Cartalax
BioregulatorsResearch Use OnlyLast reviewed: September 28, 2026
Quick Facts
- What it is
- A synthetic tripeptide (the AED peptide, Ala-Glu-Asp) from the Khavinson short-peptide bioregulator programme — the cartilage-directed member of that family. Transliterated Kartalax in the Russian literature.
- How it's taken
- Not established — the one primary study is cell culture; a review describes oral administration in patients without giving a regimen
- Half-life
- Not characterized
- Typical research dose
- No validated dose — no human regimen could be located in a readable source
- Research status
- Not FDA- or EMA-approved — US research use only. Two indexed papers, both Russian-language and from the originating institute.
On this page
Where to source Cartalax
Cartalax is not approved for human use in the US and is sold by specialty research peptide vendors for laboratory use only. The bioregulator line is more specialised than the mainstream peptide catalog, so fewer vendors carry it. Quality varies — a Certificate of Analysis is the only identity and purity check available to a buyer.
Batch-traceable COAs · cold-chain shipping
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Also stocking Cartalax
Peptides.gg, Ameano Peptides, BioLongevity Labs, Modern Aminos — each carries a current price row for this compound.
What is Cartalax?
Cartalax is a synthetic tripeptide from the Khavinson short-peptide bioregulator programme, appearing in the literature as the AED peptide (Ala-Glu-Asp) and, in one review, as “the AED tripeptide (Kartalax)”. It is the cartilage-directed member of a family whose other members target other tissues — Thymogen the thymus, Pinealon the brain, Cardiogen the heart. The bioregulator guide explains how the family is organised and where the extracts and the synthetics differ.
This is a short profile because the sourceable literature is short. Two indexed papers name the compound or its peptide sequence. Both come from the Saint-Petersburg Institute of Bioregulation and Gerontology, the institute that originated the programme; both are in Russian with an English abstract; and only one of the two is a primary study. That study is cell-culture work in chondrocytes. Everything stronger that circulates about Cartalax — efficacy in animal models, efficacy in older patients taking it by mouth — reaches the reader through the other paper, a review, and the reports behind those statements could not be located. New to reading peptide research? Start with the basics
Reported in the cited work: normalization of senescence-associated and inflammatory marker synthesis in cultured chondrocytes — p16, p21, p53, TNF-α, IL-1α and sirtuin 1 [1]; and, asserted in review, efficacy in animal models of osteoarthritis and in oral administration to older patients with the disease [2].
How is Cartalax proposed to work?
The bioregulator programme's general account is that short peptides act on gene expression rather than on a receptor in the conventional sense. For Cartalax specifically, the mechanistic content that can be sourced here is narrower than that account and comes from a single cell-culture experiment.
- Regulation of the chondrocyte senescence phenotype [1]. In chondrocyte culture, the aging-associated secretory phenotype was characterised by increased synthesis of the pro-apoptotic proteins p16, p21 and p53, increased TNF-α and IL-1α, and decreased sirtuin 1. The AED peptide was reported to normalize the synthesis of those molecules (Myakisheva et al. 2023).
- The cartilage-protection rationale [2]. A review from the same institute frames that marker profile as the mechanism behind a proposed chondroprotective effect in osteoarthritis, grouping AED with Sigumir, a cartilage and bone polypeptide complex.
- What is not established. No binding target, no receptor, no pharmacokinetics and no dose-response relationship for Cartalax appears in the literature located here. Marker normalization in cultured cells is the whole of the reported mechanism.
What is Cartalax researched for?
Cartalax's research base is small, recent in indexing, and concentrated in one place. Reading it honestly means separating what was tested from what was asserted about earlier work that cannot be retrieved.
- Chondrocyte cell culture [1]. The primary result: AED normalized senescence-associated and inflammatory marker synthesis in chondrocytes, compared against a cartilage polypeptide complex (Myakisheva et al. 2023). In vitro.
- Osteoarthritis, asserted in review [2]. A 2023 review states that AED (Kartalax) and Sigumir "have shown high efficacy in animal models of OA and oral administration in patients with OA of older age groups". Prof. Peptide reports this as the review's statement, not as a verified finding: the animal and patient studies behind it were not located as indexed records, so their design, size and outcomes cannot be checked.
- Nothing outside that. A PubMed search for "Kartalax" returns one record, the review at [2]. There is no located trial registration, no English-language primary study, and no work from a group unconnected to the originating institute.
How is Cartalax dosed, and what is known about safety?
There is no validated dose for Cartalax, and the safety record is reported here in the same section because the two share a single cause: the human work that would establish either one is not retrievable.
The only primary study located is cell-culture work, which involves no dosing of an animal or a person [1]. The review that mentions patient use describes oral administration in older adults with osteoarthritis but gives no regimen in its indexed abstract, and the underlying reports could not be located [2]. Prof. Peptide therefore publishes no milligram figure, no schedule and no route for this compound — not as a precaution, but because there is no source to report. On safety, the position is the same and worth stating plainly: no adverse-event data for Cartalax were located in either paper, and an absence of reported harm in a cell-culture study and a review is not a safety record. Long-term tolerability, interactions and effects in humans are uncharacterised in the literature available here. Research vendors sell Cartalax as lyophilised material labelled for laboratory use only; quality varies between vendors, and a Certificate of Analysis is the only check a buyer has on identity and purity.
What are the limitations of Cartalax research?
The limitation that shapes every other one is concentration of source. Both papers identified here come from the Saint-Petersburg Institute of Bioregulation and Gerontology, the institute that originated the Khavinson bioregulator programme, and share four of five authors. Both are in Russian, indexed in PubMed with an English abstract only. There is no independent replication by an unconnected group.
The strongest claims about this compound — efficacy in animal models of osteoarthritis and in older patients taking it orally — reach the reader through a review rather than through the studies themselves. Prof. Peptide could not locate those studies as separate indexed records, so their design, sample sizes, endpoints and results cannot be examined. A claim that cannot be traced to a readable report is reported here as a claim, and graded as such.
The evidence grade on this profile is In Vitro, and it rests on the chondrocyte culture study alone. Marker normalization in cultured cells is a long way from a clinical outcome; many compounds have made that step and failed.
Cartalax is not approved by the FDA or EMA. It is sold as research-use-only material in the US, and the same caveats apply that apply across this family — see the bioregulator guide .
Cartalax FAQ
What is Cartalax?
Cartalax is a synthetic tripeptide from the Khavinson short-peptide bioregulator programme, identified in the literature as the AED peptide (Ala-Glu-Asp). It is the cartilage-directed member of that family, studied alongside Sigumir, a polypeptide complex extracted from the cartilage and bone tissue of young animals. The Russian spelling transliterates as Kartalax; Western vendors sell it as Cartalax. See the bioregulator guide for how this family of compounds is organised.
Is Cartalax FDA-approved?
No. Cartalax is not approved by the FDA or EMA for any indication, and Prof. Peptide located no registration for it outside the Russian Federation. In the US it is sold as research-use-only material by specialty peptide vendors.
What does the research on Cartalax actually show?
One primary study located here tested the AED peptide directly: a chondrocyte cell-culture experiment reporting that AED normalized the synthesis of the markers that define the aging-associated secretory phenotype — the pro-apoptotic proteins p16, p21 and p53, the cytokines TNF-α and IL-1α, and sirtuin 1. That is in-vitro work. A review from the same institute states that AED has shown efficacy in animal models of osteoarthritis and in oral administration to older patients, but Prof. Peptide could not locate the underlying primary reports in PubMed.
Why is the Cartalax literature so hard to verify?
Because of who published it and where. Both papers identified here come from the Saint-Petersburg Institute of Bioregulation and Gerontology — the institute that originated the bioregulator programme — and both are in Russian, with only an English abstract indexed. That is not a reason to dismiss the work, but it means there is no independent group and no English-language primary literature to check the claims against. A search of PubMed for "Kartalax" returns exactly one record.
Is there a standard Cartalax dose?
No validated dose exists. The review that mentions patient use describes oral administration in older adults with osteoarthritis, without a regimen Prof. Peptide can report from the indexed abstract, and the primary study located here is cell-culture work with no human dosing at all. Vendors sell Cartalax as lyophilised material for laboratory use; Prof. Peptide publishes no schedule for it, because none has been established in a source that can be read.
References
- Myakisheva SN, Linkova NS, Kozhevnikova EO, Polyakova VO, Ryzhak GA. Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging. Adv Gerontol. 2023;36(2):234-238. [Article in Russian; English abstract.] PMID 37356100. https://pubmed.ncbi.nlm.nih.gov/37356100/
- Myakisheva SN, Linkova NS, Kozhevnikova EO, Ryzhak GA. Chondrocytes secretory phenotype associated with aging: role in the pathogenesis of osteoarthritis and prospects for peptide bioregulation. Adv Gerontol. 2023;36(3):313-323. [Article in Russian; English abstract. Review.] PMID 37782637. https://pubmed.ncbi.nlm.nih.gov/37782637/
Published Studies
Plain-English summaries of the two indexed papers behind the statements above. Click any title to read the source record. Both are Russian-language and from the same institute; one is a review rather than a primary study.
Myakisheva SN, Linkova NS, Kozhevnikova EO, Polyakova VO, Ryzhak GA.
The one primary study located that tests the AED peptide directly. Working in chondrocyte culture, the authors characterised the aging-associated secretory phenotype — raised p16, p21 and p53, raised TNF-α and IL-1α, and reduced Sirt1 — and compared the effect of the AED peptide against a cartilage polypeptide complex. Both were reported to normalize the synthesis of those molecules. This is in-vitro work: it describes marker changes in cultured cells, not an outcome in an animal or a person. The article is in Russian, from the Saint-Petersburg Institute of Bioregulation and Gerontology, with an English abstract indexed in PubMed.
Myakisheva SN, Linkova NS, Kozhevnikova EO, Ryzhak GA.
A review, not a primary study, and the only PubMed record that names Kartalax. It states that Sigumir and "the AED tripeptide (Kartalax)" have shown high efficacy in animal models of osteoarthritis and in oral administration to older patients with the disease. Those two claims are the strongest ones in circulation about this compound, and they arrive here at second hand: the review is from the same institute as the primary study above, it is in Russian, and Prof. Peptide could not locate the animal or patient reports it refers to as separate indexed records.
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