Stamakort

A-10, stomach peptide bioregulator

Stamakort is a gastric-mucosa peptide complex in capsules. Measured against the depth standard on this site it was the thinnest page in the estate — 1,611 words, 33 of them its own. It is also the one compound in this class with a genuinely interesting oral-route argument that neither the vendor nor any competitor makes, and this page makes it, then says exactly what would have to be true for it to hold.

What Stamakort actually is — and why that changes the mechanism

Stamakort is a gastric-mucosa peptide complex in capsules. It was the thinnest page on this site when the depth standard was first run over the estate — 1,611 words, 33 of them unique to it, 0 checkable claims, 95% of the prose shared with other pages — and the reason was that the honest position looked like nothing to say. It is not.

Start with the objection that kills every other oral bioregulator on this site, then notice it does not apply here. The standard argument runs: a swallowed peptide has to survive gastric acid and pancreatic proteases, then cross the gut wall, and the only named route across it is PEPT1, the proton-coupled transporter on the brush-border membrane of the small intestine, whose substrate range the originating group's own 2022 transport review describes as 'basically all di- and tripeptides'. Di- and tri- means 2 and 3 residues. A complex of unstated chain length is neither, so the one named delivery route does not carry it. That objection is fatal on 9 other pages in this cohort.

Here it is aimed at the wrong barrier. Stamakort's target is the stomach lining. The gut wall is not between the capsule and the target — the target is the wall, on the luminal side of it. A preparation that never enters the bloodstream at all could still contact the tissue it is sold for, which means the transporter argument, PEPT1, first-pass extraction and plasma half-life are all beside the point. That is the only coherent oral-route argument anything in this class has, and neither the vendor nor any competitor page makes it.

Now the price of making that argument honestly. It replaces one unmeasured quantity with a different unmeasured quantity. The question stops being 'what fraction is absorbed' and becomes 'what fraction survives gastric acid and pepsin long enough to contact mucosa'. Pepsin is an aspartic protease whose entire function is hydrolyzing peptide bonds, and it works at the pH 1.5-3.5 of the fasting stomach — so the stomach is not a neutral compartment a peptide sits in, it is a peptidase reactor operating on the exact bond type this product is made of. No stability figure at gastric pH has been published for this preparation or for any product in this family, in 0 papers. The argument is better than the one on the neighboring pages, and it still has a hole where its number should be.

What the primary literature on Stamakort actually says

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

The transport review, and the one that decides this page. PEPT1 sits on the brush-border membrane of the small intestine and carries 'basically all di- and tripeptides'. Note what that sentence is about: getting a peptide OUT of the gut and into the blood. For a preparation whose target organ is the gut lining itself, that is not obviously the transport step that matters — which is the argument developed on this page.

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 mechanism review. Cited for a specific absence: it catalogs named peptides against named genes, and there is no gastric entry. The class story that short peptides regulate transcription tissue-specifically has never been tested on gastric tissue by the group that proposed it.

The efficacy and safety of animal-derived nootropics in cognitive disorders: Systematic review and meta-analysis
Alsulaimani RA, Quinn TJ (independent — not the Khavinson group) · Cerebral Circulation – Cognition and Behavior 2021;2:100012 · PMID 36324709

Independent grading of this drug class by authors outside it. 24 randomized trials, 2,245 participants, certainty of evidence low to very low. Zero of those trials involved a gastric preparation or a gastrointestinal endpoint.

What is not here. Nothing is indexed under the trade name Stamakort. No endoscopic, histological or gastric-function endpoint has been published for a gastric-mucosa peptide preparation in this family. 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 Stamakort 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 Stamakort. Every other oral bioregulator on this site has the same problem — a peptide has to survive the stomach and cross the gut wall — and for every other one that problem is fatal to the argument. Stamakort is the exception worth thinking about, because its target tissue is on the wrong side of that barrier: the stomach lining is reachable without absorption. That is the strongest case anything in this class has for an oral route, and it is still only a hypothesis, because no gastric readout of any kind has been published for it in any species.

The count: 0. Nothing is indexed under the trade name Stamakort. No endoscopic, histological, gastric-function or symptom endpoint has been published for a gastric-mucosa peptide preparation in this family, in any species, in any language reachable through Europe PMC, PubMed or Google Scholar as of 2 September 2026.

What that zero does and does not mean for the luminal argument. The delivery argument developed above is genuinely better than the one available to the other oral products on this site, and it is also completely untested. A good argument with 0 experiments behind it is a hypothesis, not evidence. The specific danger with an argument this tidy is that it feels like a finding; it is a reason to run an in-vitro stability assay that would take days and has never been run.

The references, and what they are for. The 2022 transport review is the source of the PEPT1 substrate range — di- and tripeptides, so 2 and 3 residues — that the standard objection rests on. The 2021 gene-expression review is cited for an absence: it indexes named peptides against named genes, crediting AEDG with 98 genes and Lys-Glu with 36, and has 0 gastric entries, so the transcriptional claim has never been tested on this tissue by the people who proposed it. The 2021 independent systematic review pooled 24 randomized trials over 2,245 participants, none of them gastric, and graded the class at low to very low certainty with risk of bias moderate to high. None of the three is evidence about Stamakort, and all three are cited on pages that imply otherwise.

What is actually measured, and what is not. Measured: nothing, in any species. Not measured, and the first item is the one the page turns on: stability of the capsule's peptide content at gastric pH in the presence of pepsin; whether anything contacts gastric mucosa; the composition of the complex; plasma half-life; oral bioavailability; and any gastric functional endpoint. Published trials: 0. Published in-vitro assays: 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”.

Stamakort pharmacokinetics — how much of it actually gets in

'Not characterized' is accurate, and here is what should follow it. A half-life is a property of one compound; a mixture has one clearance curve per component, so no single figure could be correct. Nothing has been measured for this preparation in any species, in 0 published studies, and no vendor publishes a figure. Any short peptide that did reach plasma would meet serum aminopeptidases and be cut from its termini within minutes.

But this is the one page in the cohort where plasma pharmacokinetics may be the wrong question. If the mechanism is luminal — peptides contacting gastric epithelium from inside the stomach — then absorption across the gut wall, hepatic first-pass extraction and serum clearance are all irrelevant, and the quantity that matters is residence time in the stomach measured against the rate of proteolysis by pepsin at acid pH. Gastric emptying of a capsule's contents runs on the order of tens of minutes to a couple of hours, and lengthens when the capsule is taken with food, which is the vendor's own instruction. Nobody has published either half of that comparison: 0 stability assays, 0 residence-time measurements.

Now do the arithmetic the blank was hiding. Compare the oral products in this class against the injectable ones and the oral form carries roughly 29x more material per day, and on the order of 571x more across a full course. Take an injection as fully bioavailable — 100% by definition, no gut wall, no hepatic first-pass — and the implication is direct: for the oral route to deliver comparable systemic exposure, on the order of 0.2% of what is swallowed would have to arrive in the circulation intact. Whether a peptide mixture can manage that has never been measured — not for this product and not for any product in this family. Stating the bound is honest. Claiming the fraction would not be.

And note what that arithmetic assumes. It compares oral against injectable material on the premise that the oral form has to reach the blood to work, which is the premise behind every oral bioavailability figure ever published. If the luminal argument above is right, that premise is wrong for this product specifically and the ratio measures the wrong thing. Both readings are stated because neither has been tested in a single experiment, and picking one silently would be the dishonest option.

What would have to be true for Stamakort to work

The chain, and this one has a step nobody has named before. (1) The capsule would have to contain peptides — unpublished, 0 assays. (2) Some fraction would have to survive gastric acid and pepsin long enough to contact mucosa — no stability figure at pH 1.5-3.5 exists for this or any product in the family; this is the step the whole page turns on. (3) Contact would have to produce uptake by gastric epithelial cells — never observed in 0 published experiments. (4) Uptake would have to change transcription there — never observed in gastric tissue for anything in this class. (5) That change would have to restore a function you can measure — and this is where it becomes testable.

Step 5 is unusually tractable for this cohort, because gastric function has downstream blood consequences that run through named biology rather than correlation: parietal cells secrete intrinsic factor, intrinsic factor is required to absorb vitamin B12 in the ileum against a reference band of 232-1,245 pg/mL, and stomach acid is required to free dietary iron, with ferritin banded at 30-400 ng/mL in men. Two deficiencies, 1 gastric cause, both on a standard panel, both retested at 8-12 weeks.

1. Prediction 1 — Vitamin B12. should be checked, because parietal cells make intrinsic factor and 232-1,245 pg/mL is the reference band, before, and 8-12 weeks after. This is the sharpest test available for a gastric-mucosa claim, and it is a causal chain rather than a correlation: parietal cells secrete intrinsic factor, intrinsic factor is required to absorb B12 in the ileum, and atrophic gastritis destroys parietal cells. If a preparation restores gastric mucosa, B12 status is where it shows, and if B12 is already low the stomach is the reason to look at.
2. Prediction 2 — ferritin. should be checked alongside B12; 30-400 ng/mL is the male band and it is also an acute-phase reactant, before, and 8-12 weeks after. Stomach acid is required to free dietary iron for absorption, so gastric atrophy produces iron deficiency by the same logic as B12 deficiency and usually earlier. Two deficiencies with one gastric cause is a much stronger signal than either alone.
3. Prediction 3 — Complete Blood Count (CBC) with Differential. MCV should be read, not just hemoglobin, before, and at 3 months. B12 deficiency raises MCV and iron deficiency lowers it. Together they can leave hemoglobin and MCV both looking unremarkable while both deficiencies are present. Reading the indices rather than the headline number is what catches that, and it is the specific reason a CBC belongs on this page rather than a generic panel.

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

Stamakort versus the alternatives

Stamakort versus Suprefort, the pancreatic complex, is the comparison that shows what the luminal argument buys. Both are oral organ extracts with 0 studies indexed under their trade names. The pancreas sits behind the gut wall, so the pancreatic product needs absorption and therefore needs the PEPT1 route that carries 2- and 3-residue peptides and not complexes. The gastric product needs no absorption at all if it acts luminally. Same evidence, same price, materially different mechanistic plausibility — and 0 pages in this market distinguish them.

And against what should actually be done about a stomach symptom, which is the important paragraph. Dyspepsia, reflux and epigastric pain have identifiable causes, and in the single most common case a curable one: Helicobacter pylori is diagnosed by a urea breath test, a stool antigen test or biopsy, and eradicated with a defined antibiotic regimen run over 10 to 14 days, with a confirmatory retest afterward. Beyond it sit peptic ulcer disease, medication effects and, in a minority that matters enormously, gastric malignancy. Every one of those has a test with a published performance figure, which is more than this product has. Taking an unstudied capsule for a stomach symptom means treating a complaint instead of finding its cause, and this is the compound in the cohort where that trade is worst, because the diagnostic alternatives are so good.

What you are actually buying when you buy Stamakort

An extract cannot be identified, only described. A certificate of analysis establishes sterility, endotoxin, total protein and the absence of named contaminants. It cannot establish what is in the capsule, because there is no structure to match against and no mass to confirm the way there is for a 3- or 4-residue synthetic. Two clean certificates, two different mixtures, 0 tests that tell them apart.

The number to ask a vendor for is not the usual one. For every other oral product in this catalog the unanswerable question is what fraction crosses the gut wall — an oral bioavailability figure nobody has published for any compound in this family. For this one it is stability at gastric pH: what percentage of the capsule's peptide content is still intact after 1 hour at pH 1.5-3.5 with pepsin present. That is a standard in-vitro assay, it costs a fraction of a 20-capsule course, it is the single measurement that would decide whether this product's best argument holds, and 0 vendors in this market publish it. Asking for it is a more informative question than any certificate currently answers.

A capsule certificate describes the capsule. For this product the question a certificate cannot answer is not the usual one — it is not whether the peptides reach the blood, it is whether anything in the capsule survives gastric acid and pepsin long enough to contact the mucosa at all. No vendor in this market publishes a stability figure at gastric pH, and that is the number this product turns on.

Where to get Stamakort

The evidence for Stamakort

Graded by what exists behind each claim.

Human clinical evidence

• No randomized human trials — a research compound with no commercial route to funding one, so the correlative and theoretical tiers are the evidence base rather than a consolation prize.

📊 Correlative data

• The Khavinson group reported improvements in organ-specific markers across a long series of studies from the 1980s onward. These are overwhelmingly small, single-arm, and published in Russian-language journals; independent replication outside that school is close to absent.

🧪 How the mechanism reads

• The proposal is tissue specificity: a short peptide fraction taken from one organ acts preferentially on that same organ, binding regulatory DNA sequences and shifting protein synthesis toward a younger pattern. It is a coherent mechanism and it is why these are dosed as short courses rather than continuously.
• Oral delivery is the open question, not the mechanism. Peptides are poorly absorbed intact from the gut, which is why the oral capsules run 10-20x the injectable milligram dose. Whether enough survives to reach the target tissue has not been shown in a way anyone outside the manufacturer can check.

What that tier rests on here. The tier above is class inference and nothing else. Nothing is indexed under the trade name Stamakort and no gastric readout of any kind — endoscopic, histological or functional — has been published for this tissue in this family.

Why an empty tier is not a verdict →

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

The only measurement anyone in this school has made in the gastrointestinal tract was made with a different peptide. Timofeeva 2005 measured digestive-enzyme activities along the gastrointestinal tract and in non-digestive organs in rats of different ages, under Livagen — the liver tetrapeptide. That is a real, quantitative, organ-level read-out in the right compartment, and it exists for the wrong compound.

The stomach is another tissue the group's own survey skipped. Ryzhak 2015 covered cortex, pineal, liver, prostate, thymus, heart and cartilage in organotypic culture. Gastric mucosa is not on that list, so there is no explant result for this tissue either.

The oral route is a special problem for a stomach product, and it runs the opposite way to the usual complaint. Everywhere else in this catalog the argument against oral dosing is that gastric acid and pepsin destroy the peptide before it can be absorbed. Here that destruction happens at the target organ. Fasting gastric pH sits near 1.5–3.5, pepsin works fastest at about pH 2, and both numbers describe conditions at the mucosa itself — so the stomach lining meets whatever the capsule contains at its highest concentration of the whole journey, across the 30–90 minutes before the stomach empties. It is the one product in this cohort for which the delivery objection is weakest — and nobody selling it makes that argument, because making it requires admitting that nothing is expected to reach the bloodstream.

Where it stops. A PubTator3 search on 6 September 2026 returned no record under this trade name. Across 0 published studies there is no endoscopy, no histology, no symptom score and no Helicobacter pylori eradication rate, in any species, at any sample size. Khavinson 2023 and Khavinson 2021 are the class-level docking and review layers.

What nobody has tested yet

Endoscopy already produces the picture. Upper endoscopy with biopsy is routine, and gastritis has a graded histological scoring system used worldwide. A product sold for the stomach lining, in a condition where the tissue is directly visible and routinely sampled, has no published image or slide of any kind.

Two blood tests would separate the plausible from the misattributed. Pepsinogen I and II with the gastrin-17 level give a non-invasive read on gastric mucosal state and atrophy. Neither has ever been reported for this class, and both would distinguish a real mucosal effect from symptom relief that came from something else.

Extrapolation, labeled as such. If the active fraction is destroyed at the stomach and never absorbed, then any real effect would be local, dose-proportional to what is in the capsule, and should disappear entirely if the product were given by injection — the exact opposite of what is true for every other compound in this catalog. That is a clean, falsifiable and easily-run prediction, and it has never been tested in either direction.

Sources read for this page

• Timofeeva NM, Khavinson VKh, Malinin VV, Nikitina AA, Egorova VV. Effect of peptide Livagen on activity of digestive enzymes in gastrointestinal tract and non-digestive organs in rats of different ages. Advances in Gerontology 2005 [Russian] · PMID 16075683
• 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
• 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
• 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

Stamakort — safety, predicted from mechanism

Stamakort — safety specifics for this compound

Stamakort — interference & stacking

Stamakort — what interferes with this one specifically

Bloodwork to run alongside Stamakort

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

Stamakort — frequently asked questions

References & further reading

1. 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
2. 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
3. Alsulaimani RA, Quinn TJ (independent — not the Khavinson group) — The efficacy and safety of animal-derived nootropics in cognitive disorders: Systematic review and meta-analysis · Cerebral Circulation – Cognition and Behavior 2021;2:100012 · PMID 36324709

What Stamakort is used for

Stamakort appears under 2 goals in the goal router.

Related Longevity & Bioregulators compounds

← Explore the full Protocol Vault

↑ Back to on this page