Cartalax
Khavinson bioregulator peptide (AED tripeptide)
Also known as: Карталакс, AED, Ala-Glu-Asp, Khavinson cartilage bioregulator peptide
Evidence level: Limited data
What it is
Cartalax is a short synthetic peptide from the Russian 'Khavinson' bioregulator family, marketed for cartilage and joints. No published study of this exact sequence has actually looked at cartilage, joints, or osteoarthritis; the handful of lab studies that exist instead cover stem-cell aging, nerve cells, skin, kidney, and thymus tissue. The research is Russian-led, preclinical, hasn't been independently replicated in the West, there are no human trials, and Cartalax isn't FDA-approved.
What the research found
Cartalax is marketed for cartilage and joints, but the actual research points elsewhere. Searching the literature for its tripeptide sequence returns a small set of preclinical lab studies — in cells and animal tissue covering stem-cell aging, nerve cells, skin, kidney, and thymus — where the peptide was associated with changes in gene activity and cell-aging markers. None examined cartilage, chondrocytes, joints, or osteoarthritis. There are no human trials and the proposed mechanism is unconfirmed by Western methods, so the evidence should be read as preliminary.
Status and regulatory position
Not FDA-approved for any indication. Cartalax has never been submitted to FDA and has never been studied in a published Western Phase II or III rct. Positioned by its developers as a cartilage / joint bioregulator, but no clinical-experience publications on osteoarthritis, joint degeneration, or cartilage recovery are retrievable in PubMed for this compound — the indexed primary literature on the AED tripeptide is preclinical cell-aging and gene-expression work in non-cartilage models. Available exclusively as a research peptide through Russian or international research-supply chains and gray-market import. Not DEA-scheduled. WADA status: not explicitly named on the 2026 Prohibited List as of last review.
Safety
Cartalax is not FDA-approved and has not been studied in Western-standard clinical trials, so its safety in humans is not established; it is available only through research-supply channels. VialWise is a research and educational reference, not medical advice — consult a licensed professional.
Disclosures
⚠️ For research and educational purposes only. Cartalax is not FDA-approved for any indication and has never been studied in a published Western Phase II or III clinical trial. The Russian-language Khavinson bioregulator literature reports clinical experience but at evidence quality substantially below Western evidence-based-medicine standards. Cartalax is available exclusively as a research peptide through Russian or international research-supply chains and gray-market import. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.
⚠️ The Khavinson bioregulator framework is substantially less characterized in Western peer-reviewed literature than in the Russian Khavinson publication corpus. The same evidence-base caveat applies across the Khavinson product line. The Khavinson hypothesis — that short tissue-specific peptides act as transcriptional regulators via DNA promoter binding — is reported in extensive Russian-language Khavinson Institute publications but has not been validated through Western Phase II or III RCTs. The Russian publications report clinical experience across the Khavinson bioregulator product line (Cartalax = cartilage/joint; Epitalon = pineal; Pinealon = neuropeptide; Bonomarlot = bone marrow; many others) using methodology that does not meet Western evidence-based-medicine standards. Research-community use of Khavinson bioregulators including Cartalax in the US/Western context operates on this evidence-base gap.
⚠️ The cartilage / joint label on Cartalax is not supported by the compound's own published literature. Cartalax is *named and marketed* as a cartilage / joint / connective-tissue bioregulator, and the Khavinson framework hypothesizes the AED (Ala-Glu-Asp) tripeptide is tissue-specifically targeted to chondrocyte and cartilage-matrix function. But every PubMed-indexed primary study on this sequence is a cell-aging or gene-expression model — mesenchymal stem cells, neuronal differentiation, skin fibroblasts, kidney tissue, thymocytes — and not one of them examines cartilage, chondrocytes, joints, or osteoarthritis. A direct PubMed query pairing the sequence with cartilage / chondrocyte / osteoarthritis / joint terms returns zero results. The specific molecular mechanism — claimed transcriptional regulation via DNA promoter binding in chondrocytes — is not validated by standard Western mechanism characterization. Treat the cartilage positioning as derived from the compound's name and the Khavinson tissue-extract origin narrative, not from published cartilage data.
⚠️ Cartalax overlaps in research-community use with established cartilage / joint-support modalities (BPC-157, TB-500, glucosamine/chondroitin, hyaluronic acid injections, biologics like Synvisc). Researchers seeking joint or cartilage support have substantially better-characterized alternatives in the Vialwise library, including BPC-157 (published preclinical tendon/ligament/cartilage healing data; established research-community use), TB-500 (Tβ4 fragment with cartilage matrix synthesis evidence), and the BPC-157+TB-500 blend (combined healing protocol). Cartalax's evidence base is qualitatively weaker than these established alternatives. The research-community case for Cartalax over BPC-157 / TB-500 for cartilage/joint use is not well-supported by published evidence.
⚠️ The Khavinson bioregulator cluster is now multi-entry in the Vialwise library. Including Epitalon (pineal axis), Pinealon (neuropeptide), and this Cartalax entry — plus the related Russian-tradition neuropeptides Selank and Semax from related research groups. All entries in the Khavinson cluster share the limited-Western-primary-literature evidence-base constraint and should be interpreted within that consistent framing.
Quick reference
| Compound class | Khavinson bioregulator tripeptide. Sequence AED (Ala-Glu-Asp). MW ~333 Da. Russian-tradition "tissue-specific peptide bioregulator" research class. |
|---|---|
| Common research-supply sizes | lyophilized vials. Available primarily through Russian and international research-supply chains and gray-market import. |
| Frequency | Daily SC or IM dosing during 10–30 day treatment cycles is the dominant Russian Khavinson pattern. Cycle repetition pattern varies; common pattern is 1–2 cycles per year. |
| Half-life | Plasma elimination half-life not characterized in published Western literature. The Khavinson bioregulator framework hypothesizes rapid plasma clearance but sustained tissue-specific effects via the claimed transcriptional regulation mechanism. |
| Route | Subcutaneous and intramuscular (the dominant routes in Russian Khavinson Institute protocols). Some research-community protocols report intra-articular injection at the affected joint — this is not a Khavinson Institute standard protocol and is not supported by published evidence; intra-articular injection of research-supply Cartalax carries elevated infection and joint-cartilage damage risk and is not recommended. |
| Onset of action | Subjective effects (when reported) typically within the treatment cycle (10–30 days). Cartilage / joint effects emerge over weeks to months in Russian Khavinson protocol reports. |
In depth
Cartalax is a Khavinson bioregulator tripeptide with sequence AED (Ala-Glu-Asp), MW ~333 Da. In PubMed it is indexed under its own NLM supplementary concept ("alanyl glutamyl aspartic acid") and, in the Khavinson group's internal numbering, as T-31.[⁴][⁶] The compound is part of the broader Khavinson bioregulator product line developed at the St. Petersburg Institute of Bioregulation and Gerontology under the direction of Vladimir Khavinson beginning in the 1970s-1980s. Cartalax is marketed within the Khavinson series as a cartilage / joint / connective-tissue bioregulator — but the indexed literature on this sequence does not cover cartilage. The six PubMed-indexed primary studies on AED are aging and gene-expression models in bone-marrow mesenchymal stem cells,[¹] periodontal-ligament stem cells differentiating toward neurons,[²] senescing skin fibroblasts,[³] rat kidney explants and renal cell cultures,[⁴][⁵] and aging thymocytes.[⁶] None examines cartilage, chondrocytes, joints, or osteoarthritis, and a direct PubMed query pairing the sequence with those terms returns zero results. In two of the six, AED was tested but was not the peptide that produced the reported effect.[²][⁶]
The Khavinson bioregulator framework — short synthetic tissue-specific peptides as transcriptional regulators via DNA promoter binding and modulation of gene expression in target tissues. The framework remains substantially less characterized in Western peer-reviewed literature than in the Russian Khavinson publication corpus. See the Epitalon and Pinealon entries for further treatment of the framework's evidence-base status.
What the indexed AED studies actually measured — including where AED did nothing. In human bone-marrow mesenchymal stem cell aging cultures, AED was among the peptides reported to stimulate NF-κB expression, alongside a 3.5–5.6-fold rise in IGF1 expression attributed to the peptides collectively; the reported FOXO1 and TNKS2 effects in that paper belong to other peptides, not AED.[¹] In senescing skin fibroblasts, all four tested peptides inhibited MMP-9 and raised Ki-67 and CD98hc, and AED specifically was reported to suppress caspase-dependent apoptosis.[³] In organotypic rat kidney cultures, AED (as T-31) stimulated proliferation and reduced apoptosis, though less than the calf-kidney polypeptide complex the study centered on.[⁴] In aging rat renal cell culture, AED lowered the senescence markers p16, p21, and p53 and raised SIRT-6.[⁵] Two of the six are weaker than they first look: in the neuronal-differentiation study, the reported GAP43/Nestin increases came from the combined peptide compound and from KED alone, not from AED,[²] and in the thymocyte-aging study only AB-9 showed a geroprotective effect — T-31 (AED) did not.[⁶] All of this is cell-culture and animal-tissue work, not human outcomes, and none of it is a cartilage or joint model.
Cartalax-specific use-case claims (vendor and Khavinson-tradition framing, unsourced). Research-supply vendor pages describe Cartalax use in age-related joint degeneration / osteoarthritis, post-injury cartilage recovery, and as an adjunct combined with Bonomarlot and other Khavinson products. No PubMed-indexed publication supports any of these use cases for this compound, and none is validated by a Western Phase II or III rct.
Mechanism (claimed by the Khavinson framework, not validated by Western mechanism characterization). The framework hypothesizes: SC or IM administration → systemic circulation → cell membrane penetration → nuclear entry → binding to specific DNA promoter regions → modulation of gene transcription in the target tissue. The chondrocyte-specific version of this chain — transcriptional regulation of cartilage-matrix-synthesis genes — has no published study behind it, and none of the mechanism steps has been validated by Western mechanism characterization for the AED tripeptide.
Comparison to BPC-157 and TB-500 (the established cartilage/joint-support library entries). BPC-157 has substantially better-characterized cartilage/joint-healing evidence than Cartalax, including published preclinical tendon-to-bone healing data, ligament repair models, and broader gut-healing-pleiotropic-effects research. TB-500 (Tβ4 fragment) has published cartilage matrix synthesis evidence and is used adjunctively in cartilage-recovery research. The BPC-157+TB-500 blend is the dominant research-community joint/cartilage-healing protocol. Researchers seeking cartilage/joint support should consider BPC-157 / TB-500 first given the substantially stronger evidence base; Cartalax is at most a Russian-tradition adjunct option, not a primary cartilage-healing intervention.
Regulatory status (US — current). Cartalax is not FDA-approved for any indication and has never been submitted to FDA. The compound is available exclusively through Russian or international research-supply chains and gray-market import; not legally compoundable through US 503A pharmacies. Not DEA-scheduled.
Regulatory status (Russia / former Soviet states / Eastern Europe). Cartalax and related Khavinson bioregulators are marketed in Russia and some former Soviet states under the Khavinson Institute product line. Regulatory specifics vary by country.
Regulatory status (sport — WADA). Cartalax is not explicitly named on the 2026 WADA Prohibited List as of last review. The broader Khavinson bioregulator class is not currently a WADA-targeted category. Users in regulated sport should verify the current WADA status directly.
Common research interests. Despite the absent Western Phase II/III evidence base, Cartalax is used in research-community contexts for: - Putative cartilage / joint support — the dominant research-community use case, extrapolating from the compound's name and vendor framing. No PubMed-indexed study of this sequence examines cartilage or joint tissue. - Adjunct to broader Khavinson bioregulator protocols — combined research-community use with Epitalon, Pinealon, Bonomarlot, and other Khavinson products. Common in Russian-tradition longevity-research practice. - Adjunct to BPC-157 / TB-500 cartilage-healing protocols — research-community use as a supplemental cartilage-axis bioregulator. Not supported by published evidence. - Post-orthopedic-injury recovery support — extrapolating from the Russian Khavinson Institute clinical-experience publications.
Reported side effects
Commonly reported
- Mild injection-site reactions — typical of SC and IM injection
- Subjective improvements in joint function / pain — reported in research-community use; not characterized in Western evidence
- Mild headache — uncommon
- Mild GI symptoms — uncommon
- The published Western evidence base for Cartalax is essentially absent. Russian Khavinson Institute publications report clinical experience but at evidence quality below Western standards.
- The Khavinson bioregulator framework's claimed mechanism has not been validated by Western mechanism characterization specifically for the AED tripeptide.
- Long-term safety in chronic use is essentially unknown outside the Russian Khavinson clinical-experience corpus.
- Intra-articular administration is not a Khavinson Institute standard protocol and carries elevated infection and joint-damage risk in research-community use.
Serious
- Severe allergic / hypersensitivity reaction — rare but warrants immediate medical evaluation given absent Western safety data
- New or worsening joint inflammation, redness, warmth, severe pain — could suggest joint infection, gout, or other inflammatory joint pathology; warrants immediate medical evaluation
- Severe injection-site reaction (induration, abscess, signs of infection) — warrants medical evaluation
- Systemic inflammatory symptoms (fever, severe fatigue, generalized malaise) — warrants medical evaluation
- Unexpected musculoskeletal symptoms (new joint pain in untreated joints, severe muscle cramps) — warrants medical evaluation
Contraindications and warnings
Active joint infection — caution
Active autoimmune joint disease (rheumatoid arthritis, psoriatic arthritis, etc.) — caution given immune-axis Khavinson framework effects
Pregnancy and lactation — no human data; default to contraindicated
Pediatric use — no Western clinical-trial evidence base; default to contraindicated
Known hypersensitivity to short peptides or Khavinson bioregulators — contraindicated
Active severe systemic infection — caution
Regulatory note (US): Cartalax is not FDA-approved for any indication and is not legally compoundable through US 503A pharmacies.
Regulatory note (sport): Not explicitly named on the 2026 WADA Prohibited List as of last review.
Not DEA-scheduled.
Key terms
- Khavinson bioregulator
- A class of short peptides from a Russian/Soviet research program proposed to act as tissue-specific regulators; far less studied in Western literature.
- Peptide
- A short chain of amino acids, the building blocks of proteins. Many compounds in this library are peptides.
- Subcutaneous
- An injection into the fatty layer just under the skin, rather than into a muscle or vein.
- Western clinical trial
- A study run to the evidence standards used by regulators like the FDA (randomized, controlled, peer-reviewed).
Sources
- Ashapkin V, Khavinson V, Shilovsky G, Linkova N, Vanuyshin B. (2020). Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides. Molecular Biology Reports, 47(6):4323–4329.(PMID 32399807)
- Caputi S, Trubiani O, Sinjari B, Trofimova S, Diomede F, Linkova N, Diatlova A, Khavinson V. (2019). Effect of short peptides on neuronal differentiation of stem cells. International Journal of Immunopathology and Pharmacology, 33:2058738419828613.(PMID 30791821)
- Lin'kova NS, Drobintseva AO, Orlova OA, Kuznetsova EP, Polyakova VO, Kvetnoy IM, Khavinson VKh. (2016). Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro. Bulletin of Experimental Biology and Medicine, 161(1):175–8.(PMID 27259496)
- Chalisova NI, Lin'kova NS, Nichik TE, Ryzhak AP, Dudkov AV, Ryzhak GA. (2015). Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals. Bulletin of Experimental Biology and Medicine, 159(1):124–7.(PMID 26033601)
- Khavinson VKh, Tarnovskaia SI, Lin'kova NS, Poliakova VO, Durnova AO, Nichik TE, Kvetnoĭ IM, D'iakonov MM, Iakutseni PP. (2014). [Tripeptides slow down aging process in renal cell culture]. Advances in Gerontology, 27(4):651–6. Russian-language; no DOI indexed.(PMID 25946838)
- Lin'kova NS, Polyakova VO, Trofimov AV, Kvetnoy IM, Khavinson VKh. (2011). Peptidergic regulation of thymocyte differentiation, proliferation, and apoptosis during aging of the thymus. Bulletin of Experimental Biology and Medicine, 151(2):239–42.(PMID 22238759)
Related entries
Entry last updated 2026-09-03. Sourced from published literature and regulatory labelling; see Sources above.