Cartalax Research

Cartalax is a synthetic tripeptide, sequence Ala-Glu-Asp or AED ^[1]. It belongs to a group of short peptides developed in Russia and marketed as peptide bioregulators. This page sets out what has been published about Cartalax. Very little has been.

Identity and naming

The US National Library of Medicine indexes the concept under the entry terms alanyl-glutamyl-aspartic acid, Ala-Glu-Asp, cartalax and T-31 peptide ^[1]. PubChem holds it as CID 87815447, molecular formula C12H19N3O8. The registry number 85806-95-7 resolves to that same record, re-checked directly ^[1].

One database error is worth knowing about. Both the NLM record and PubChem also carry the synonym H-Asp-Glu-Asp-OH ^[1]. That string reads Asp-Glu-Asp, which would be C13H19N3O10. The formula on the record is C12H19N3O8, which is Ala-Glu-Asp. The Asp-Glu-Asp synonym is wrong, and two databases propagate it.

The brand name has no research literature

A PubMed title and abstract search for cartalax returns zero records ^[3]. A bare-term search, which also reaches indexing terms, returns six ^[3]. The peptide is reachable in the literature only under its sequence. A title and abstract search for "AED peptide" returns four records ^[3]. Those four are the core of the compound-specific evidence base.

One research group produced all of it

Vladimir Khavinson and the St Petersburg Institute of Bioregulation and Gerontology discovered these peptides, hold patents covering members of the family, and sell them ^[8]. Khavinson is a named co-inventor on a granted family patent assigned to his own institute's clinic company, and declared no patent or licensing arrangement in a 2020 paper ^[8]. That is family background, not evidence about this compound.

For Cartalax specifically, all four AED records carry Linkova NS of that institute, and Khavinson co-authors two of them ^[4]. No group unconnected to the network has published on the AED peptide ^[3]. Nothing here is independent.

What the four records are

Two are Russian-language 2023 papers in Advances in Gerontology, with English abstracts only ^[4]. One is cell culture work in human mesenchymal stem cells, on chondrogenic differentiation ^[4]. The other is cell culture work in human chondrocytes ^[4]. It concerns the senescence-associated secretory phenotype, with markers including p16, p21, p53 and Sirt1 ^[4]. One is a 2020 English-language paper comparing the KE and AED peptides ^[4]. It is cell culture work in human skin fibroblasts ^[4]. One is a 2015 English-language animal study, in a rat model of cisplatin kidney injury ^[4]. It was led from Bukovinian State Medical University in Ukraine ^[4].

Two of the four report a result attributed to AED on its own. In the rat model, AED decreased protein excretion and electrolyte concentration in the urine ^[4]. In replicatively aging human skin fibroblasts, AED activated synthesis of sirtuin-1, sirtuin-6 and collagen I ^[4]. The authors of that second paper read the change as a geroprotective effect ^[4]. The two Russian-language papers report no AED-attributed outcome that their English abstracts allow to be stated here ^[4]. The rat paper also reports results for the sibling peptides EDL and AEDG, which are not results for Cartalax ^[4].

Beyond those four, three further laboratory reports name AED. In cultured human fetal mesenchymal stem cells, AED was tested alongside KED and KE in aging models ^[5]. In cultured human periodontal ligament stem cells, AED was tested alongside KED, KE and AEDG ^[6]. Both are in vitro, both carry authors from the developer's institute, and the second reports marker expression rather than function ^[6]. A 2015 report stated that T-31, which is AED, stimulated proliferation and reduced apoptosis of kidney cells ^[2]. That report is cell and tissue work, not a result in an animal or a person ^[2]. It is a different paper from the 2015 rat study above ^[2][4].

What has not been studied

No lifespan or longevity study of Cartalax exists in any species ^[3]. There is no human clinical study of any kind ^[3]. No trial of Cartalax is registered on ClinicalTrials.gov; the single search hit is an enteral nutrition study unrelated to the peptide ^[3]. No pharmacokinetic study has been located, so no plasma concentration, half-life or clearance figure exists ^[3]. No formal toxicology package has been published. Absence of published toxicology is not evidence of safety.

Cartalax and its siblings

AED is the first three residues of epitalon (AEDG), cortagen (AEDP), bronchogen (AEDL) and cardiogen (AEDR) ^[7]. The last two of those sequences are less secure than the first two ^[7]. Bronchogen appears in the literature as both AEDL and ADEL ^[7]. Cardiogen has no named sequence record in either database, so AEDR rests on the developer's own table ^[7]. No published study explains what functionally distinguishes Cartalax from the longer peptides it sits inside. The literature is silent there. Results reported for those compounds are not results for this one.

Longevity and mortality figures circulating for "Khavinson peptides" belong to other substances, including crude bovine extracts that are not Cartalax. Material sold under this name is for laboratory research use only and is not for human consumption.

Frequently Asked Questions

Is there human evidence for Cartalax? There is no human clinical study of Cartalax of any kind ^[3]. All work on human material is cell culture ^[4][5][6]. It covers skin fibroblasts, mesenchymal stem cells, chondrocytes and periodontal ligament stem cells ^[4][5][6]. Every one of those reports carries authors from the developer's institute ^[4][5][6]. None is a study in people. No trial of Cartalax is registered on ClinicalTrials.gov ^[3].

Why does searching for Cartalax return nothing? The brand name has no title or abstract presence in PubMed at all ^[3]. The peptide appears in the literature only under its sequence code AED, or as T-31 ^[1][3]. Four records are reachable that way, and all four come from one research network ^[3][4].

Is Cartalax the same as Asp-Glu-Asp? No. Both the NLM record and PubChem carry H-Asp-Glu-Asp-OH as a synonym, and that string is an error ^[1]. The formula on the record is C12H19N3O8, which is Ala-Glu-Asp. Asp-Glu-Asp would be C13H19N3O10 ^[1].

References

1. 1

   NLM supplementary concept record C572340, entry terms alanyl-glutamyl-aspartic acid, Ala-Glu-Asp, H-Asp-Glu-Asp-OH, cartalax, T-31 peptide; PubChem CID 87815447, C12H19N3O8, molecular weight 333.29, CAS 85806-95-7. Both records re-resolved directly, 27 August 2026. (CAS 85806-95-7 returns the Ala-Glu-Asp structure; the H-Asp-Glu-Asp-OH synonym is contradicted by the formula on the same record.)
2. 2

   Chalisova NI, et al. Bulletin of Experimental Biology and Medicine. 2015;159(1). PMID 26033601. DOI: 10.1007/s10517-015-2906-9. (Names T-31 (AED) and T-35 (EDL); reports that both stimulate proliferation and reduce apoptosis of kidney cells. The paper does not use the trade name Cartalax.)
3. 3

   PubMed E-utilities counts and absence searches, and ClinicalTrials.gov API v2 query, run 27 August 2026. (cartalax[tiab] = 0; bare-term cartalax = 6; "AED peptide"[tiab] = 4, matching the four records at reference 4; no lifespan or longevity record; no human clinical study; no pharmacokinetic study; ClinicalTrials.gov returns one hit, NCT06852014, an enteral nutrition study unrelated to the peptide.)
4. 4

   Myakisheva SN, et al. Advances in Gerontology (Uspekhi Gerontologii). 2023. PMID 37782646. (cell culture, human mesenchymal stem cells; chondrogenic differentiation) and PMID 37356100. (cell culture, human chondrocytes; senescence-associated secretory phenotype; p16, p21, p53, TNF-alpha, IL-1alpha, Sirt1). Both Russian, English abstracts only, and neither abstract yields an AED-attributed outcome that can be stated. Fridman NV, et al. Bulletin of Experimental Biology and Medicine. 2020. PMID 33231794. DOI: 10.1007/s10517-020-05022-1 ("Comparison of the Effects of KE and AED Peptides..."; cell culture, human skin fibroblasts in replicative aging; reports that the AED peptide activates synthesis of sirtuin-1, sirtuin-6 and collagen I, which the authors read as a geroprotective effect; the KE finding in the same abstract belongs to a different compound and is not carried here). Zamorskii II, et al. Bulletin of Experimental Biology and Medicine. 2015. PMID 26515176. DOI: 10.1007/s10517-015-3062-y (in vivo, rats with cisplatin-induced acute renal failure; Bukovinian State Medical University, Chernovtsy, Ukraine, with Lin'kova NS of the St Petersburg institute; reports that the AED peptide decreased protein excretion and electrolyte concentration in the urine. The same abstract reports a nephroprotective effect for EDL, and effects on diuresis, urine creatinine and glomerular filtration rate for EDL and AEDG; those belong to sibling compounds and are not carried here). Linkova NS co-authors all four; Khavinson co-authors PMID 33231794. and PMID 26515176.
5. 5

   Ashapkin V, Khavinson V, Shilovsky G, Linkova N, Vanyushin B. Molecular Biology Reports. 2020;47(6):4323-4329. PMID 32399807. DOI: 10.1007/s11033-020-05506-3. (Names Ala-Glu-Asp (AED), Lys-Glu-Asp (KED) and Lys-Glu (KE); tested in human fetal mesenchymal stem cell aging models. Sequence codes only, no trade names.)
6. 6

   Caputi S, Trubiani O, Sinjari B, Trofimova S, Diomede F, Linkova N, Diatlova A, Khavinson V. International Journal of Immunopathology and Pharmacology. 2019;33. PMID 30791821. DOI: 10.1177/2058738419828613. (Names AED, KED, KE and AEDG; tested on human periodontal ligament stem cells. Conclusions are marker-expression findings, not functional outcomes.)
7. 7

   Khavinson V, et al. International Journal of Molecular Sciences. 2022;23(14):7733. PMID 35887081. DOI: 10.3390/ijms23147733. (Table 2 gives name and sequence for the family, including AEDG, AEDP, AEDL and AEDR. Note the table spells two members Korthagen and Prostomax.) Bronchogen sequence conflict: Monaselidze JR, et al. Bulletin of Experimental Biology and Medicine. 2011. PMID 21240358. DOI: 10.1007/s10517-011-1146-x gives Ala-Asp-Glu-Leu in its title, against Ala-Glu-Asp-Leu in PMID 22117547. and PMID 28371610. Cardiogen: NLM holds no supplementary concept record for the name, and a PubMed search pairing cardiogen with Ala-Glu-Asp-Arg or AEDR returns zero records, so the AEDR assignment rests on reference 7's own table.
8. 8

   Khavinson V, Popovich I, Mikhailova O. Acta Biomedica. 2020. PMID 32921699. (Conflict of interest statement declaring no commercial associations including patent or licensing arrangement.) USPTO US6727227B1, granted 27 April 2004, four named inventors including Vladimir K. Khavinson, assignee the institute's clinic LLC. (Family patent, covering the tetrapeptide epitalon, not Cartalax.)