Glandokort
A-17, adrenal peptide bioregulator
Glandokort is an adrenal-derived peptide complex, listed as A-17. It is sold into the largest and least well-defined complaint in wellness, and the useful thing this page can do is separate the parts of that complaint that have real measurements from the parts that do not. The adrenal cortex is not one gland doing one job; it is three zones making three classes of hormone under three different controls, and 'adrenal support' names none of them.
Glandokort quick facts
| Reported research dose | 40-160mg daily (1-2 capsules, 1-2x daily with food · 40mg/capsule) |
| Route | Oral |
| Frequency | 1-2x Daily · Daily during a course |
| Half-life | Not characterized |
| Forms | Oral |
| Evidence level | Theoretical — Khavinson-school work, largely Russian-language and rarely replicated outside it |
The Khavinson literature behind this is decades deep, almost entirely Russian-language, and rarely replicated by any independent group — small single-arm series rather than controlled trials. Absence of replication is not evidence it fails; it is an absence of the evidence that would settle it either way. Dose and course length follow the manufacturer's convention, not a trial. Adrenal insufficiency is a real diagnosis with a real treatment; this is not it. Adrenal-directed, usually run for fatigue reasons. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, morning cortisol and DHEA-S, drawn at the same time of day both times. Run it as an experiment you measure, not a protocol you trust.
What Glandokort actually is — and why that changes the mechanism
Glandokort is an adrenal-derived peptide complex in capsules, listed as A-17. It is sold into the biggest and vaguest complaint in the wellness market, and the most useful thing this page can do is take the word 'adrenal' apart, because the gland does not behave the way the marketing assumes.
The adrenal cortex is 3 tissues, not 1. The zona glomerulosa makes aldosterone under the renin-angiotensin system and serum potassium, with an upright reference band of 4-31 ng/dL. The zona fasciculata makes cortisol under pituitary ACTH, banded 6.2-19.4 µg/dL on a 7-9am draw, with the peak arriving 30-45 minutes after waking. The zona reticularis makes DHEA and other androgen precursors, read as DHEA-S at roughly 280-640 µg/dL in the twenties falling to 40-330 µg/dL by the seventies — a fall of about 2-fold at the top of the band and about 7-fold at the bottom. 3 zones, 3 hormone classes, 3 control systems, and inside the same organ a medulla of completely different embryonic origin making catecholamines, whose plasma half-life is measured in minutes. 'Adrenal support' selects none of them, and the interventions for problems in each are unrelated to each other.
What the complex commits to, quantified. A peptide of 2 residues has 20 × 20 = 400 possible identities and one of 3 residues has 8,000; the label chooses among none. The 2021 gene-expression review carrying this class's mechanism is indexed by sequence — 98 genes for AEDG, 36 for Lys-Glu — and holds 0 adrenal entries.
And the version of the claim that would actually be worth testing. Strip away the syndrome language and there is a real research question underneath: does the cortisol rhythm flatten with age and chronic stress? Cortisol peaks 30-45 minutes after waking and falls through the day, and the shape of that curve is a measurable thing. A product claiming to restore adrenal function is, at its most defensible, claiming to steepen a flattened diurnal slope. That is specific, it is falsifiable, a 4-point salivary series across 1 day measures it, and 0 studies have done it for this product in the 5 years since the independent 2021 review of this class.
What the primary literature on Glandokort actually says
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 2021 gene-expression review, source of the class mechanism, indexed by peptide sequence — 98 genes credited to AEDG, 36 to Lys-Glu. There is no adrenal entry, because a complex has no sequence to index. Every transcriptional claim made for this capsule is borrowed.
Peptides of pineal gland and thymus prolong human life
Khavinson VKh, Morozov VG · Neuro Endocrinology Letters 2003;24(3-4):233–240 · PMID 14523363
The 266-subject elderly series, cited for its actual content: thymus and pineal preparations, injected, over 6-8 years. No cortisol measurement, no ACTH, no DHEA-S, no adrenal endpoint of any kind.
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 2019 docking screen — 108,800 peptide-DNA complexes at a binder threshold near -32. Defined sequences only, and nothing derived from adrenal tissue has been identified, let alone screened.
What is not here. Nothing is indexed under the trade name Glandokort. No cortisol, ACTH, DHEA-S or aldosterone endpoint has been published for an adrenal-derived 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 Glandokort 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 Glandokort. The specific weakness here is that the product is sold for a syndrome that is not a diagnosis, while the real adrenal disorders it could be confused with are diagnosable and dangerous. Cortisol runs 6.2-19.4 µg/dL on a 7-9am draw and follows a strong circadian rhythm, peaking 30-45 minutes after waking and falling through the day, so a single random value answers almost nothing. DHEA-S falls with age from roughly 280-640 µg/dL in the twenties to 40-330 µg/dL by the seventies. ACTH at 7.2-63 pg/mL separates a primary adrenal problem from a pituitary one. None of those numbers has ever been reported before and after a course of this product, in 0 published studies.
The count: 0. Nothing is indexed under the trade name Glandokort, and 0 cortisol, ACTH, DHEA-S or aldosterone results have been published for an adrenal-derived peptide preparation in this family. Searched through Europe PMC, PubMed and Google Scholar on 2 September 2026.
The harder point, and it is about the market rather than the molecule. This product is sold against a syndrome that is not a recognized diagnosis, and that matters in a specific way: an unfalsifiable target guarantees an unfalsifiable result. If the endpoint is 'feeling less depleted', every course succeeds. If the endpoint is a diurnal cortisol slope, or a DHEA-S value against a band that runs 280-640 µg/dL in the twenties and 40-330 µg/dL by the seventies, a course can fail. Only the second kind of endpoint is worth anybody's money, and the second kind has never been reported at 8-12 weeks or at any other interval.
What the citations are for. The 266-subject elderly series used thymus and pineal preparations by injection over 6-8 years with 0 adrenal endpoints — no cortisol against the 6.2-19.4 µg/dL band, no ACTH against 7.2-63 pg/mL, nothing. The 2021 gene-expression review is keyed on sequences this product does not have. The 2021 independent review pooled 24 randomized trials over 2,245 participants on cognitive outcomes and graded certainty low to very low. None of them is evidence about the adrenal cortex.
What is actually measured, and what is not. Measured for this product: nothing, in 0 studies. Measurable by anyone, and never reported for it: a morning cortisol against 6.2-19.4 µg/dL, ACTH against 7.2-63 pg/mL, DHEA-S against a band that falls from roughly 280-640 µg/dL in the twenties to 40-330 µg/dL by the seventies, and an upright aldosterone against 4-31 ng/dL. The measurement that would actually test the interesting version of the claim — a diurnal cortisol slope across 4 points — has also never been done.
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”.
Glandokort pharmacokinetics — how much of it actually gets in
The half-life field reads 'not characterized' and that is correct. A mixture has one clearance curve per component; 0 measurements exist for this preparation in any species.
What can be reasoned, and one comparison that is specific to this gland. A short peptide reaching plasma meets serum aminopeptidases and clears in minutes. Hold that against the system it is aimed at: ACTH, the native peptide signal to the adrenal cortex, is itself a short-lived circulating peptide, which is precisely why cortisol is pulsatile and why the time of a blood draw matters so much. A short half-life therefore does not argue against a peptide acting here. What it does argue is that serum concentration of the product is the wrong thing to chase, and the endpoint has to be the hormone output rather than the input.
The oral barrier. Swallowed, a peptide meets gastric acid, pancreatic proteases and then the brush border of the small intestine, where PEPT1 carries di- and tripeptides — 2 and 3 residues — and not complexes; whatever crosses faces hepatic first-pass extraction before reaching an artery. 0 oral bioavailability figures have been published for any product in this family, and an injection is 100% bioavailable by definition.
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.
What would have to be true for Glandokort to work
The chain. (1) The capsule would have to contain active peptides — 0 published assays. (2) A fraction would have to cross the gut wall intact — the named route carries 2- and 3-residue peptides. (3) It would have to reach cortical cells in 1 of the 3 zones — never measured, and the product names neither a zone nor which hormone it means: aldosterone at 4-31 ng/dL, cortisol, or DHEA-S. (4) It would have to change transcription there — never observed in adrenal tissue for anything in this class. (5) A hormone output would have to move in a stated direction — and the direction has never been stated.
The measurement that separates a real claim from a comfortable one. A single morning cortisol between 6.2-19.4 µg/dL cannot see a rhythm that takes 24 hours to trace, and rhythm is where the interesting question lives. Anyone making a serious version of this claim should be measuring the slope — waking, 30-45 minutes after waking, midday and evening — before and after. That is the difference between an endpoint and a feeling.
- Prediction 1 — Cortisol (AM). a morning draw at 7-9am, banded 6.2-19.4 µg/dL, is the baseline — but the slope matters more than the value, before, and after a full course. This is the prediction that shows what a serious version of the claim would look like. Cortisol peaks 30-45 minutes after waking and falls through the day, and the interesting research question about aging and stress is whether that slope flattens. A single morning number cannot see a slope. A 4-point salivary series can, and it is the measurement anyone making a rhythm claim should be held to.
- Prediction 2 — dhea-s. should rise if an adrenal-cortex claim means anything; the band falls with age from about 280-640 µg/dL in the twenties to about 40-330 µg/dL by the seventies, 8-12 weeks. DHEA-S is the most abundant circulating adrenal steroid, the sulfated form is stable through the day so timing barely matters, and its age-related decline is exactly the phenomenon this product is sold against. If the claim has any content, this is the cheapest place it would appear.
- Prediction 3 — ACTH (Adrenocorticotropic Hormone). read with cortisol at 7.2-63 pg/mL, because the pair says where a problem sits, with the cortisol draw. This is the fork. A low cortisol with a high ACTH points at the adrenal gland itself; a low cortisol with a low or inappropriately normal ACTH points at the pituitary. Those are different diseases. An adrenal-directed product is only on topic for the first, and buying it without the pair means never finding out which one you have.
- Prediction 4 — aldosterone. worth knowing exists; upright 4-31 ng/dL, and it varies with posture, sodium and time of day, only if blood pressure or potassium is abnormal. This entry is here to make the zonal point concrete. Aldosterone comes from a different zone of the same gland, under a different control system entirely, and is the one adrenal hormone with a common, treatable, frequently missed excess state that presents as hypertension. A product that says 'adrenal' without saying 'zone' is not addressing it.
Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Glandokort did to it — and that difference is the entire point of testing.
Glandokort versus the alternatives
Glandokort versus finding out what the fatigue actually is, which is the paragraph worth the page. Persistent tiredness has a differential that ordinary tests cover: hypothyroidism, iron deficiency, anemia, sleep apnea, depression, poorly controlled glucose, and medication effects. Every one of those has a treatment with real evidence, several are cheap to fix, and none of them improves because an adrenal capsule was added on top. The single most common outcome of buying a product like this is 3 months spent not looking.
And against the adrenal diagnoses that are real. Adrenal insufficiency exists, it is dangerous, and it is not diagnosed by a random cortisol against the 6.2-19.4 µg/dL morning band — it is diagnosed with a stimulation test, and ACTH at 7.2-63 pg/mL separates a primary adrenal cause from a pituitary one. Cortisol excess exists too and is investigated with its own protocol. Primary aldosteronism is a common, missed and treatable cause of hypertension, measured against an upright aldosterone band of 4-31 ng/dL and interpreted with renin. Those are the conditions the word 'adrenal' properly refers to, all 3 have defined diagnostic pathways, and 0 of them are managed with an extract.
What you are actually buying when you buy Glandokort
A certificate cannot identify an extract — sterility, endotoxin, total protein and named contaminants are establishable, contents are not, because the product is defined by a process and there is no mass to check against the way there is for a 3- or 4-residue synthetic.
The anatomical question here is sharper than usual. The adrenal gland is a cortex wrapped around a medulla, and the two have different embryonic origins and completely different products: steroids on the outside, catecholamines on the inside. Separating them cleanly is a dissection step, not a purification step, and no routine certificate reports a marker that would show whether it was done — not a catecholamine, not a steroid, not a protein band. A buyer of an 'adrenal cortex' preparation has the vendor's word and nothing else. That is not an allegation about anyone; it is a description of what a certificate covers.
A certificate cannot identify an extract. The specific question for an adrenal preparation is anatomical: the cortex and the medulla are different tissues with different embryonic origins inside the same organ, and the medulla makes catecholamines. A buyer has no way to confirm which part of the gland a preparation came from, and no routine certificate reports a marker that would distinguish them.
Where to get Glandokort
Buy Glandokort at BioLongevity Supplements →The evidence for Glandokort
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. Nothing is indexed under the trade name Glandokort and 0 cortisol, ACTH, DHEA-S or aldosterone results have been published for an adrenal-derived preparation — which matters because the syndrome this product is sold against is not itself a diagnosis, and the real adrenal disorders have defined tests.
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
A PubTator3 search on 6 September 2026 for this school's peptides against adrenal and corticosterone endpoints returned one record, and it was about vasopressinergic regulation of the stress axis — not about a peptide bioregulator at all. Under the trade name itself, nothing. That is the state of the evidence for an adrenal peptide preparation: zero cell studies, zero animal studies, zero human studies, in any language.
The adrenal is also missing from the group's own survey. Ryzhak 2015 compared seven calf-tissue extracts in organotypic culture — cortex, pineal, liver, prostate, thymus, heart, cartilage. No adrenal. So unlike thymus or prostate, this tissue does not even have an explant growth index behind it.
What remains is doctrine. Khavinson 2012 asserts that peptides stimulate differentiation tissue-specifically; Khavinson 2021 reviews the gene-expression claim across the family; Kolchina 2019 models how a short peptide might contact DNA; Khavinson 2022 docks these molecules against peptide and amino acid carriers without measuring transport in a living cell. Every one of those is a general statement about a class. None of them is a measurement in an adrenal gland.
And the adrenal is the organ where that is least forgivable. It is the one tissue in this catalog with a validated, cheap, dynamic function test in everyday clinical use. An 8 a.m. cortisol with ACTH, and where it is equivocal a stimulation test, settles adrenal function in a morning. It has never been applied to this product.
What nobody has tested yet
The test that would settle it is already standard of care. A morning cortisol and ACTH pair, before and after, would show within weeks whether an adrenal preparation moves the axis at all. If a stimulation test is added, the answer becomes unambiguous. No study of any product in this family has reported a cortisol value.
The DHEA-S question is the one people actually mean. DHEA-sulfate falls steadily with age, is a single stable blood test, and is the adrenal number most often invoked in the marketing around this category. It has never been reported for this product either, which means the claim most commonly made for it has never been checked.
Extrapolation, and a caution that belongs with it. If an adrenal preparation did influence the axis, the direction is not obvious — anything that raises cortisol output chronically carries the metabolic and bone costs that go with it, and anything acting centrally could suppress ACTH instead. Both are hypotheses, neither has been measured. Separately and more practically: the complaint this product is bought for — persistent fatigue — overlaps with genuine adrenal insufficiency, which is uncommon, diagnosable with the same cheap test, and dangerous if missed. Measuring first is the useful move regardless of what the capsule does.
Sources read for this page
- 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 VKh. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine 2012 · PMID 22808515
- 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
- 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
Glandokort — 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.
Glandokort — safety specifics for this compound
Specific to Glandokort: 0 adverse-event data exist for any adrenal-derived preparation in this family. The named risk is that the symptom this product is bought for overlaps with conditions that are dangerous when missed. Adrenal insufficiency presents as fatigue, weight loss, low blood pressure, salt craving and dizziness on standing, and it is diagnosed with a stimulation test rather than a single cortisol against the 6.2-19.4 µg/dL morning band; untreated, it can decompensate into an adrenal crisis. Anyone already on prescribed corticosteroids is in a different situation again, because stopping or tapering them without supervision is genuinely hazardous, and nothing on this page is a reason to change them. The second risk is ordinary and more common: 3 months on a capsule while an untreated thyroid problem, iron deficiency or sleep apnea keeps running is a real cost, and each of those has a test that takes 1 blood draw or 1 night.
Glandokort — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Glandokort 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.
Glandokort — what interferes with this one specifically
The interference that matters here is with the cortisol measurement itself, and it is large. Any exogenous corticosteroid — oral, injected, inhaled, or a potent topical used over a wide area — suppresses ACTH and drives measured cortisol down, so a value drawn during or shortly after steroid treatment describes the prescription rather than the gland. Some steroid preparations also cross-react with the cortisol assay itself and read as a falsely high result. Estrogen, whether from combined oral contraception or hormone therapy, raises cortisol-binding globulin and therefore raises TOTAL cortisol without changing the free fraction, which is a classic false positive against the 6.2-19.4 µg/dL band. Draw timing is the third: a 7-9am reference range applied to an afternoon sample is not a comparison. Second, and specific to this class: 0 interaction studies exist for any bioregulator, so every line here is predicted from known endocrinology rather than observed with this product.
- 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
- 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 — Glandokort in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Glandokort
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
Glandokort — frequently asked questions
Is Glandokort a peptide or an extract?
An extract — a peptide complex from adrenal cortex, not a single defined molecule. That is why a certificate of analysis cannot confirm its identity the way it can for a synthetic peptide.
Is there a human trial of Glandokort?
Nothing is indexed under the trade name Glandokort. No cortisol, ACTH, DHEA-S or aldosterone endpoint has been published for an adrenal-derived peptide preparation in this family.
What should I measure if I run Glandokort?
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
- 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, Morozov VG — Peptides of pineal gland and thymus prolong human life · Neuro Endocrinology Letters 2003;24(3-4):233–240 · PMID 14523363
- 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
What Glandokort is used for
Glandokort appears under 2 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.