Cartalax

Dosing from the Literature

Published for the joints: 1 μg to 5.0 mg injected into muscle once a day for 20 days, in adults with knee osteoarthritis, in the developers' patent; the Russian product instructions give capsules and drops, not a peptide dose. Not published: a human trial in a medical journal.

No human dose comes from a trial published in a medical journal. The table gives the regimens the Russian product instructions and the developers' patent describe, with a rat dose from the same patent. Not FDA-approved prescribing; not a rheumatology therapy.

What It Is

Cartalax is a synthetic short peptide within the Khavinson bioregulator program. Its sequence is Ala-Glu-Asp (AED), a tripeptide (a chain of 3 amino acids) with an approximate molecular weight of 333 daltons. It shares the "Ala-Glu-Asp" acidic core with several Khavinson tetrapeptide (a chain of 4 amino acids) siblings (Epithalon AEDG, Cortagen AEDP, Bronchogen AEDL, Cardiogen AEDR) — Cartalax is the shorter, three-residue version lacking the C-terminal residue. It is sometimes listed under the alias "AC-4." The two acidic residues (Glu, Asp) plus the small hydrophobic Ala give the tripeptide a net-anionic character under most buffer conditions, which the Khavinson framework links to DNA binding; the group's computer models place AED in the minor groove of an AT-rich DNA stretch (Khavinson 2014, Advances in Gerontology, PMID 25946838) or on the sequence ACCT (Khavinson 2016, PMID 27909961).

Within the Khavinson framework, short peptides like Cartalax were designed from the amino-acid composition of tissue extracts (Khavinson 2002, PMID 12374906); Cartalax is the one assigned to cartilage. The parent complex in earlier Russian work was derived from cartilage and joint-tissue extracts. As with other Khavinson bioregulators, Cartalax is presented as a chemically defined synthetic replacement for the crude tissue extract — synthesized, purified, and available as lyophilized research peptide or oral-capsule dietary supplement. The group's 2022 review lists Cartalax (AED) as a "chondroprotector" on the strength of the developers' Russian patent, published in 2007 (Khavinson et al., 2007), and as a regulator of skin-fibroblast function on the strength of a 2020 cell study (Khavinson 2022, PMID 35887081).

Cartalax is sold as an oral capsule in the dietary-supplement line of Khavinson's institute (IBG product pages), and seller listings give it as lyophilized research peptide in 20 mg vials. Neither form is registered as a pharmaceutical in any jurisdiction. In Russia it is sold as a BAD (biologically active additive); outside Russia it is research-only.

Cartalax is not a drug used or recognized in evidence-based rheumatology or orthopedics. Guideline-directed osteoarthritis management — weight optimization, exercise / physical therapy, topical and oral NSAIDs, intra-articular corticosteroids or hyaluronic acid, DMOADs in trial, and joint replacement in advanced disease — does not include Cartalax.

Who Khavinson was, and what his record supports →

Mechanism of Action

The Khavinson framework proposes that short bioregulator peptides act as sequence-specific DNA-binding molecules or intracellular epigenetic modulators that can enter cells and reach nuclear chromatin (Khavinson 2021, PMID 34834147). Cartalax's mechanism is described within this framework. Independent structural validation is limited.

• Proliferation signal (kidney, not cartilage) — The young-and-aged proliferation finding for AED comes from rat kidney-cell cultures and kidney explants (Khavinson 2014, Advances in Gerontology, PMID 25946838; Chalisova 2015, PMID 26033601); no study naming AED in chondrocyte proliferation was found.
• Anti-apoptotic / survival — AED suppressed caspase-dependent apoptosis in aging rat skin fibroblasts (Lin'kova 2016, PMID 27259496); no study of AED in chondrocytes under oxidative or mechanical stress was found. In a 2023 study of aging chondrocytes from Khavinson's institute, AED brought the age-related rise in p16, p21, p53, TNF-α and IL-1α and the fall in Sirt1 back toward normal, as a cartilage polypeptide complex did (Myakisheva 2023, PMID 37356100).
• Collagen and proteoglycan synthesis — No study measuring type II collagen (COL2A1) or aggrecan (ACAN) in chondrocytes given AED was found. The one study that measured these proteins with AED, from Khavinson's institute, used human mesenchymal stem cells: in cultures aged by repeated passaging, AED at 200 ng/mL raised gene expression and protein synthesis of SOX9, aggrecan, type II collagen and COMP, as a cartilage polypeptide complex did at 2,000 ng/mL (Myakisheva 2023, PMID 37782646).
• Anti-inflammatory / MMP modulation — AED lowered MMP-9 in aging skin fibroblasts (Lin'kova 2016, PMID 27259496) and normalized TNF-α and IL-1α in aging chondrocytes (Myakisheva 2023, PMID 37356100); no study of AED and MMP-13 was found.
• Fibroblast (a cell that builds collagen) / connective-tissue aging (sibling-peptide evidence) — Linkova 2016 (PMID 27259496) tested AED itself, with KE, KED and AEDG, in aging skin-fibroblast cultures: all four lowered MMP-9 and raised Ki-67 and CD98hc, and AED and AEDG also suppressed caspase-dependent apoptosis.
• DNA / chromatin interaction (proposed) — Fedoreyeva 2011 (PMID 22117547) showed nuclear penetration of fluorescence-labeled epithalon, pinealon and testagen; AED was not tested. The group's claim is that short peptides bind DNA in a sequence-specific way, including in gene promoters, and bind histones in ways that make promoters more accessible (Khavinson 2021, PMID 34834147); the framework applies this to Cartalax. For AED itself, the group's computer-docking model places it on the DNA sequence ACCT (Khavinson 2016, PMID 27909961).
• Thyroid C-cells (claimed) — The developers' patent claims that AED increases the number and activity of the thyroid's calcitonin-producing C-cells, from a study in rats whose pineal gland had been removed (0.5 μg per rat injected under the skin over 10 days); its own figures show fewer C-cells than in operated rats given saline (12 days after the course, about as many as in unoperated rats), with denser calcitonin staining (Khavinson et al., 2007). No peer-reviewed study of AED and C-cells was found.

Limitation: the group itself calls the molecular mechanism of short peptides unclear and offers DNA binding as its supposition (Khavinson 2016, PMID 27909961); for AED, the evidence of DNA binding is the group's computer modeling (Khavinson 2014, Advances in Gerontology, PMID 25946838; Khavinson 2016, PMID 27909961), and no study of AED from outside the group was found.

What the Research Shows

All 17 journal papers cited on this page come from Khavinson's institute or teams writing with it (Khavinson is an author on 12), and 6 are in Russian. The journal evidence is cell-culture and animal data, with no randomized controlled human trial; the developers' patent describes one small study in people with knee osteoarthritis (Khavinson et al., 2007).

• Kidney-cell aging (Khavinson, Tarnovskaya, Linkova et al. — Advances in Gerontology 2014; 27(4):651-656, PMID 25946838) — In young and aged rat kidney-cell cultures, AED and EDL raised cell proliferation and SIRT-6 and lowered the aging markers p16, p21 and p53; the paper's computer models place both peptides in the minor groove of the DNA sequence ATATATATAT. It is a kidney study, not a cartilage one.
• Fibroblast aging (Linkova 2016, PMID 27259496) — AED, KE, KED and AEDG all lowered MMP-9 and raised the proliferation and regeneration markers Ki-67 and CD98hc in aging skin fibroblasts; AED and AEDG also suppressed caspase-dependent apoptosis.
• Human skin fibroblasts (Fridman 2020, PMID 33231794) — In human skin fibroblasts aged by repeated passaging, AED raised the synthesis of sirtuin-1, sirtuin-6 and type I collagen. A cell study from Khavinson's institute.
• Stem cells and chondrocytes (Myakisheva 2023) — Two 2023 Russian-language cell studies from Khavinson's institute tested AED on cartilage-related cells: it raised SOX9, aggrecan, type II collagen and COMP in aging human mesenchymal stem cells (Myakisheva 2023, PMID 37782646) and normalized aging markers in chondrocytes (Myakisheva 2023, PMID 37356100).
• Kidney (Khavinson 2014; Chalisova 2015; Zamorskii 2018) — Much of AED's published cell and animal work is in kidney rather than cartilage. In aging rat kidney-cell cultures, AED (coded T-31) activated cell-renewal markers (Khavinson 2014, Bull Exp Biol Med, PMID 24958378); in kidney explants from young and old rats it raised proliferation and reduced apoptosis, though less than a calf-kidney peptide extract (Chalisova 2015, PMID 26033601); and in old rats it raised urine output and sodium excretion and lowered urine protein (Zamorskii 2018, PMID 30607912).
• Bone density in rats (Povorozniuk 2007, PMID 18306703) — In ovariectomized rats, a model of postmenopausal bone loss, a cartilage-extract preparation and a substance coded T-31 (the code the group's later papers use for AED) both prevented the drop in bone mineral density and raised it again after it had fallen, the extract more strongly. A Russian-language study co-authored by Khavinson.
• Tissue-specific differentiation (Khavinson/Linkova 2012, PMID 22808515) — Short peptides (pancragen, bronchogen and vesugen; not AED) raised differentiation markers in aged pancreatic, bronchial and prostate-fibroblast cultures.
• Gene-regulation review (Khavinson 2021, PMID 34834147) — Framing AED-class peptides within the broader epigenetic-bioregulator model.
• Nuclear penetration (Fedoreyeva 2011, PMID 22117547) — Labeled epithalon, pinealon and testagen reached the nuclei of HeLa cells; AED was not tested.
• Systemic immune context (Gumen 2006, PMID 17426849) — Vilon, Epithalon and Cortagen changed lymphocyte-activating-factor production by macrophages from young and old mice; AED was not tested.
• No osteoarthritis RCTs — No published randomized placebo-controlled human trials of AED for osteoarthritis, post-injury cartilage recovery, rheumatoid arthritis, or any joint-related endpoint exist in English-indexed peer-reviewed journals.
• No head-to-head vs standard osteoarthritis therapies — No trial has tested AED against or alongside NSAIDs, intra-articular corticosteroids, hyaluronic acid, PRP, or orthopedic surgical management.
• No imaging-based cartilage outcome data — No MRI-based cartilage-volume, T2-mapping, or Kellgren-Lawrence-progression data in humans.

Human Data

Synthetic Cartalax (AED) has not been evaluated in a randomized controlled trial published in a medical journal. The developers' patent describes one small study: 29 people aged 52–72 with knee osteoarthritis, randomly split into a group given AED injections into muscle once a day for 20 days and 12 controls given saline. It reports less pain and better joint movement in 54.5–62.7% of cases, depending on severity, and no significant change on X-ray, and it gives no results for the saline group (Khavinson et al., 2007). Other accessible human-use information consists of:

• Parent-extract Soviet-era observational use — Earlier Russian orthopedic and rheumatology observational reports on the polypeptide cartilage extract (not the defined AED tripeptide) describe anecdotal joint-pain and mobility improvements. These predate modern trial methodology.
• Supplement-line post-market — Oral AED capsule has been sold in Russia as a dietary supplement since the 2000s. Observational reports exist but do not constitute controlled human evidence. A 2023 review from Khavinson's institute states that AED, which it calls Kartalax, and a cartilage-and-bone extract "have shown high efficacy" in animal models of osteoarthritis and when taken by mouth by older patients with osteoarthritis; its English abstract names no study design or size (Myakisheva 2023, PMID 37782637).
• No human PK/PD — No human pharmacokinetic or pharmacodynamic data published for AED.
• No WADA-relevant performance data — No evidence of effect on athletic performance or anti-doping-relevant endpoints.
• No rheumatology society recognition — ACR, EULAR, OARSI, and AAOS do not mention Cartalax in any guidance document, scientific statement, or clinical practice guideline.

Where the Cartalax program intersects with the broader osteoarthritis and connective-tissue research literature — collagen biology, proteoglycan metabolism, MMP regulation, and chondrocyte survival pathways — there are thousands of peer-reviewed publications describing each of these biological axes in detail, but virtually none of them reference AED. The Khavinson-program contribution sits outside the mainstream rheumatology research community; there is essentially no citation crosstalk between the two. For a user evaluating Cartalax, the practical implication is that the compound's narrative and biological framing come almost entirely from a single lab group's papers, and independent verification at the level of cartilage-volume imaging, synovial-fluid biomarkers, histological scoring, or patient-reported outcome measures has not occurred.

Position Within Evidence-Based Osteoarthritis Care

Understanding where Cartalax fits — or does not fit — relative to current osteoarthritis management is important context for anyone considering it. OARSI 2019 and ACR 2019/2020 guidelines structure osteoarthritis treatment around a tiered model: foundational non-pharmacological management (exercise, weight management, education, patellofemoral offloading), then topical and oral NSAIDs, then intra-articular injections (corticosteroids, hyaluronic acid where indicated), then surgical options (arthroscopic where narrowly indicated, joint replacement in advanced disease). Every element of that model has RCT-level or meta-analytic support. Cartalax is not referenced in any of those guidelines, meta-analyses, or Cochrane reviews.

Within the pipeline of "disease-modifying osteoarthritis drugs" (DMOADs) — a research priority for two decades — compounds such as sprifermin (recombinant FGF-18), cindunistat, and lorecivivint have advanced through Phase 2/3 with MRI-based cartilage-volume endpoints. These programs sit in a completely separate research tradition from Cartalax and have orders-of-magnitude more evidence. When a community-level user considers "a peptide for cartilage," the scientific baseline comparison is with these clinical-development programs and standard-of-care management, not a Khavinson cross-referential claim.

Reconstitution & Storage

Seller listings give research-peptide Cartalax as lyophilized powder in 20 mg vials. The Russian supplement comes as 0.2 g capsules, 0.16 g and 0.3 g tablets and a sublingual liquid (RLS, 2022).

• Reconstitution — Reconstitution guides describe injecting BAC water slowly down vial wall at 45°, then swirling gently rather than shaking.
• Storage — A seller listing gives a 36-month shelf life for the powder, without a storage temperature; no storage figures for mixed vials were found. The Russian registration data list the capsules and tablets at 2–25°C, dry and away from light, for 5 years, and the sublingual liquid at 2–25°C, away from direct sunlight, for 3 years (RLS, 2022).

→ Calculator — vial-to-syringe math

Side Effects & Risks

• Tolerability — Khavinson's institute states that no side effects were found with its Cytogens, Cartalax among them (IBG product pages); the knee-osteoarthritis study in the developers' patent does not mention side effects (Khavinson et al., 2007). No other report on side effects in people was found.
• Toxicology — The only toxicity data found are the developers' own: no toxic reactions in mice after one injection of 1–5 mg/kg, and no changes in blood or organs in rats injected daily for 90 days or guinea pigs for 6 months at 1 μg/kg to 1 mg/kg (Khavinson et al., 2007). They are not peer-reviewed, and no reproductive or genotoxicity study was found.
• Not a substitute for rheumatology / orthopedic care — Cartalax does not replace physical therapy, NSAIDs, intra-articular injections, DMARDs, or joint replacement where indicated.
• Allergy / hypersensitivity — The institute's instructions and the Russian registration data list individual intolerance of the components as a contraindication (IBG product pages; RLS, 2022); no report of an allergic reaction to Cartalax was found.
• Purity / source concerns — Sold outside Russia as a research chemical, it is not held to drug-quality standards.
• Pregnancy / lactation / pediatric — The same instructions and registration data list pregnancy and breastfeeding as contraindications (IBG product pages; RLS, 2022); no safety study in pregnancy, breastfeeding or children was found.
• WADA status — Not specifically named on the 2026 WADA Prohibited List; its S0 clause covers substances no other section names and no government has approved for human therapeutic use (WADA Prohibited List 2026).
• Theoretical epigenetic concerns — The Khavinson group attributes AED's effects on gene expression to DNA binding (Khavinson 2014, Advances in Gerontology, PMID 25946838); if that is right, effects on genes other than the intended ones are a theoretical risk. No long-term safety study in people was found.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for Cartalax. The one human study found, in the developers' patent, judged it by pain, joint movement and knee X-rays; the patent's toxicity tests in rats and guinea pigs measured blood counts and blood chemistry (Khavinson et al., 2007).

Commonly Stacked With

No study of Cartalax given together with another compound was found. The combined-use schemes of Khavinson's institute list it with two other of its Cytogen capsules, Vesugen and Crystagen, for the musculoskeletal system (IBG product pages).

Stacking this? Read the receipt →

→ Calculator — vial-to-syringe math

Legal Status

Related Compounds

People researching Cartalax usually also check these Khavinson siblings:

Next Steps

References

1. Khavinson VKh, Tarnovskaia SI, Lin'kova NS, Poliakova VO, Durnova AO, Nichik TE, Kvetnoĭ IM, D'iakonov MM, Iakutseni PP. Tripeptides slow down aging process in renal cell culture. Advances in Gerontology. 2014;27(4):651-656. PMID: 25946838. (In Russian.)
2. Lin'kova NS, Drobintseva AO, Orlova OA, Kuznetsova EP, Polyakova VO, Kvetnoy IM, Khavinson VKh. Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro. Bulletin of Experimental Biology and Medicine. 2016;161(1):175-178. PMID: 27259496.
3. Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine. 2012;153(1):148-151. PMID: 22808515.
4. Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules. 2021;26(22):7053. PMID: 34834147.
5. Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Moscow). 2011;76(11):1210-1219. PMID: 22117547.
6. Gumen AV, Kozinets IA, Shanin SN, Malinin VV, Rybakina EG. Production of lymphocyte-activating factors by mouse macrophages during aging and under the effect of short peptides. Bulletin of Experimental Biology and Medicine. 2006;142(3):360-362. PMID: 17426849.
7. Khavinson VKh. Peptides and ageing. Neuroendocrinology Letters. 2002;23(Suppl 3):11-144. PMID: 12374906.
8. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
9. Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M. Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers. International Journal of Molecular Sciences. 2022;23(14):7733. PMID: 35887081.
10. Myakisheva SN, Linkova NS, Kozhevnikova EO, Polyakova VO, Ryzhak GA. Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging. Advances in Gerontology. 2023;36(2):234-238. PMID: 37356100. (In Russian.)
11. Myakisheva SN, Linkova NS, Diatlova AS, Polyakova VO, Ryzhak GA. The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging. Advances in Gerontology. 2023;36(3):383-390. PMID: 37782646. (In Russian.)
12. Khavinson VK, Lin'kova NS, Tarnovskaya SI. Short Peptides Regulate Gene Expression. Bulletin of Experimental Biology and Medicine. 2016;162(2):288-292. PMID: 27909961.
13. Fridman NV, Linkova NS, Kozhevnikova EO, Gutop EO, Khavinson VK. 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;170(1):154-157. PMID: 33231794.
14. Khavinson VKh, Lin'kova NS, Polyakova VO, Durnova AO, Nichik TE, Kvetnoi IM. Peptides regulate expression of signaling molecules in kidney cell cultures during in vitro aging. Bulletin of Experimental Biology and Medicine. 2014;157(2):261-264. PMID: 24958378.
15. Chalisova NI, Lin'kova NS, Nichik TE, Ryzhak AP, Dudkov AV, Ryzhak GA. Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals. Bulletin of Experimental Biology and Medicine. 2015;159(1):124-127. PMID: 26033601.
16. Zamorskii II, Shchudrova TS, Zeleniuk VG, Linkova NS, Nichik TE, Khavinson VK. The influence of peptides on the morphofunctional state of old rats kidneys. Advances in Gerontology. 2018;31(4):498-504. PMID: 30607912. (In Russian.)
17. Povorozniuk VV, Khavinson VKh, Makogonchuk AV, Ryzhak GA, Kreslov EA, Gopkalova IV. Effect of peptide regulators on the structural and functional status of bone tissue in ageing rats. Advances in Gerontology. 2007;20(2):134-137. PMID: 18306703. (In Russian.)
18. 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. Advances in Gerontology. 2023;36(3):313-323. PMID: 37782637. (In Russian.)
19. Khavinson VKh, Grigoriev EI, Malinin VV, Ryzhak GA. Peptide substance normalizing the metabolism in osseous and cartilaginous tissues, pharmaceutical composition on its base and the method of its application. Russian patent RU 2299741 C1; filed May 30, 2006, published May 27, 2007; patent holder SIA Peptides. International application WO 2007/139433 A1; December 6, 2007. patents.google.com/patent/RU2299741C1/ru and patents.google.com/patent/WO2007139433A1/en. Read October 4, 2026. (The developers' patent on Cartalax's peptide, H-Ala-Glu-Asp-OH; in Russian, with the international application in English.)
20. St. Petersburg Institute of Bioregulation and Gerontology. Cytogens; How to take. Product pages for its Cytogen capsules, Cartalax among them (state registration certificate No. 77.99.23.3.У.9174.8.06). old.gerontology.ru/pills/cytogens/ and old.gerontology.ru/pills/intake/. Read October 4, 2026. (In Russian.)
21. RLS (Register of Medicinal Products of Russia). Cartalax (capsules 0.2 g; tablets 0.16 g and 0.3 g) and Cartalax lingual (liquid): dietary supplement registration data, updated August 8, 2022. rlsnet.ru/baa/kartalaks-30386 and rlsnet.ru/baa/kartalaks-lingval-66642. Read October 4, 2026. (In Russian.)
22. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.

Related Research

• BronchogenKhavinson Bronchial Bioregulator
• CardiogenKhavinson Cardiac Bioregulator
• ChonlutenKhavinson Bronchial-Mucosal Bioregulator
• CortagenKhavinson Cortical / Neural Bioregulator
• FDA TrackerPCAC voted on 7 of the 12 peptides on July 23–24, 2026; FDA plans a PCAC review of the other 5 before the end of February 2027.