Ovagen
Liver/GI peptide bioregulator
Ovagen (Liver/GI peptide bioregulator) is a longevity & bioregulators research compound. Liver, GI and immune bioregulator — proposed to support hepatic/intestinal protein synthesis and detox-related function.
Ovagen quick facts
| Reported research dose | 2mg-5mg (per course) |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~30 min |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
Gut/liver bioregulator — course-based. Aimed at the gut-liver axis rather than the liver alone, which is the argument for it over the purely hepatic peptides. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, a CMP for liver enzymes, and your own digestion is the honest readout. Run it as an experiment you measure, not a protocol you trust.
How Ovagen works
Liver, GI and immune bioregulator — proposed to support hepatic/intestinal protein synthesis and detox-related function.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Ovagen
Buy Ovagen at Biolongevity Labs →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Ovagen
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
- Sold for liver, gut and immune support — a broad positioning that is broad because the peptide was isolated from tissue serving all three, not because three separate effects have been shown.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- Glu-Asp-Leu — a synthetic tripeptide proposed to support hepatic and intestinal protein synthesis.
- The shared claim across the Khavinson series: peptides this short are proposed to enter the cell nucleus and bind promoter regions of DNA, shifting tissue-specific gene expression.
- Liver is the tissue with the clearest available readout in the whole series — ALT, AST and GGT are on every routine panel, so anyone using this can generate their own before-and-after data at near-zero cost. That is worth doing regardless of what the label claims.
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 →
What Ovagen actually does
Start with the thing that is wrong on every page selling this. Ovagen is sold as a liver and gut bioregulator. The sequence attached to that name by vendor consensus is Glu-Asp-Leu. And the peer-reviewed literature that uses Glu-Asp-Leu is renal. The originating group's own 2021 gene-expression review places EDL in the regulation of kidney cell function Khavinson 2021, and the one animal paper published on the sequence is a nephroprotection study Zamorskii 2017. Not one indexed paper studies EDL in liver tissue. That is not a small mismatch between marketing and evidence; it is a different organ.
The molecule itself. Three residues, Glu-Asp-Leu, formula C15H25N3O8, average mass 375.39 Da. Two acidic side chains plus the C-terminal carboxyl against one protonated N-terminal amine gives a computed net charge near −2.06 at blood pH and an isoelectric point of 3.55. So it is a small dianion, and small dianions do not diffuse across membranes. Every claim about what it does inside a cell depends on something carrying it there.
And this is the one place the transport argument works in the compound's favor. The carriers proposed for this family are PEPT1 and PEPT2 and the amino-acid transporters LAT1 and LAT2, and their described substrate range is di- and tripeptides Khavinson 2022. EDL has exactly 3 residues, so unlike the tetrapeptides in this catalog — Bronchogen, Cardiogen, Pancragen, Epitalon, all 4 residues — it sits inside the stated range rather than outside it. That is a real mechanistic distinction and no vendor page draws it. The qualifier is that the 2023 assessment of 26 of these peptides against those transporters was molecular docking scored against all 8,400 possible di- and tripeptides, with no uptake measured in a cell Khavinson 2023. A good binding energy is a hypothesis about transport, not transport.
The catalog line on this page says the half-life is about 30 minutes. Treat that as an expectation rather than a measurement: 0 pharmacokinetic studies of this peptide have been published in any species, and the figure is what a small unmodified peptide facing plasma aminopeptidases would be expected to do, not what anybody watched it do.
Cell, rodent, human — and where it stops
In cells. The 2021 systematic review of peptide effects on gene expression assigns EDL to the regulation of renal cell function Khavinson 2021. The same review is where the wider claim for this family comes from — that these peptides reach chromatin and bind histone proteins — and the search for structural motifs that would let a 3-residue peptide recognize a specific double-stranded DNA sequence is a hard problem the group has published on directly Kolchina 2019. Nothing in the cell-level record puts EDL in a hepatocyte. And the nuclear entry the whole argument depends on was shown for short fluorescence-labeled peptides in HeLa cells Fedoreyeva 2011, which are neither hepatocytes nor renal tubule cells.
In rodents, and this is a genuinely good animal study for the wrong organ. Rats, two separate models of acute kidney injury — gentamicin-induced nephropathy and ischemia/reperfusion — with EDL reported to prevent oliguria and azotemia, reduce proteinuria and sodium excretion, preserve antioxidant enzyme activity, suppress lipid peroxidation, and restore cellular energy metabolism Zamorskii 2017. Two independent injury mechanisms, one toxic and one ischemic, converging on the same protective readout is a stronger design than most of this class manages. The abstract states neither the route nor the duration, and reports direction rather than effect size, so the size of the protection cannot be quoted from it.
In humans: 0. No randomized trial, no controlled series, no published human data of any kind on this sequence, for the kidney or for the liver. The independent systematic review that covers this general family pooled 24 randomized trials over 2,245 participants with cognitive endpoints, rated the risk of bias moderate to high and the certainty of evidence low to very low, and includes nothing on either organ Alsulaimani 2021.
The obstacles, and the first one is unique to this page. (1) The translation chain does not point at the organ the product is sold for. Cell work: kidney. Animal work: kidney. Marketing: liver and gut. Every link in the chain would have to be re-run in hepatic tissue before the liver claim has an evidence base at all. (2) Acute kidney injury in a rat given a nephrotoxin is a different problem from slow age-related decline in filtration, and a compound that blunts an acute insult has not been shown to do anything over years. (3) Nothing has measured where the peptide goes after a dose in any species, so tissue specificity remains an assumption for this molecule as for every other one in the class. (4) The trade name and the sequence are joined by vendor consensus rather than by a publication: no paper this page could find states that Ovagen is Glu-Asp-Leu.
What would have to be true, and how you would know it was not
Three predictions. The first is the one that argues against the product as sold, and it is the honest headline of this page.
1. The liver numbers should not move, and if they do, look elsewhere first. If the mechanism is renal, there is no reason to expect ALT, AST, ALP or bilirubin on a CMP to change over a 10 to 20-day course, and no reason for GGT to change either. GGT is the trap: it is the marker people watch for liver improvement, it responds strongly to alcohol and to weight change, and this site's own guidance is to allow 6 weeks minimum after any change before re-drawing it, because of its 2 to 3-week half-life. A GGT that falls during a course in which somebody also cut their drinking has told you about the drinking. Run the CMP at baseline and again at 3 to 6 months, which is the window this site uses for anyone on an ongoing compound, and expect a flat line.
2. If anything moves, it should be a kidney number, and creatinine is the wrong one to trust. Creatinine-based eGFR is confounded by muscle mass, by meat intake and by creatine supplementation, all of which are common in the population buying peptides. Cystatin C is independent of muscle and this site already positions it as the test that confirms or overturns an abnormal creatinine-based eGFR. Pair it with a urinalysis for protein, which is the readout closest to the proteinuria the rat study reported. A falling urine protein with a stable eGFR would be the first human signal that the animal result transferred; a change in creatinine alone would not be.
3. The prediction that would falsify the marketing rather than the molecule. If a group of people ran a course and their liver panel moved while their kidney markers stayed flat, the renal mechanism described above would be wrong and the vendor positioning would be right — which would be a genuinely interesting result and the opposite of what the published record predicts. Nobody has collected the paired draw that could settle it, and it costs one CMP and one cystatin C.
What nobody has tested yet
Four things nobody has done, in ascending order of how strange it is that nobody has done them.
1. Nobody has given this peptide to an animal with liver injury. The hepatic equivalents of the two rat models that were run are standard, cheap and decades old — acetaminophen overdose, carbon tetrachloride, hepatic ischemia/reperfusion — and the readouts are the same transaminases a person can order. The same group that ran 2 kidney models has run 0 liver models, and the product has been sold as a liver peptide throughout.
2. Nobody has measured where it goes. One radiolabeled or fluorescently tagged biodistribution study in rodents — count per gram in kidney, liver, gut, plasma, at 4 or 5 timepoints — would test the tissue-specificity claim that the whole Khavinson catalog rests on, not just this compound's. It has never been published for any member of the family.
3. Nobody has run it against a real membrane. EDL is one of the few peptides in this catalog whose length falls inside the stated PEPT1 substrate range, which makes it the best candidate in the set for a Caco-2 permeability assay Khavinson 2023. A single apparent-permeability number would convert the strongest theoretical argument on this page into evidence, or kill it.
4. Nobody has published the name. There is no paper stating that the product called Ovagen contains Glu-Asp-Leu. The sequence reaches this page through vendor listings, and the same market has already been caught mapping one product to another product's sequence. A lot-level tandem mass spectrometry result would cost a fraction of a course and would be the first published identification of what is actually in the vial. There is a practical wrinkle worth knowing before anybody tries to check this themselves: the name is not unique to this peptide. A PubMed search for Ovagen returns veterinary papers on a commercial follicle-stimulating hormone preparation used to superovulate ewes and cattle. Anyone searching the literature for this product will find a livestock gonadotropin unless they search the sequence instead, which is one more reason the sequence and not the trade name is the thing to ask a vendor about.
Ovagen — its own safety story, not its class's
The class safety block on this page is about injecting peptides in general. Three things specific to this one.
Using a liver product for a liver symptom is how a treatable cause gets missed. Raised transaminases have a short list of causes worth excluding before anything else: hepatitis B and C, alcohol, hemochromatosis, autoimmune hepatitis, drug effect, and metabolic dysfunction-associated steatotic liver disease. Each has a test, most are on a standard panel or one step past it, ferritin and a CMP catch several of them, and several have treatments with actual trials. This compound has 0 human studies and 0 published results in any liver condition.
If the renal literature is the real mechanism, the population that should be most careful is the one with reduced kidney function. Anything given to a person whose filtration is impaired is cleared differently, and this molecule has no measured clearance in any species. That is an argument for a baseline cystatin C and a urinalysis before a course rather than an argument that it is dangerous, because there is no evidence either way — but the asymmetry matters: the group with most to gain from a nephroprotective peptide is also the group in which an unstudied one is least predictable.
What the silence is worth. 0 adverse events have been published for this compound. With 0 human trials, there was never an arm in which an adverse event could have been recorded, so the number describes the absence of observation rather than the presence of safety. The concrete risks on a course are the ones that belong to the needle and to the vial: sterile technique, injection-site reaction, and a preparation whose contents nobody has independently identified.
Sources read for this page
- Fedoreyeva LI, et al. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Moscow) 2011;76(11):1210–1219 · PMID 22117547
- 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
- Zamorskii II, Shchudrova TS, Lin'kova NS, Nichik TE, Khavinson VKh. Nephroprotective Effect of EDL Peptide at Acute Injury of Kidneys of Different Genesis. Bulletin of Experimental Biology and Medicine 2017;163(3):389–393 · PMID 28744634
- 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
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 2023;13(3):552 · PMID 36979488
- Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M. Systematic search for structural motifs of peptide binding to double-stranded DNA. Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
- 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
Ovagen — 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.
Ovagen — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Ovagen moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
These are short peptide fragments given in microgram amounts and there is no mechanism predicting a specific marker shift. Listing markers here would be padding.
What to do: Test the organ system the bioregulator is aimed at, not a generic panel — that is the only measurement that would tell you anything.
The evidence base here is almost entirely one research group's, largely in Russian, and rarely replicated independently. That is the single most important thing to know before running a course, and it is more useful than any interaction list.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Ovagen in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Ovagen
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
Ovagen — frequently asked questions
What is Ovagen?
Ovagen (Liver/GI peptide bioregulator) is a longevity & bioregulators research compound. Liver, GI and immune bioregulator — proposed to support hepatic/intestinal protein synthesis and detox-related function.
Is the full Ovagen protocol on this page?
The reported research dose is on this page, along with how Ovagen works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Ovagen?
Ovagen has an approximate half-life of ~30 min, which is part of what determines how often it's dosed.
What's the evidence behind Ovagen?
Current evidence level: Russian studies; limited. Ovagen is offered for research purposes only and is not an approved medicine.
Ovagen inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Ovagen is used for
Ovagen appears under 1 goal in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Ovagen is the hepatocyte arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.