Epiphamin
Pineal cytamin — Khavinson-school organ peptide fraction, oral tablet
Epiphamin (Pineal cytamin — Khavinson-school organ peptide fraction, oral tablet) is a longevity & bioregulators research compound. A Khavinson-school polypeptide fraction from animal pineal gland, 155mg per tablet, from the older cytamin line. Unlike every other organ on this shelf the pineal makes a claim with a hormone attached, so the mechanism is testable: melatonin is measurable in saliva, in overnight urine as its metabolite, and as dim-light melatonin onset. The school's position is that the peptide fraction restores the gland's own rhythm rather than supplying the hormone.
Epiphamin quick facts
| Route | Oral |
| Frequency | Not established · Not established |
| Half-life | Not characterized — no analytical method for this preparation has been published |
| Forms | Oral |
| Evidence level | No published study of this product. The literature belongs to the parenteral extracts and the synthetic peptides of the same school. |
The most expensive tablet on the cytamin shelf at $101 for 40, against $42 for most of the line, and the one with the least product-specific evidence. The single PubMed record naming it is a 2002 hypothesis paper on aspirin-sensitive asthma that proposes the pineal extracts as an approach; no trial followed. Every human melatonin result attributed to this family belongs to the injectable extract Epithalamin. Dim-light melatonin onset before and after a course is the measurement nobody has taken.
How Epiphamin works
A Khavinson-school polypeptide fraction from animal pineal gland, 155mg per tablet, from the older cytamin line. Unlike every other organ on this shelf the pineal makes a claim with a hormone attached, so the mechanism is testable: melatonin is measurable in saliva, in overnight urine as its metabolite, and as dim-light melatonin onset. The school's position is that the peptide fraction restores the gland's own rhythm rather than supplying the hormone.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Epiphamin
Buy Epiphamin at RUPharma →The evidence for Epiphamin
Graded by what exists behind each claim.
✅ Clinically validated
- None. The single PubMed record naming this product is a 2002 hypothesis paper on aspirin-sensitive asthma whose closing sentence proposes the pineal extracts as an approach to correcting melatonin (Evsyukova 2002). No trial followed it in the twenty-four years since.
📊 Correlative data
- The human melatonin record in this school belongs to the injectable pineal extract: restoration of the night melatonin rise in old monkeys and elderly people (Korkushko 2007), increased pineal melatonin synthesis in elderly people under a related preparation (Trofimova 2017), and a long-running follow-up of elderly coronary patients (Korkushko 2011). A hormone moved, in more than one species. It moved after an injection of a different product.
🧪 Theoretical / extrapolated
- The restorative-versus-substitutive question is the whole argument. If the tablet raises melatonin by supplying it, plain melatonin does the job better and cheaper. If it restores the gland's own rhythm, that is a genuinely different claim — and the only measurement that separates them, a melatonin read-out after a washout, has never been published.
- At $101 for 40 tablets against $42 for most of the line, this is the most expensive cytamin and the one with the least product-specific evidence.
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 →
What Epiphamin actually does
The name is spelled two ways and only one of them finds the literature. A PubTator3 query for epiphamin returns a single record. A query for epifamin, the transliteration the Russian journals actually print, returns seven, and four of those are reports in patients. Both queries were run 9 September 2026. An earlier version of this page carried the first number and concluded that no trial had ever followed; that was a fact about a spelling rather than about a product, and it is corrected throughout what follows.
The record the first spelling finds. Evsyukova 2002 is a hypothesis paper about aspirin-sensitive asthma, arguing that the condition is an apudopathy driven by dysfunction of melatonin-producing cells: lower daytime melatonin output, a disordered platelet membrane-receptor complex, enhanced lipid peroxidation, reduced inhibition of 5-lipoxygenase and NO-synthase, and increased leukotriene production. Its closing sentence proposes correcting melatonin with the epiphysis extracts Epithalamin and Epiphamin. It is a proposal, it is twenty-four years old, and no study has ever tested it in asthma.
The gland this is made from does one measurable thing, and that is a gift to a page like this. Unlike a liver or a cartilage extract, a pineal product makes a claim with a hormone attached: melatonin, measurable in saliva, in overnight urine as its metabolite, and as dim-light melatonin onset. Nothing else on the cytamin shelf has a read-out that clean. Hold on to it, because the four human studies of this tablet measured caspases, catalase, glutathione and citrate, and did not measure that hormone once.
The product, stated plainly, including its price. A 155 mg tablet of a nucleoprotein fraction from animal pineal gland, 40 per pack, listed by a partner at $101 — against $42 for most of the rest of the line. It is the most expensive tablet on the shelf, and on the corrected search it is also the only one of the seventeen with a published human series behind it — which is a point in its favor, and is why the rest of this page is about what that series did and did not measure rather than about a hole in the record. One more, because it will confuse anybody comparing the page to the product listing: the vendor's own title calls this an endocrine bioregulator and never uses the word pineal. The name derives from epiphysis, and the one paper that mentions the product names it among the epiphysis extracts Evsyukova 2002 — so pineal is right, but it is the literature saying so and not the label.
What the underlying mechanism claim actually is. The school's position is that organ-derived peptide fractions act on gene expression in the tissue they came from — not by supplying a hormone, but by restoring the gland's own output. That distinction matters more here than anywhere else in the line, because a pineal product has an obvious substitutive alternative and the restorative claim is the only thing that separates the two. It is also, conveniently, the version that is harder to test — and it has not been tested.
Cell, rodent, human — and where it stops
Four reports in patients, one research group, and every endpoint is blood chemistry. Between 2010 and 2015 a group in Voronezh published four studies in which epifamin was added to standard treatment and compared against standard treatment alone: thyrotoxicosis Popov 2010, drug-induced hepatitis twice Popov 2011 Popov 2012, and type 2 diabetes complicated by steatohepatitis Popov 2015. Two studies in diabetic rats from the same laboratory sit underneath them Popova 2013 Agarkov 2014. That is a product-specific human record, it is more than any other tablet in this line has, and no page on this site had found it before 9 September 2026.
What they measured, and how much weight it carries. Biochemiluminescence, catalase, superoxide dismutase, reduced glutathione, glutathione peroxidase and reductase, glucose-6-phosphate dehydrogenase, aconitate hydratase, citrate, caspase-1 and caspase-3. Popov 2015 adds ALT, AST, cholesterol and fasting and postprandial glucose — the only numbers in the series a reader could order at a lab. The largest stated sample is 25 people, split 12 and 13 Popov 2010; no abstract in the series describes randomization, blinding or a placebo, none reports a symptom, function or survival endpoint, and every one of them is an add-on to therapy that was itself working. Open add-on studies of surrogate chemistry are the weakest design that still counts as human evidence, and that is the correct grade for this.
Every paper explains itself with melatonin and none of them measured melatonin. The mechanism asserted across the series is that epifamin corrects the melatonin level. Popova 2013 says apparently; Popov 2015 says obviously; Agarkov 2014 says probably. Not one abstract in the six reports an assay of melatonin, of its urinary metabolite, or of any circadian measure at all. The hormone the product is bought for is the single variable the studies supporting it left unmeasured.
Twice the same group ran plain melatonin beside it. Melaxen is a melatonin tablet. Popov 2011 added melaxen or epifamin to standard hepatitis therapy and reports both correcting antioxidant status. Agarkov 2014 put the two side by side in diabetic rats and reports reduced glutathione rising 1.6-fold on epifamin and 1.7-fold on melaxen. The comparator the school chose for itself is the cheapest thing on the pharmacy shelf, and on the numbers it published, the comparator was not behind.
The tablet in those studies and the tablet on sale are not obviously the same tablet. Popov 2010 dosed one 10 mg tablet three times a day before meals for seven days. The product a partner lists is 155 mg per tablet. Those two numbers could be a peptide content and a whole tablet mass, or they could be two different preparations; the vendor publishes no composition and the paper names no manufacturer, so nothing available settles it. Until something does, this series is evidence about a 10 mg Russian pharmacy tablet and reading it onto a 155 mg import is an assumption, not a citation. The class word Tokaev 2007 adds only a nutrition review about liver disease.
What exists instead is a body of work on the INJECTABLE pineal extract, and it is the strongest human record anywhere in this school. Korkushko 2007 reported that night melatonin release and circadian amplitude decline with age in both old monkeys and elderly people, and that pineal peptide preparations restore the night rise. Goncharova 2003 is the primate arm. Trofimova 2017 reported increased pineal melatonin synthesis in elderly people under a related preparation. Korkushko 2011 followed elderly coronary patients given courses of the extract over years and reported slower cardiovascular aging alongside a normalized melatonin rhythm. A hormone moved, in more than one species, more than once.
The explant rung included pineal tissue, and named the product. Khavinson 2002 lists the epiphysis preparation Epithalamin among the polypeptide preparations applied to organotypic explants from rats of different ages, with the tissue-specificity claim as the reported result.
Now the break, and it is a route and a product, not a species. Every measurement in the paragraph above was made on Epithalamin or a close relative, administered by injection, in a research setting. Epiphamin is a swallowed tablet from the same manufacturer and the same gland, and it shares with those studies a tissue of origin and nothing else — not a dose, not a route, and not one overnight urine sample. The pineal literature is real. It is still not this product's literature, and the Voronezh series does not close that gap, because it measured antioxidant chemistry in sick patients rather than melatonin in anybody.
Epiphamin pharmacokinetics — how much of it actually gets in
What degrades it. The same gastric and pancreatic proteolysis that meets any dietary protein: acid denaturation, pepsin, trypsin and chymotrypsin, then brush-border peptidase hydrolysis to amino acids and short peptides. No enteric coating is claimed and no dissolution or stability data has been published for the tablet.
The oral barrier, and the one number that makes this page different. Melatonin's own oral pharmacology is the reference point nobody on this shelf wants to stand next to: it is a small lipophilic indoleamine that crosses the gut wall and the blood-brain barrier without help, and a milligram of it raises circulating melatonin far above any physiological night peak. So the question this product has to answer is not whether melatonin can be raised orally. It is whether a 155 mg protein fraction, of which some unknown fraction survives digestion, can make a gland do it — which is a much harder claim and a much more interesting one.
The arithmetic that bounds it. Suppose 1% of the tablet reached the circulation intact: 1.55 mg into roughly 5 liters is about 310 ng/ml, which sits above the 0.01-100 ng/ml band used in the organotypic work on this class. At 0.1% it is 31 ng/ml and still inside it. The concentration argument is therefore not the weak link. The weak link is that every human melatonin result in this family came from an injection, which bypasses the gut entirely, so nobody has ever had to find out what the intact absorbed fraction is, and nobody has looked. There is no published comparison of a swallowed tablet against an injection of the same gland's extract.
Half-life is unstatable and should be said so. No analyte has been defined for this preparation, so nothing can be followed in plasma. What can be reasoned is that the school's own protocol shape — a 20 to 40 day course from a 40-tablet pack, then months off — is a claim about a durable change in gland behavior, not about an exposure that persists. That claim has a measurement attached to it and the next section names it.
What would have to be true, and how you would know it was not
Four predictions, and this is the cytamin where they are cheapest to run.
1. Dim light melatonin onset, before and after a course. Saliva samples every 30 minutes across the evening under dim light, twice: once before the pack is opened, once when it is finished. DLMO is the reference standard for circadian phase and it is the exact quantity the underlying literature says these preparations restore Korkushko 2007. Prediction if the restorative claim is real: onset moves earlier and the night rise is steeper. Zero published studies of this tablet have measured it.
2. Overnight urinary 6-sulfatoxymelatonin as the cheap version. One overnight collection, no clinic, no dim-light protocol, and it integrates the whole night's output rather than sampling a curve. Weaker than DLMO and roughly a tenth of the hassle.
3. Against the product: actigraphy will show nothing. If the effect is a genuine restoration of pineal rhythm, sleep onset latency and sleep efficiency on a wrist tracker should shift measurably across a 40-day course. Prediction: they will not, because the tablet does not deliver a hormone and the gland is unlikely to be reachable by an orally digested protein fraction. This is the prediction that would cost the product most if it were run and came back flat, which is precisely why it belongs on the page.
4. The comparison that would settle the interesting question. Substitution and restoration look identical on a single melatonin measurement and completely different after washout. Measure DLMO one month after a course ends. A substitutive effect is gone; a restorative one persists. No published series in this family has ever reported a washout measurement, which means the school's central claim has never been tested in the one way that could distinguish it.
What nobody has tested yet
The asthma hypothesis has sat unanswered for over twenty years. Evsyukova 2002 proposed correcting melatonin in aspirin-sensitive asthma with the pineal extracts and named this product. That is a testable clinical hypothesis with a defined population, a defined intervention and obvious endpoints — peak flow, leukotriene metabolites, aspirin challenge threshold. Nobody ran it. A page that cites the paper without saying that is quoting a proposal as though it were a result.
Nobody has assayed a tablet for melatonin. This is the obvious control and it is missing. If a pineal-gland extract contains residual melatonin, a share of any effect is substitutive and the restorative story is partly wrong; if it contains none, the restorative story is the only one available. One high-performance liquid chromatography run answers it. That exact experiment has been done on other glandular supplement categories and it changed what was known about them Kang 2013; it has never been done here.
The head-to-head against plain melatonin exists and it was run on the wrong endpoint. Popov 2011 and Agarkov 2014 both set epifamin beside melaxen, which is melatonin, and both scored the comparison on antioxidant chemistry. The comparison that would decide anything is the same two arms with dim light melatonin onset as the endpoint and a washout, because substitution and restoration diverge only after the last tablet. That version has never been run, and it is the study that decides whether a $101 pack has a rationale a bottle of melatonin does not.
Extrapolation, labeled as such. If the mechanism is restorative, three consequences follow and none has been looked for: the effect should be largest in the people whose baseline night melatonin is lowest, which is measurable before dosing; it should outlast the course, which the washout above would show; and it should be absent in anyone whose pineal gland is calcified, which is visible on a head CT already taken for other reasons. Three testable consequences of the product's own claim, and zero published attempts.
Epiphamin — its own safety story, not its class's
Three things this tablet owns that the class block cannot say.
Six studies exist and none of them was designed to find harm. The Voronezh reports Popov 2010 Popov 2011 Popov 2012 Popov 2015 are add-on studies of blood chemistry running 7 days to a few weeks, in groups of a few dozen, with no abstract reporting an adverse-event table and none describing a safety endpoint. A tolerability signal needs either a large sample or a long one and this series has neither. So the reassurance available here is narrow: nothing alarming was reported, by studies that were not looking and could not have seen much.
A pineal product interacts with the one thing everybody self-medicates already. Anyone taking this is very likely also taking melatonin, and the two claims are not additive in any established way. If the tablet does nothing, the melatonin explains any effect seen. If the tablet does something restorative, adding exogenous hormone is the intervention most likely to mask it. Either way, running both at once makes the result uninterpretable, and the circadian read-outs above are only meaningful if one variable moves at a time.
The undisclosed-composition problem is sharper here than elsewhere on the shelf. The gland this material comes from produces a hormone, and no vendor publishes an assay for hormone content. The precedent for why that matters is not hypothetical: when a comparable category of glandular supplements was tested by chromatography, 9 of 10 products contained active hormone, some at doses exceeding normal treatment Kang 2013. Nobody is claiming that result transfers to this tissue. The point is that the measurement is easy, it has been informative before, and for this product it has never been made.
Sources read for this page
- Evsyukova HV. Aspirin-sensitive asthma due to diffuse neuroendocrine system pathology. Neuro Endocrinology Letters 2002 · PMID 12195225
- Popov SS, Pashkov AN, Zoloedov VI, Popova TN, Rakhmanova TI. [Antioxidant status of patients with thyrotoxicosis syndrome treated with the combined regimen containing epifamin]. Biomeditsinskaia Khimiia 2010 [Russian] · PMID 20695219
- Popov SS, Shul'gin KK, Pashkov AN, Zoloedov VI, Shvedov GI. [Intensity of free radical oxidation and superoxide dismutase activity in patients with drug hepatitis in combination therapy with melaxen or epifamin]. Eksperimentalnaia i Klinicheskaia Gastroenterologiia 2011 [Russian] · PMID 22629773
- Popov SS, Shul'gin KK, Pashkov AN, Zoloedov VI, Shvedov GI, Rakhmanova TI. [Peculiar properties of glutathione system and NADPH-generated enzymes functioning in blood of patients with drug-induced hepatitis under combined treatment with epifamin]. Biomeditsinskaia Khimiia 2012 [Russian] · PMID 22642157
- Popov SS, Pashkov AN, Agarkov AA, Shulgin KK. [Intensity of apoptotic processes, aconitate hydratase activity and citrate level in patients with type 2 diabetes mellitus complicated steatohepatitis under application of epifamin at basic therapy]. Biomeditsinskaia Khimiia 2015 [Russian] · PMID 26215420
- Popova TN, Agarkov AA, Verevkin AN. Intensity of Free Radical Processes in Rat Liver under Type 2 Diabetes and Introduction of Epifamin. Acta Naturae 2013 · PMID 24455191
- Agarkov AA, Popova TN, Verevkin AN, Matasova LV. Activity of the glutathione antioxidant system and NADPH-generating enzymes in blood serum of rats with type 2 diabetes mellitus after administration of melatonin-correcting drugs. Bulletin of Experimental Biology and Medicine 2014 · PMID 24952485
- Trofimova SV. Pineamin increased pineal melatonin synthesis in elderly people. Advances in Gerontology 2017 [Russian] · PMID 28849889
- Korkushko OV. Normalizing effect of the pineal gland peptides on the daily melatonin rhythm in old monkeys and elderly people. Advances in Gerontology 2007 [Russian] · PMID 17969590
- Goncharova ND. Peptide correction of age-related pineal disturbances in monkeys. Advances in Gerontology 2003 [Russian] · PMID 14743609
- Korkushko OV, Khavinson VKh, Shatilo VB, Antonyk-Sheglova IA. Peptide geroprotector from the pituitary gland inhibits rapid aging of elderly people: results of 15-year follow-up. Bulletin of Experimental Biology and Medicine 2011 · PMID 22451889
- Khavinson VKh, Malinin VV, Chalisova NI, Grigor'ev EI. [Tissue-specific action of peptides in tissue culture of rats of various ages]. Advances in Gerontology 2002;9:95-100 [Russian] · PMID 12096446
- Tokaev ES. [Bioactive substance used for treatment and preventive maintenance of liver diseases]. Voprosy Pitaniia 2007 [Russian] · PMID 17802767
- Kang GY, Parks JR, Fileta B, Chang A, Abdel-Rahim MM, Burch HB, Bernet VJ. Thyroxine and triiodothyronine content in commercially available thyroid health supplements. Thyroid 2013 · PMID 23758055
Epiphamin — 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.
Epiphamin — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Epiphamin 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.
- Dose range and how to work up to it
- 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 — Epiphamin in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Epiphamin
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
Epiphamin — frequently asked questions
What is Epiphamin?
Epiphamin (Pineal cytamin — Khavinson-school organ peptide fraction, oral tablet) is a longevity & bioregulators research compound. A Khavinson-school polypeptide fraction from animal pineal gland, 155mg per tablet, from the older cytamin line. Unlike every other organ on this shelf the pineal makes a claim with a hormone attached, so the mechanism is testable: melatonin is measurable in saliva, in overnight urine as its metabolite, and as dim-light melatonin onset. The school's position is that the peptide fraction restores the gland's own rhythm rather than supplying the hormone.
Where can I find Epiphamin dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Epiphamin protocol are available to members inside Skool. This public page covers what Epiphamin is, how it works and the evidence.
What is the half-life of Epiphamin?
Epiphamin has an approximate half-life of Not characterized — no analytical method for this preparation has been published, which is part of what determines how often it's dosed.
What's the evidence behind Epiphamin?
Current evidence level: No published study of this product. The literature belongs to the parenteral extracts and the synthetic peptides of the same school.. Epiphamin is offered for research purposes only and is not an approved medicine.
What Epiphamin is used for
Epiphamin appears under 1 goal 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.