or AEDG ^[4].

The result separates the three, and the separation is the point. This tripeptide decreased protein excretion and electrolyte concentration in the urine — a narrow effect. The kidney complex, EDL and AEDG normalised a much wider set of parameters: diuresis, urinary creatinine and its excretion, glomerular filtration rate, absolute sodium resorption, urinary protein and sodium and potassium concentrations. The paper's summary names EDL as producing the potent nephroprotective effect, not this compound ^[4].

A peptide named for cartilage doing less in a kidney model than two peptides assigned elsewhere is consistent with the series' tissue-specificity premise, and it is reported here for that reason as much as any other. The indexed abstract gives no group sizes and no statistical detail.

Findings in this section were obtained in rats. Nothing in them establishes anything about humans.

What Is Cartalax Being Researched For?

• Chondrogenic differentiation of ageing stem cells — SOX9, aggrecan, type II collagen and COMP, at gene and protein level ^[2].
• Chondrocyte senescence — the p16, p21, p53, tumour necrosis factor alpha, interleukin-1 alpha and sirtuin-1 profile ^[3].
• Dermal fibroblast function during replicative ageing — sirtuins, type I collagen, MMP-9, Ki-67 and caspase-3 ^{[1, 5]}.
• Gene expression in ageing mesenchymal stem cells — IGF1, FOXO1, TERT, TNKS2 and NFkB ^[6].
• Acute renal failure in rats — as the least effective of three peptides tested ^[4].

None of that is research into, or evidence about, research-grade material supplied for laboratory use.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Cartalax vs Related Compounds

The cartilage polypeptide complex

The extract this tripeptide was designed from, and the comparator that matters most. Both were tested in the same two 2023 experiments, with the tripeptide effective at one tenth the concentration by mass ^[2]. A defined molecule outperforming its parent mixture by mass is the shape the series' founding claim predicts.

Vilon :: Lys-Glu, compared head to head with this tripeptide in dermal fibroblasts, where the two changed different proteins ^[1]. Epitalon and Ovagen :: The two peptides tested beside this one in the rat renal model, both of which acted on more parameters than it did ^[4]. Cortagen and Cardiogen :: Ala-Glu-Asp-Pro and Ala-Glu-Asp-Arg — this exact sequence with one residue added. Whether a tripeptide and its own C-terminal extensions should be expected to act on different organs is the series' premise at its most demanding, and no experiment testing this tripeptide against either extension has been located.

Evidentiary position

Not approved by the U.S. Food and Drug Administration, no registered trial, no clinical report of any design, and a record that is almost entirely cell culture.

No comparison of effect between these compounds is made on this page.

Chemical & Molecular Characteristics

This is the most strongly acidic peptide in the batch. Three residues supply three ionisable acidic groups — the glutamate side chain, the aspartate side chain and the C-terminal carboxyl — against a single N-terminal amine and no basic side chain at all. At physiological pH the molecule carries a net charge near −2, is extremely water-soluble, and has essentially no hydrophobic surface. That combination argues strongly against passive membrane crossing, which is worth holding against every intracellular observation reported for it.

No aromatic residue, so no absorbance at 280 nm. Quantification has to rely on peptide-bond absorbance near 214 nm, where solvents and buffer components also absorb.

Reversed-phase retention is poor. A 333-dalton peptide of this polarity is weakly retained on conventional C18 columns and can elute near the void volume alongside salts and synthesis-related impurities. Ion-pairing or mixed-mode separation is usually needed to say anything meaningful about purity, and a bare "purity by HPLC" figure without a method is close to uninformative for this compound.

Adjacent acidic residues make isomerisation the principal identity risk. Glutamate followed directly by aspartate is a motif prone to the alpha/beta and alpha/gamma rearrangements characteristic of Asp- and Glu-containing peptides, favoured by heat and by acidic conditions. The rearranged products have identical molecular formulas and identical masses. A mass spectrum confirming 333.29 daltons is consistent with the intended tripeptide and with several isomers of it, and only a sequencing method distinguishes them.

The synonym discrepancy is a reason to check. The PubChem record for this compound carries a synonym reading H-Asp-Glu-Asp-OH, a different sequence of different composition. The record's structure, formula and CAS number correspond to Ala-Glu-Asp, so the synonym is best treated as an aggregation error — but a compound whose register entry contains a conflicting sequence string is one whose certificate of analysis is worth reading for what it actually confirms.

One register field is empty. CAS registry number 85806-95-7 and PubChem compound identifier 87815447 both resolve; no FDA/NCATS unique ingredient identifier does. That field is shown as unknown above rather than filled from a neighbouring substance.

Frequently Asked Questions

Scientific References

1. Fridman NV, Linkova NS, Kozhevnikova EO, et al.. Comparison of the Effects of KE and AED Peptides on Functional Activity of Human Skin Fibroblasts during Their Replicative Aging Bulletin of experimental biology and medicine; 2020. PMID 33231794 doi:10.1007/s10517-020-05022-1
2. Myakisheva SN, Linkova NS, Diatlova AS, et al.. [The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging.] Advances in gerontology = Uspekhi gerontologii; 2023. PMID 37782646
3. Myakisheva SN, Linkova NS, Kozhevnikova EO, et al.. [Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging.] Advances in gerontology = Uspekhi gerontologii; 2023. PMID 37356100
4. Zamorskii II, Shchudrova TS, Lin'kova NS, et al.. Peptides Restore Functional State of the Kidneys During Cisplatin-Induced Acute Renal Failure Bulletin of experimental biology and medicine; 2015. PMID 26515176 doi:10.1007/s10517-015-3062-y
5. Lin'kova NS, Drobintseva AO, Orlova OA, et al.. Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro Bulletin of experimental biology and medicine; 2016. PMID 27259496 doi:10.1007/s10517-016-3370-x
6. Ashapkin V, Khavinson V, Shilovsky G, et al.. Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides Molecular biology reports; 2020. PMID 32399807 doi:10.1007/s11033-020-05506-3
7. Khavinson V, Linkova N, Kozhevnikova E, et al.. Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers International journal of molecular sciences; 2022. PMID 35887081 doi:10.3390/ijms23147733

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.