Important limitations
- Individual claims and source links have not yet completed editorial verification.
- Evidence level, applicable study model, formulation, route and population remain unassigned.
Ovagen
Ovagen, a tripeptide bioregulator, primarily targets the liver and gastrointestinal (GI) tract.
Dosing & scaling, explained
The moderated mass amounts below are retained for comparison. Near-duplicates, mix-dependent volumes and device markings are excluded. This is educational source context, not a protocol or recommendation.
Mass amounts available for comparison
- Lower range1 mgDose
Recorded example with no verified study backing; shown for amount literacy only.
- Mid range5 mgDose
Recorded example with no verified study backing; shown for amount literacy only.
Only mcg or mg amounts are retained. The calculator derives mL, syringe units or pen clicks from the current vial strength, water volume and device.
No independently verified schedule
Evidence context
No clinical amount or schedule is inferred from this material. Source verification is pending, and every displayed amount remains educational context rather than guidance.
Storage, handling and interpretation
Product identity
Verify the exact compound, formulation and amount against the product label or certificate before calculation.
Storage & handling
Follow the product label, certificate and validated laboratory SOP; no universal storage assumption is applied here.
Prepared solutions
Label concentration and preparation date, use sterile technique where applicable, and follow a validated stability protocol.
Reported protocols for Ovagen
What published studies and recent community write-ups report about amounts, timing and course length. 6 preclinical and 3 community-reported rows, each linked to its source. These are descriptions of what others report, not instructions, and nothing here is medical advice.
| Context | Dose | Frequency | Route | Course | Source |
|---|---|---|---|---|---|
| Preclinical6 rows | |||||
| Rat cisplatin-induced acute renal failureRats with cisplatin-induced acute renal failure, comparing a kidney polypeptide complex with the short peptides AED, EDL and AEDG | Dose per kilogram not reported in the abstract; 3 short peptides were compared against the whole kidney extract | Given across the days of the injury model | Injection | Duration of the acute injury modelNot applicable | Bulletin of Experimental Biology and Medicine (PubMed)2015 |
| EDL and AEDG normalized urine output, urinary creatinine and its excretion, glomerular filtration rate and absolute sodium resorption while reducing urinary protein, and the authors singled out EDL as having a potent nephroprotective effect. The abstract does not state the dose per kilogram, so no human-relevant amount can be derived from it. | |||||
| Rat gentamicin nephropathy and ischemia-reperfusion injuryRats with gentamicin-induced nephropathy and with ischemia-reperfusion kidney injury | Dose per kilogram not reported in the abstract; 2 separate injury models were used | Given across the injury models | Injection | Duration of each modelNot applicable | Bulletin of Experimental Biology and Medicine (PubMed)2017 |
| EDL prevented oliguria and retention azotemia, lowered proteinuria and sodium excretion, stopped antioxidant enzyme activity collapsing, suppressed lipid peroxidation and normalized kidney cell energy supply. This is the clearest EDL-specific animal paper and it concerns the kidney, not the liver or ovary that vendors describe. | |||||
| Aged rat kidney function studyOld rats given a kidney polypeptide complex or the peptides AED, EDL or AEDG | Dose per kilogram not reported in the abstract; effects reported as 1.2 to 1.6-fold changes | A course of administrations | Injection | Course length not stated in the abstractNot applicable | Advances in Gerontology (PubMed)2018 |
| EDL raised urine output 1.2 to 1.4-fold, distal sodium transport 1.2 to 1.3-fold and sodium excretion 1.6-fold, with higher antioxidant enzyme activity, lower lipid peroxidation and no morphological sign of kidney toxicity. The paper is in Russian in the institute's own journal, with only an abstract in English. | |||||
| Aging kidney cell culture, senescence markersYoung and aged renal cell cultures treated with AED or EDL | Culture-medium concentrations; 3 senescence markers (p16, p21, p53) were tracked alongside SIRT6 | Added to the culture medium | Cell culture | Through the aging of the cultureNot applicable | Advances in Gerontology (PubMed)2014 |
| Both peptides raised proliferation and SIRT6 expression while lowering p16, p21 and p53, and the authors modelled the peptides binding an alternating AT sequence in the DNA minor groove as the proposed cause. The DNA interaction was computed rather than measured, and lowering tumour-suppressor and senescence markers is not self-evidently desirable. | |||||
| Organotypic kidney tissue culture, cell renewalKidney explants from young and old rats | Culture-medium concentrations of T-31 (AED) and T-35 (EDL), compared with the whole calf kidney polypeptide complex | Added to the culture medium | Organotypic tissue culture | Duration of the explant cultureNot applicable | Bulletin of Experimental Biology and Medicine (PubMed)2015 |
| The short peptides raised the proliferation marker Ki-67 and lowered the pro-apoptotic protein p53 in explants from both young and old animals, but did so less strongly than the whole kidney extract. A 2014 companion paper from the same group, listed in the sources below, found that the gelatinase MMP-14 rather than cell renewal was the main target of EDL specifically, while the related peptide AED drove the proliferation effect. | |||||
| Independent enzymology: HIV-1 protease inhibitionPurified mature HIV-1 protease, with pepsin as a selectivity control | Ki of about 50 micromolar for Glu-Asp-Leu (about 20 micromolar for Glu-Asp-Phe) | Enzyme kinetic assays and crystallography at pH 4.2 | In vitro enzymology | Not applicableNot applicable | Biochemistry (PubMed)1998 |
| A National Institutes of Health group found Glu-Asp-Leu to be the smallest potent analog of an octapeptide from the HIV-1 Gag-Pol transframe region, acting as a competitive inhibitor while being a poor inhibitor of pepsin (Ki about 7.5 millimolar). This is the only independently published bioactivity for the sequence, and it is unrelated to the kidney or liver claims made for the supplement. | |||||
| Community-reported3 rows | |||||
| Khavinson-line oral capsule course | About 200 mcg of peptide per capsule, 1-2 capsules daily | Once daily during a course, sometimes split morning and evening | Oral capsule or sublingual; no widely circulated injectable protocol exists | 10-day courses, with some protocols extending a single course to 20-30 daysCourses repeated 2-4 times a year; continuous dosing is not part of the convention | Community resource2026 |
| This September 2026 directory entry describes Ovagen as commercially an oral-only product, with injectable protocols existing as forum constructions rather than conventions. It states that the peptide has no indexed pharmacokinetic characterization at all, so even oral bioavailability claims rest on extrapolation from related short peptides, and that no Western clinician runs an Ovagen protocol. | |||||
| Research-chemical vials and the absence of any dose basis | Sold as 20 mg lyophilised vials or as capsules; median listed price about 3 US dollars per mg across 44 suppliers | Course lengths copied from the institute's supplement marketing | Reconstituted powder for injection, or oral capsules | As stated by the supplier; no published study supports any of themNot established | Community resource2026 |
| This September 2026 review states plainly that no human dose exists because there are no human studies, that the rat papers do not give a dose per kilogram in their abstracts, and that cell work used nanogram-per-millilitre concentrations. It also notes that EDL altered sodium and water handling in rats, so its effect in someone with kidney disease, on diuretics or with high blood pressure is unknown. | |||||
| Evidence grading and product identity | 0 registered clinical trials and 0 human studies recorded for the compound | Not applicable | Oral capsule in commercial reality | Not applicableNot applicable | Community resource2026 |
| This tracker grades the evidence D and flags a discrepancy worth knowing about: the Russian capsule product lists lysine, glutamic acid and aspartic acid among its ingredients, which suggests the sequence Lys-Glu-Asp rather than the Glu-Asp-Leu identified in the research literature. It also notes that vendor citations for carbon tetrachloride and paracetamol liver-injury protection could not be verified in accessible databases. | |||||
How a course is commonly described
- Days 1-10Community-reported
The canonical Khavinson schedule for this family is a 10-day course of 1-2 capsules a day, taken at a consistent time with or without food. Nothing measurable is expected within a course, and no study has tracked an endpoint over one.
- Extended courseCommunity-reported
Some supplier protocols stretch a single course to 20 or 30 days rather than 10. The same source notes that continuous chronic dosing is not part of the published convention for the Khavinson line and that no chronic-dosing data exist in any species at any dose.
- Between coursesCommunity-reported
Courses are described as repeated two to four times a year, with the gap justified by the framework claim that gene-expression changes persist after dosing stops. For this peptide specifically that persistence has never been demonstrated.
- Preclinical comparisonPreclinical
In the animal work there was no course in this sense: EDL was injected during the days of an acute kidney injury model and the effect was read at the end of it, or given as a course to old rats with urine output measured afterward. None of those timings maps onto someone swallowing a capsule.
- There are no human studies of Glu-Asp-Leu, no registered trials and no pharmacokinetic data, so the capsule courses above are supplement marketing conventions rather than tested schedules. The published evidence is rat kidney injury models and kidney cell culture from one research network, several papers in Russian with English abstracts only.
- The marketing and the literature disagree about the target organ. The institute lists Ovagen as both a nephroprotector and a hepatoprotector, but the hepatoprotector label is supported by a patent rather than a published experiment, and no study of this sequence in liver tissue or in ovarian tissue appears to exist.
- EDL changed urine output and sodium handling in rats and lowered p16, p21 and p53 in kidney cells, so it is not an inert molecule; its effect in a person with kidney disease, on diuretics or with raised blood pressure has not been studied. It is not approved as a medicine anywhere. The rows above record what sources report, not endorsements of use.
Sources for this section (10)
- Peptides Restore Functional State of the Kidneys During Cisplatin-Induced Acute Renal Failure
- Nephroprotective Effect of EDL Peptide at Acute Injury of Kidneys of Different Genesis
- The influence of peptides on the morphofunctional state of old rats kidneys
- Tripeptides slow down aging process in renal cell culture
- Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals
- Peptides regulate expression of signaling molecules in kidney cell cultures during in vitro aging
- Hydrophilic peptides derived from the transframe region of Gag-Pol inhibit the HIV-1 protease
Plus 3 community resources (dosing guides, forum threads and vendor write-ups), reported above but not linked.
Overview
Ovagen is the trade name for the synthetic tripeptide Glu-Asp-Leu, one of the short peptide bioregulators designed at Vladimir Khavinson's St Petersburg Institute of Bioregulation and Gerontology, where it also appears under the laboratory code T-35. Despite the name, nothing published concerns the ovaries: the institute lists it as a nephroprotector and hepatoprotector, and every indexed experiment on the sequence is either a rat kidney study or kidney cell culture from that institute and its collaborators in Chernivtsi, Ukraine. There are no human studies, no registered trials and no pharmacokinetic data for it, and it is not an approved medicine anywhere; in Russia it is sold as a dietary supplement capsule and elsewhere as an unlicensed research chemical. The one independent finding about the sequence comes from structural biology rather than gerontology: Glu-Asp-Leu is a weak competitive inhibitor of the HIV-1 protease.
What researchers are exploring
These themes organize the educational information currently available. Individual claims remain under source review and are not treatment claims.
- 1
Ovagen and the Liver
Bioregulator effects on GI tract and liver health
What is known and what still needs verification
Available context is organized without assigning unsupported study models or evidence grades.
- Not graded
Ovagen and the Liver
Bioregulator effects on GI tract and liver health
Amounts recorded for Ovagen
These amount records are independent from vial strength, reconstitution volume and measuring device. A recorded source is not the same as study backing, and these values are not recommendations.
- 1Dose · lower endpointSign in for schedule, duration and source context.1 mg
- 2Dose · upper endpointSign in for schedule, duration and source context.5 mg
Chemistry identifiers
Sequence, synonyms and registry identifiers as recorded in PubChem, the National Library of Medicine's open chemistry database. Formula, mass and CAS number are summarized at the top of the page.
Sequence
Glu-Asp-Leu
Also listed as
Glu-Asp-Leu, EDL, glutamyl-aspartyl-leucine, L-Glutamyl-L-aspartyl-L-leucine, NH2-Glu-Asp-Leu-COOH, T-35 (code used in the developer's papers), CHEBI:137252, PDB ligand 1a30
InChIKey
JVSBYEDSSRZQGV-GUBZILKMSA-N
IUPAC name
(2S)-2-[[(2S)-2-[[(2S)-2-amino-4-carboxybutanoyl]amino]-3-carboxypropanoyl]amino]-4-methylpentanoic acid
Limitations and unknowns
Sources
1 link carried over from the earlier page, awaiting verification.