Cartalax
AED (Ala-Glu-Asp)
Cartalax is Ala-Glu-Asp, the connective-tissue tripeptide. It is also the compound whose entry in this Vault was wrong until this page was written — it carried Vesugen's sequence. What follows is what the cartilage literature actually attaches to AED, and what it does not.
Cartalax quick facts
| Reported research dose | 1-2mg (can be escalated to 5mg) |
| Route | Subq |
| Frequency | 1x Daily |
| Half-life | Short |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
Cartilage and connective-tissue bioregulator. Short-course tool, sparse Western data. Vascular tissue with a connective-tissue emphasis, often run in joint protocols rather than cardiac ones. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, hs-CRP, and honestly, joint comfort under load. Run it as an experiment you measure, not a protocol you trust.
How Cartalax works — what 3 residues can and cannot do
Cartalax is Ala-Glu-Asp — a tripeptide, molecular weight 333.3 g/mol, isoelectric point 3.55, net charge about -2.1 at blood pH. Those four numbers are computed from the sequence, not quoted from a vendor.
Start with a correction, because this page carried a false statement until it was rebuilt. This Vault recorded Cartalax as KED (Lys-Glu-Asp). That is Vesugen's sequence. Two different products were listed as the same molecule, and the error is the kind that only shows up when someone actually reads across the catalog. Cartalax is AED, Ala-Glu-Asp. Linkova et al. name it directly — the cartilage polypeptide complex contains short peptides of 75 to 846 Da “including the tripeptide AED (Ala-Glu-Asp)” — and every vendor listing agrees. Corrected in the source data, and flagged here rather than changed quietly.
What the corrected sequence changes. Alanine's side chain is a methyl group: no charge, no hydrogen bonding, nothing to contact DNA with. So AED is a peptide with two acidic residues and one inert one, carrying a net charge near −2 at blood pH — the most negative peptide on these pages, and therefore the most strongly repelled by a polyanionic DNA backbone. Vesugen's lysine, one residue away, halves that repulsion. If the DNA-interaction mechanism is real, AED should be the weaker binder of the two, and that is a prediction the literature has never checked.
Three residues against the standard. A zinc finger reads three base pairs with about 30 amino acids. Three side chains, one of them inert, cannot carry promoter-address information — and the counting confirms it: a four-base site recurs every 44 = 256 base pairs, about twelve million times across the genome. What the originating group actually proposes is groove binding and local destabilization of base pairing, which is chemistry rather than gene targeting. Their systematic screen was run on dipeptides, found the vast majority could not bind double-stranded DNA at all, and expects longer peptides to be more selective without having measured it.
Ala-Glu-Asp. This corrects the Vault's own data. Cartalax was recorded here as KED (Lys-Glu-Asp), which is Vesugen's sequence — the two entries were identical, which is how the error shows. Linkova et al. 2023 identify AED as the tripeptide component of the cartilage polypeptide complex, and every vendor listing for Cartalax names Ala-Glu-Asp. Corrected, and flagged here rather than changed quietly.
What the primary literature on Cartalax actually says
Peptide Regulation of Chondrogenic Stem Cell Differentiation
Linkova N, Khavinson V, Diatlova A, Myakisheva S, Ryzhak G · International Journal of Molecular Sciences 2023;24(9):8415 · PMID 37176122
The cartilage-specific review. AED is described as 'a component of the polypeptide complex isolated from animal cartilage tissue'. In mesenchymal stem-cell ageing models it is reported to stimulate NFκB and IGF1 gene expression and to affect TNKS2; in replicative ageing of rat skin fibroblasts it is reported to regulate Ki67, CD98hc, caspase-3 and MMP9. MMP9 is the interesting one — it degrades collagen, so a compound claimed to help cartilage should be lowering it, and the paper's claim is regulation rather than a stated direction.
Peptide Regulation of Gene Expression: A Systematic Review
Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR · Molecules 2021;26(22):7053 · PMID 34834147
Places AED alongside KED and KE as regulators of IGF1, FOXO1, TERT, TNKS2 and NFκB in bone-marrow MSC cultures, and reports p53 effects in renal cell cultures.
Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers
Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M · International Journal of Molecular Sciences 2022;23(14):7733 · PMID 35887081
A tripeptide sits inside the PEPT1/PEPT2 substrate range, which is the only reason an oral form of anything in this class is arguable at all.
What is not here. Nothing is indexed under the trade name Cartalax. The AED record is cell work. Searched through Europe PMC, PubMed and Google Scholar on 2 September 2026. Naming the gap is more useful than filling it with a paragraph of hedging.
Why the Cartalax evidence is weak — and what it still showed
Almost every human result in this class comes from one school — Vladimir Khavinson's institute in St Petersburg and the groups around it. That means single-center data, collected by the people who developed the compound, rarely blinded, never pre-registered, and reported across enough endpoints that something was always going to move. Read anything below against that.
Specific to Cartalax. Every AED result in the literature is a cell-culture readout. There is no animal joint model published under this compound's name, no imaging endpoint, and no human trial. The mechanistic story is specific enough to be interesting — NFκB, IGF1, MMP9 are the right genes for a cartilage claim — and specific enough to be tested, which is precisely why the absence of any test is the honest headline.
What the data does support. The cartilage-specific review reports that AED stimulates NFκB gene expression in both replicative and stationary models of mesenchymal stem cell ageing, stimulates IGF1 expression in the same models, and affects TNKS2 in the replicative model. It separately reports that AED regulates the proliferation protein Ki67, the glycoprotein CD98hc, caspase-3 and MMP9 in a model of replicative ageing of rat skin fibroblasts.
MMP9 is the interesting one and the paper does not resolve it. Matrix metalloproteinase 9 degrades collagen. A compound sold to support cartilage should be lowering it. The paper says AED regulates MMP9 without stating a direction, and a reader is entitled to notice that “regulates” is doing a lot of work in a sentence where the direction determines whether the finding is good news or bad.
The specific epistemic position: named genes, named proteins, real cell-culture experiments — in mesenchymal stem cells and rat skin fibroblasts, not in chondrocytes and not in a joint. Nothing is indexed under the trade name Cartalax. No animal model of osteoarthritis, no imaging endpoint, no human anything. This is an absence of evidence, not evidence of absence, and the distinction is load-bearing here because the underlying cell work is genuinely real.
What is actually measured, and what is not. Measured, in cell culture: NF-kB and IGF1 gene expression stimulated in mesenchymal stem-cell ageing models; TNKS2 affected; Ki67, CD98hc, caspase-3 and MMP9 regulated in rat skin fibroblasts — with the direction of the MMP9 change not stated. Not measured: anything in chondrocytes; anything in a joint; delivery through avascular cartilage matrix; plasma half-life; clearance; and any human endpoint.
Not proven is not the same as disproven. Everything above says the evidence is weak. None of it says the compound does nothing. There is no adequately powered trial that ran and came back null, because outside Russia there is essentially no trial at all — this class is unfunded, not failed. A reader who leaves thinking “disproven” has learned something false, and so has one who leaves thinking “proven”.
Cartalax pharmacokinetics — how much of it actually gets in
What degrades it. Two peptide bonds, an exposed N-terminal alanine, no protecting groups. Serum and tissue aminopeptidases cleave it directly. The Vault lists the half-life as “Short”, and that is honest as far as it goes — no measured plasma half-life for Ala-Glu-Asp has ever been published, in any species.
What “Short” should say next. A tripeptide is inside PEPT1's described substrate range — “basically all di- and tripeptides” — so an oral form would at least have a named mechanism behind it, and Cartalax is sold injectable only. Subcutaneous injection is 100% bioavailable by definition: no gastric acid, no brush border, no hepatic first-pass. That matters more for this compound than for its siblings, because the claimed target is cartilage.
And cartilage is the hardest tissue in the body to reach. Articular cartilage is avascular — it has no blood supply at all, and nutrients arrive by diffusion through the matrix from synovial fluid. A systemically injected peptide with a minutes-scale serum half-life has to leave the circulation, cross into synovium, diffuse through a dense proteoglycan matrix, and reach chondrocytes before it is degraded. Nobody has measured any step of that for this molecule. It is the single biggest pharmacokinetic obstacle on any page in this cohort, and no other write-up of this compound mentions that cartilage has no blood supply.
The ratio the catalog itself implies. Across this class, the oral products carry a median of roughly 29x more material per day than the injectable ones. Nobody arrived at that by measuring absorption — no oral bioavailability figure has been published for any compound in this family — but the gap is the vendors' own implicit answer to the question: swallowing it is assumed to deliver a small fraction of what an injection delivers, and an injection is fully bioavailable by definition. Treat that as a bound on the plausible exposure, not as a measurement, because a measurement is exactly what is missing.
What would have to be true for Cartalax to work
What would have to be true. Ala-Glu-Asp would have to survive minutes in serum; leave the circulation into synovium; diffuse through avascular cartilage matrix to reach chondrocytes; enter those cells and their nuclei; and shift transcription enough to change matrix turnover. Step three is the one no other compound in this catalog has to solve, and it is unaddressed. The cell work jumps straight to the last step by putting the peptide in a dish with the cells.
Cartilage change is slow and hard to measure, so the honest predictions are about inflammation and function rather than about cartilage itself.
- Prediction 1 — hs-CRP (High-Sensitivity C-Reactive Protein). should fall if the NFκB claim holds in a whole organism, within a course. The named mechanism has a cheap systemic readout. Use it.
- Prediction 2 — ESR (Sed Rate). should track hs-CRP, or the signal is noise, within a course. Two inflammatory markers moving together is weak evidence; one moving alone in a single person is none.
- Prediction 3 — grip strength. should not change — this is a tissue claim, not a strength claim. Named to stop the wrong outcome being read as success. Connective-tissue compounds get credited with training adaptations constantly.
Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Cartalax did to it — and that difference is the entire point of testing.
Cartalax versus the alternatives
Cartalax versus Vesugen — and the reason this pairing matters. These two were recorded as the same molecule in this Vault until now. They are not: AED versus KED, one residue apart, differing by about one unit of net charge, sold for cartilage and for blood vessels respectively. Their published cell-culture profiles overlap heavily — both are reported to act on IGF1, TNKS2 and NFκB in marrow mesenchymal stem cells — which means the evidence that supposedly distinguishes them is largely the same evidence. If tissue specificity is real, one of these should work where the other does not; that experiment has never been run, and the two products are sold as though it had.
Cartalax versus Sigumir, the cartilage extract, is the same extract-versus-peptide trade as everywhere else: a product with no verifiable identity against a product with no clinical record.
And against the credible alternative. For joints, the things with human trial data are progressive loading, bodyweight management and structured rehabilitation — and for symptomatic relief, established pharmacology. They are less interesting and they work. A tripeptide with fibroblast data and an avascular target tissue is not a substitute for any of them.
What you are actually buying when you buy Cartalax
Defined tripeptide: one correct mass, confirmable by mass spectrometry, with HPLC purity beside it.
And the reason to check it here more than anywhere else. Until this rebuild, this Vault — and a good deal of the market it reads from — had Cartalax's sequence wrong. If the catalog can carry the wrong sequence, so can a vendor's label, and the buyer has exactly one defense: the expected mass of Ala-Glu-Asp against what the mass spectrum says. A certificate that reports purity without confirming identity is not answering the question that actually went wrong here.
Expect/mol. Because the Vault itself had this sequence wrong, assume a vendor can too: ask what sequence they are actually shipping, in three-letter code, and check the mass against it.
Where to get Cartalax
Buy Cartalax at Flawless Compounds →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Cartalax
Graded by what exists behind each claim.
Human clinical evidence
- The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.
📊 Correlative data
- Used for joint and connective tissue support, often in courses alongside Sigumir. Reported experience is slow and modest, and hard to separate from the natural fluctuation of joint symptoms.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- Ala-Glu-Asp-Gly — a defined tetrapeptide targeting connective and vascular tissue, proposed to normalize gene expression in vessel walls and cartilage matrix.
- The shared claim across the Khavinson series: peptides this short are proposed to enter the cell nucleus and bind promoter regions of DNA, shifting tissue-specific gene expression.
- Cartilage is the hardest tissue in the body to affect from the outside — it is avascular, so anything systemic has to diffuse in through synovial fluid. That is a real pharmacokinetic obstacle nobody in this series has addressed.
What that tier rests on here. The tier above rests on cell-culture work in mesenchymal stem cells and rat skin fibroblasts — not in chondrocytes and not in a joint. Nothing is indexed under the trade name Cartalax.
What community dosing logs are worth → · How to read the Soviet clinical series → · The Khavinson series, in full →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
Cell, rodent, human — and where it stops
Cartalax is the one bioregulator here whose tissue claim is backed by a paper about that exact molecule in that exact tissue. Linkova 2023 is about peptide regulation of chondrogenic stem cell differentiation, and Ala-Glu-Asp is the tripeptide in it. Three residues, 333.3 g/mol, two acidic side chains, computed net charge about −2.1 at blood pH. That is a rare thing in this catalog and it is worth saying before the qualification arrives.
Now the qualification. The paper is cell biology. Stem cells in culture, differentiation markers as the read-out, no joint, no animal, no person. The distance from a differentiation marker in a dish to a cartilage surface in a knee is the entire unsolved problem of this field, and nothing in the published record crosses it.
The delivery step is worse here than almost anywhere. Khavinson 2023 scored 26 of these peptides against LAT and POT carriers by molecular docking, comparing them against all possible di- and tripeptides, and measured no transport in any living cell. Khavinson 2022 is the earlier version of the same argument. Even if the carrier story were right, it delivers into the bloodstream. Cartilage is avascular. The last step of the journey is diffusion from synovial fluid into a dense matrix, and no paper in this class has measured that for anything.
Where it stops. No human study. No radiographic or MRI endpoint. No pain score. Khavinson 2021 is the class-wide gene-expression review, not a cartilage result, and Kolchina 2019 is structural modeling.
What nobody has tested yet
Does any of it reach synovial fluid? Joint aspiration is a routine clinical procedure, and mass spectrometry on aspirate would say within one sample whether an injected tripeptide arrives at the tissue it is named for. This has never been done for any compound in this class, and it is the step every claim on this page depends on.
The cartilage turnover markers already exist. CTX-II in urine and serum COMP are validated markers of cartilage degradation and are used in osteoarthritis trials. A compound claiming to support chondrogenesis has an obvious pair of numbers waiting for it and has never been measured against either.
Extrapolation, labeled as such. If AED works by driving mesenchymal cells down a chondrogenic path, the population in which it could plausibly matter is not an older knee with worn cartilage — it is a healing one, where progenitor cells are already mobilized. That predicts the effect would be largest after a cartilage injury or a microfracture procedure and near zero in established osteoarthritis. It is a specific, falsifiable and unflattering prediction about who this would help, and nobody has tested it in either direction.
Sources read for this page
- Linkova N, Khavinson V, Diatlova A, Myakisheva S, Ryzhak G. Peptide Regulation of Chondrogenic Stem Cell Differentiation. International Journal of Molecular Sciences 2023;24(9):8415 · PMID 37176122
- 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
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 2023;13(3):552 · PMID 36979488
- Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M. Systematic search for structural motifs of peptide binding to double-stranded DNA. Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
- Khavinson VKh. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine 2012 · PMID 22808515
- 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
Cartalax — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These are short peptide fragments of organ extracts, and the honest starting point is that the mechanism itself is not established in a way that lets anyone predict harm precisely. The proposal is gene-regulatory — short peptides binding DNA and modulating transcription in a tissue-specific way. If that is what they do, the theoretical concern is influencing transcription in tissue you were not aiming at.
- In practice the doses are tiny, the peptides are short, and they are degraded quickly — which is also the argument that they may do very little at all. Those two possibilities are the same uncertainty viewed from opposite ends, and you should hold both.
What has actually been reported
- Decades of Russian clinical use with a strikingly clean tolerability record — injection-site reactions and little else reported.
- That record comes almost entirely from one research school, is largely unreplicated outside it, and safety data from a group with an interest in the outcome is worth less than the same data from a skeptic. This is not an accusation; it is how evidence weighting works.
How to reduce the risk
Same mechanism as the prediction.
- Follow the course printed on the label rather than running continuously. These are the one class in the Vault where a duration is STATED rather than inferred, and it is typically 10–20 days repeated a few times a year. Read the box.
- Run one at a time. They are cheap and it is tempting to stack six. If something changes, a stack of six tells you nothing about which one did it — and given the evidence base, attribution is the entire value of your own experiment.
- Decide your endpoint before you start, and make it a marker or a measurable symptom rather than a feeling. With a compound class this under-evidenced, an unfalsifiable endpoint means you will conclude it worked no matter what happened.
- Buy from a source that publishes third-party testing. Where the molecule itself is uncertain, identity and purity are the only variables you can actually control.
What it does to your bloodwork
A fact about the assay.
- Test the ORGAN, not the peptide. A thymic peptide is judged on immune markers, a pineal one on sleep and IGF-1, a vascular one on lipids and inflammatory markers. There is no assay for the compound itself.
Don't run this if
- Pregnancy — not because of a specific finding, but because nobody has studied it and the mechanism claim is transcriptional.
- Active malignancy, on the same reasoning as any tissue-growth signal: unproven, mechanistically arguable, and not worth finding out.
The honest unknown
- Essentially everything a skeptic would want: independent replication, pharmacokinetics, and whether the oral forms survive digestion at all. Unproven is not the same as ineffective — but here it is a large unproven.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Cartalax — safety specifics for this compound
Specific to Cartalax: the cell-culture work reports stimulation of NFκB expression, which is an inflammatory transcription factor, in a compound sold for a condition whose main symptom is inflammation. The paper frames that as regulation of stem-cell differentiation; a reader with joint pain is entitled to notice that the named direction is upward. Nothing in the literature examines what that does in an inflamed joint, and no study has looked at MMP9 direction — the enzyme that degrades the tissue this compound is sold to protect. For a safety reader the NFκB finding is the whole point and it is worth stating twice: the cell-culture work reports AED stimulating NFκB gene expression in both replicative and stationary mesenchymal stem-cell ageing models, alongside IGF1 and TNKS2. NFκB is the transcription factor that runs the inflammatory response. Sold for joint pain, that is a mechanism pointed at the symptom, and hs-CRP is the marker that would show it — measured before and after in 0 studies, in any species.
Cartalax — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Cartalax moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
These are short peptide fragments given in microgram amounts and there is no mechanism predicting a specific marker shift. Listing markers here would be padding.
What to do: Test the organ system the bioregulator is aimed at, not a generic panel — that is the only measurement that would tell you anything.
The evidence base here is almost entirely one research group's, largely in Russian, and rarely replicated independently. That is the single most important thing to know before running a course, and it is more useful than any interaction list.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Reconstitution maths — the calculator
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Cartalax in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Cartalax
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Cartalax — frequently asked questions
What is the amino acid sequence of Cartalax?
Cartalax is Ala-Glu-Asp — 3 residues, 333.3 g/mol, isoelectric point 3.55. Those figures are computed from the sequence rather than quoted.
Can a peptide that short really bind DNA?
Not the way a transcription factor does. A zinc finger needs about 30 residues to read three base pairs. When Khavinson's group docked all 400 dipeptides against DNA, the vast majority could not bind double-stranded DNA at all. The claim is a computational prediction supported by gene-expression readouts in cells, not a measured binding event.
Is there a human trial of Cartalax?
Nothing is indexed under the trade name Cartalax. The AED record is cell work.
What should I measure if I run Cartalax?
Before and after, not after alone. The falsifiability section on this page names the specific markers, the direction each should move and the timescale — and says what a null result would rule out.
References & further reading
- Linkova N, Khavinson V, Diatlova A, Myakisheva S, Ryzhak G — Peptide Regulation of Chondrogenic Stem Cell Differentiation · International Journal of Molecular Sciences 2023;24(9):8415 · PMID 37176122
- 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
- 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
Cartalax inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Cartalax is used for
Cartalax appears under 3 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Cartalax is the cardiac & vascular arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.