Sigumir

Val-Glu-Pro-Asp (cartilage)

Sigumir is sold as a cartilage peptide complex, and this site's own record contradicts itself about what it is: the display field names a four-residue sequence, while everything else on the card describes an organ extract. Those cannot both be the top-level description, one mass spectrum would settle it, and nobody has published one. That contradiction is the most useful thing on this page, so it is the first thing on it.

What Sigumir actually is — and why that changes the mechanism

This page has to start with a contradiction in its own data, because everything else depends on which half of it is true. The card for this compound describes a cartilage peptide complex — an extract. The same card's display field names a four-residue sequence, Val-Glu-Pro-Asp. A product cannot be both. An extract is a mixture defined by its process and has no formula; a tetrapeptide is one molecule with one mass.

The sequence claim is checkable, so check it. If Sigumir really were Val-Glu-Pro-Asp, the consequences are computable and none of them are opinions: molecular weight 458.5 g/mol, molecular formula C₁₉H₃₀N₄O₉, isoelectric point 3.55, and a net charge of about −2.1 at blood pH, because two of the four residues are acidic. A single mass spectrum distinguishes that from an extract in one run. Nobody has published one.

Where the sequence claim comes from matters too. It is in a display field, not in this site's verified sequence record — the file that exists precisely so a sequence used for chemistry is never seeded from recall. That record already caught one error of exactly this kind in this catalog: Cartalax was listed with Vesugen's sequence until a peer-reviewed source named the cartilage tripeptide as Ala-Glu-Asp. Val-Glu-Pro-Asp appears in no source in this reference list. Treat it as a vendor claim awaiting a mass, which is what it is.

And now the physical problem that applies whichever answer is right. Articular cartilage is avascular. It has no blood supply, so nothing injected subcutaneously arrives there by circulation the way it arrives at the kidney or the liver; it has to reach chondrocytes by diffusion from synovial fluid, through a dense matrix, to cells that make up a small minority of the tissue's volume. That barrier is why cartilage-directed drugs are hard in general, and it is a real obstacle rather than a rhetorical one. No compound in this class has been shown to cross it, and no page in this market mentions that it exists.

What the primary literature on Sigumir 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 one paper in this reference list that is genuinely about this tissue. It reviews peptide regulation of chondrogenic stem-cell differentiation and names the cartilage tripeptide as AED, Ala-Glu-Asp — the compound this site carries separately as Cartalax. It does not study a cartilage extract, it does not name Sigumir, and it reports cell-culture differentiation rather than any joint outcome.

Systematic search for structural motifs of peptide binding to double-stranded DNA
Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M · Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715

The docking screen, 108,800 complexes, binder threshold about -32. Cited here for the arithmetic it makes possible rather than for cartilage: it is a screen over defined sequences, so it can say something about a tetrapeptide and nothing at all about a complex. Which of those two things Sigumir is has not been established.

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

The gene-expression review. It indexes by sequence, and there is no cartilage-extract entry. The chondrocyte gene-regulation claim printed on vendor pages for this product is a claim about a peptide, transferred to a preparation that may or may not contain it.

What is not here. Nothing is indexed under the trade name Sigumir. The cartilage peptide literature that does exist is published on the tripeptide AED, which this site carries separately as Cartalax. 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 Sigumir 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 Sigumir. Two things are wrong with the Sigumir record and they are different in kind. The first is an evidence gap: no trial, no animal study, no joint endpoint, under this name, anywhere. The second is an identity problem that sits upstream of the first — the product is described simultaneously as a tetrapeptide and as an organ extract, and until that is resolved there is no way to say which body of reasoning even applies to it. Every other page in this cohort can at least say what the thing is.

The count: 0. Nothing is indexed under the trade name Sigumir. No joint endpoint, no imaging endpoint, no cartilage histology, no pain score, in any species, in 0 papers. Searched through Europe PMC, PubMed and Google Scholar on 2 September 2026 under the trade name and the tissue name.

What the one on-tissue paper actually reports. The chondrogenic differentiation review is a real paper about this tissue, and it is about the tripeptide Ala-Glu-Asp in cell culture — the compound this site carries separately as Cartalax. Published in 2023, it does not study an extract, does not name Sigumir, and reports differentiation markers in cultured cells rather than anything that happened in a joint. Citing it on this page without saying that is how a cell-culture result becomes a cartilage claim, and that transfer is made routinely in this market.

The epistemic position, and it is the odd one in this cohort. Every other page here can at least state what the product is before reporting that nothing has been published about it. This one cannot. The identity question sits upstream of the evidence question, and it is the cheaper of the two to answer: a mass spectrum costs a fraction of a 10-20 day course and would settle in 1 run, against a target of 458.5 g/mol, what the entire literature has not.

What is actually measured, and what is not. Measured: nothing about this product. Computable from the sequence its own listing claims, if that claim is true: molecular weight 458.5 g/mol, formula C₁₉H₃₀N₄O₉, isoelectric point 3.55, net charge about −2.1 at blood pH. Not measured: a mass spectrum that would confirm or refute that sequence; the composition if it is an extract; delivery into avascular cartilage; and any joint endpoint in any species. Published trials under this name: 0.

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”.

Sigumir pharmacokinetics — how much of it actually gets in

The half-life on this card is about 15-30 min, and that figure has no study behind it. If the product is an extract it cannot have a single half-life at all, because a mixture has one clearance curve per component. If it is the tetrapeptide, then serum aminopeptidases and proteases cut it from the termini within minutes and the figure is plausible — but it would then be a computed expectation, not a measurement, and it has never been measured for this product in any species.

Why the number matters less here than usual, and what replaces it. Plasma clearance is the wrong quantity for an avascular target. The rate that governs whether anything reaches a chondrocyte is diffusion from synovial fluid into a dense extracellular matrix, and that is slow, concentration-driven, and nobody has measured it for anything in this class. A short plasma half-life and a slow diffusion barrier in series is the least favorable combination in this catalog, and it is a structural argument that would hold even if the identity question were settled tomorrow.

The oral form adds the standard barrier on top. A swallowed peptide meets gastric acid, pancreatic proteases and then the brush border of the small intestine, where the class's named transport route, PEPT1, carries di- and tripeptides; anything absorbed then passes hepatic first-pass extraction. Oral bioavailability has never been published for this product. An injection skips all of that and is 100% bioavailable by definition, which is why the two routes cannot be treated as interchangeable even though this product is sold as though they are.

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 Sigumir to work

Two chains, because the product has two possible identities, and they fail differently. If it is Val-Glu-Pro-Asp: the mass must confirm at 458.5 g/mol — never published; the peptide must survive to reach synovial fluid — never measured; it must diffuse into avascular matrix and enter chondrocytes — never observed for any compound in this class; and it must alter transcription there in a way that changes tissue behavior — observed for a different tripeptide in cultured cells, never in a joint.

If it is an extract: every one of those steps still applies, and step one becomes unanswerable rather than merely unanswered, because there is no mass to confirm. The first experiment is the same either way and it is not a clinical trial. It is one run on a mass spectrometer, and the fact that it has not been done is the most concrete thing this page can tell you.

1. Prediction 1 — hs-CRP (High-Sensitivity C-Reactive Protein). should be flat in a mechanical joint problem and may fall in an inflammatory one, 3 months. This is the prediction that sorts the two kinds of joint pain before you spend anything. Osteoarthritis is largely mechanical and typically leaves hs-CRP under 3.0 mg/L; an inflammatory arthritis does not. A cartilage product bought for a joint whose problem is inflammatory is aimed at the wrong tissue entirely.
2. Prediction 2 — ESR (Sed Rate). should be within 0-15 mm/hr; a persistently raised value points away from cartilage, 3 months. Paired with hs-CRP for the same reason as above, and slower, so it is harder to move by accident. Two normal inflammatory markers alongside joint pain is a reasonable argument that the problem is structural — which is the only situation where a cartilage claim is even on topic.
3. Prediction 3 — Vitamin D (25-Hydroxy). should be in the sufficient band of 30-100 ng/mL before anything else is tried, before starting, then 8-12 weeks after a change. Deficiency is under 20 and insufficiency 20-29, both common, both cheap to fix, and both associated with musculoskeletal pain that people spend far more than this product costs trying to treat. Correcting it first is what makes any later result interpretable.
4. Prediction 4 — osteocalcin. worth a baseline; 9-42 ng/mL is the reference band, annually. Osteocalcin is made by osteoblasts and reports bone formation, not cartilage. It is on this list precisely to mark the boundary: there is no blood marker of cartilage turnover on this site, or on most panels, which is a limitation of the testing rather than of the product and should be said plainly.

Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Sigumir did to it — and that difference is the entire point of testing.

Sigumir versus the alternatives

Sigumir versus Cartalax is the comparison the data forces. Cartalax is Ala-Glu-Asp — three residues, confirmed against a peer-reviewed source that names the cartilage tripeptide explicitly, with a mass a laboratory can verify. Sigumir is a product whose own listing cannot decide whether it is a tetrapeptide or an extract. On verifiability that is not close. On clinical evidence both stand at 0 joint endpoints, and the cell-culture work that exists belongs to the tripeptide.

And against what actually has evidence in osteoarthritis, which is unglamorous and works. Progressive loading and strength training have randomized trial evidence for pain and function; body-weight reduction has evidence for knee load; and where there is inflammatory rather than mechanical joint disease, that is a diagnosis with disease-modifying treatment and a peptide is not part of it. The two blood markers that separate those cases — hs-CRP against the under 3.0 mg/L band and ESR against 0-15 mm/hr — cost less than a course and decide which conversation you are in. Running them first is worth more than anything on this page.

What you are actually buying when you buy Sigumir

This is the one product in the cohort where the identity section is not boilerplate, because the identity is genuinely unresolved. If the vendor stands behind the 4-residue sequence, then a certificate of analysis is meaningful: mass spectrometry can confirm 458.5 g/mol and the formula C₁₉H₃₀N₄O₉, and HPLC can put a number on purity. Ask for both, and check the mass — it is the one claim on the vial a laboratory can falsify.

If the vendor says it is an extract, the sequence should come off the label, and what remains cannot be identity-tested at all: a certificate can establish sterility, endotoxin, total protein and the absence of named contaminants, and nothing more, because a preparation defined by its process has no structure to match. The useful move is to ask the question directly and see which answer comes back. A vendor that answers 'both' has answered 'neither' — and 0 vendors in this market have published a mass spectrum for any extract they sell.

Ask for the mass. If the vendor's own listing names a four-residue sequence, then mass spectrometry can confirm or refute it in one run, and a vendor unwilling to produce that has told you which of the two descriptions is real. If the answer is that it is an extract, then the sequence should come off the label, and no certificate can establish identity for what remains.

Where to get Sigumir

The evidence for Sigumir

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

• The cartilage/bone extract, sold for joint support and age-related bone change. Same practical position as the rest of the extract arm.
• Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.

🧪 Theoretical / extrapolated

• A cartilage and bone-derived peptide complex proposed to regulate chondrocyte gene expression.
• Two things at once: the mechanism is a real, testable hypothesis with published cell-level work behind it, and essentially all of that work is one group's, unreplicated at scale.
• Bone density is one of the easiest endpoints to measure objectively — a DEXA scan before and after a year of use would produce a real answer. That such a test has never been published is the most useful thing to know here.

What that tier rests on here. The tier above rests on cell-culture work about a different compound: the chondrogenic differentiation literature is published on the tripeptide Ala-Glu-Asp, which this site carries as Cartalax. Nothing is indexed under the trade name Sigumir, and the product's own listing has not settled whether it is a peptide or an extract.

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

Cartilage is one of the seven tissues the group's own extract survey actually tested, which makes this one of the better-documented extracts here. Ryzhak 2015 compared calf-derived polypeptide preparations from cortex, pineal, liver, prostate, thymus, heart and cartilage in organotypic culture, using explants from rats of different ages. That is the closest thing to a Sigumir experiment in the literature: a cartilage extract, in a dish, with an explant growth index as the read-out.

What it is not. An organotypic explant is a fragment of tissue in a nutrient medium with the compound added directly to it. It bypasses the stomach, the liver, the bloodstream and the synovial membrane — every barrier that decides whether an oral capsule does anything. It also bypasses load, which is the variable that actually governs cartilage health in a living joint.

The other paper on this tissue is about a different molecule. Linkova 2023 concerns chondrogenic stem cell differentiation and the tripeptide Ala-Glu-Asp, which this site sells separately as Cartalax. It is a defined molecule with a mass a laboratory can confirm. Sigumir is not that molecule, and the two results are not interchangeable.

What a search actually returns, which is not nothing and is not the product either. A PubTator3 search on 6 September 2026 returned three records, and no record carries this trade name in its title. Two of the three are worth naming. Myakisheva 2023 is a 2023 review of the aging chondrocyte secretory phenotype in osteoarthritis and the prospects for peptide bioregulation — the right tissue, the right disease, and a review rather than a result. Iordanishvili 2012 is the closest thing in this whole class to a human joint endpoint: bioregulating therapy in the treatment of temporomandibular joint disease in elderly and senile patients, in 2012. A jaw joint is a joint. It is also a different joint, a mixed therapy, and a paper that does not name this product.

Where it stops. For Sigumir itself there is no pain score, no radiograph, no MRI cartilage thickness and no histology, in any species, at any sample size. Kolchina 2019 and Khavinson 2021 are the structural and review layers under the whole class, not evidence about a knee.

What nobody has tested yet

WOMAC and a walking test would cost nothing and have never been run. Osteoarthritis research has validated, free, patient-reported instruments and timed functional tests that any trial can use. A cartilage product with decades of availability and zero published functional data has not been tested against the standard of its own field.

The biochemical markers exist too. Urinary CTX-II tracks type II collagen breakdown and serum COMP tracks cartilage turnover. Both are used in real osteoarthritis trials, both are orderable, and neither has ever been reported for this class.

Extrapolation, labeled as such. Cartilage has no blood supply, so anything reaching a chondrocyte arrives by diffusion from synovial fluid through a dense proteoglycan matrix — a process measured in hours to days, not minutes. That predicts something specific: a plasma half-life measured in minutes is almost irrelevant here, because the rate-limiting step is on the far side of the joint capsule. It also predicts that if anything works, it works slowly and would need months rather than weeks to show on any structural measure. Nobody has measured joint-space diffusion for any peptide, so this remains a physical argument rather than a finding.

Sources read for this page

• Myakisheva SN. Chondrocytes secretory phenotype associated with aging: role in the pathogenesis of osteoarthritis and prospects for peptide bioregulation. Advances in Gerontology 2023 [Russian] · PMID 37782637
• Iordanishvili AK. Application of bioregulating therapy in complex treatment of temporomandibular joint diseases in people of elderly and senile age. Advances in Gerontology 2012 [Russian] · PMID 22708467
• 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
• Ryzhak AP, Chalisova NI, Lin'kova NS, Khalimov RI, Ryzhak GA, Zhekalov AN. [Polypeptides influence on tissue cell cultures regeneration of various age rats]. Advances in Gerontology 2015;28(1):97-103 [Russian] · PMID 26390619
• 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, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules 2021;26(22):7053 · PMID 34834147
• Khavinson VKh. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine 2012 · PMID 22808515

Sigumir — safety, predicted from mechanism

Sigumir — safety specifics for this compound

Sigumir — interference & stacking

Sigumir — what interferes with this one specifically

Bloodwork to run alongside Sigumir

Baseline first, then again at 8–12 weeks.

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

Sigumir — frequently asked questions

References & further reading

1. 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
2. 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
3. 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

Sigumir inside a finished plan

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What Sigumir is used for

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