Ovagen
Also known as: EDL, Glu-Asp-Leu, T-35 peptide, T-35
3 notable studies · 3 references
TLDR
Ovagen is generally identified as the synthetic tripeptide Glu-Asp-Leu (EDL/T-35), with limited direct preclinical evidence involving kidney-cell aging, tissue remodeling, and experimental kidney injury, but no established human efficacy and no convincing published evidence supporting the ovarian implication of its name or many of its liver-focused marketing claims.
Research Supports
- Studied (as EDL/T-35) in kidney-cell aging and kidney tissue-culture experiments, not ovarian research
- Investigated for effects on extracellular-matrix remodeling via MMP-14
- Studied in experimental models of acute kidney injury, including rhabdomyolysis-associated injury
- Investigated for effects on cell proliferation and apoptosis in aging kidney tissue
Observations Reported in Research
- T-35/EDL specifically affected MMP-14 expression in aging primary kidney-cell cultures (Khavinson et al., 2014)
- In kidney tissue from young and old rats, T-35/EDL stimulated proliferation and reduced apoptosis, though less than the full kidney-peptide complex (Chalisova et al., 2015)
- T-31 and T-35 were among the kidney-associated peptides studied in a rhabdomyolysis-induced kidney-injury model (Zamorskiĭ & Shchudrova, 2014)
- No peer-reviewed study was identified examining Ovagen/EDL in ovarian tissue or function
These are brief summaries of what the referenced research examined or reported — not conclusions about safety or effectiveness, and not medical advice. See Notable Studies and Sources & References below for the full context and citations.
At a Glance
Classification: Synthetic tripeptide; short peptide bioregulator; experimental renal-associated peptide
Ovagen is generally identified in the peptide-bioregulator market as Glu-Asp-Leu or EDL. Despite the name “Ovagen,” the identifiable peer-reviewed EDL research isn't ovarian research. It's primarily kidney research. EDL appears in published experiments under the laboratory designation T-35. Researchers have studied it in aging kidney-cell cultures, kidney tissue cultures, experimental acute kidney injury, and rhabdomyolysis-associated kidney injury. For example, a 2014 paper explicitly identifies T-35 (EDL) and reports effects on MMP-14 in aging primary kidney-cell cultures. There is no comparable peer-reviewed evidence establishing Ovagen/EDL as an ovarian therapy.
What Is Ovagen?
Ovagen is generally identified as the tripeptide Glu-Asp-Leu (EDL) and EDL appears in the Khavinson literature as T-35. It belongs to the same short-peptide research family as Cartalax / AED / T-31, Pinealon / EDR, Vesugen / KED, and Chonluten / EDG. Commercial sources variously call Ovagen ovarian, liver, gastrointestinal, or renal. The strongest verifiable peer-reviewed evidence for EDL/T-35 is clearly renal. For Aminodex, classify it scientifically as an experimental renal-associated short peptide while mentioning the conflicting commercial classifications.
What Are Researchers Studying?
Kidney-cell aging
A 2014 experiment studied a kidney-derived polypeptide complex together with T-31 / AED and T-35 / EDL. Researchers used primary kidney-cell cultures during in-vitro aging. They measured Ki-67, p53, MMP-14, and IL-8. T-35/EDL specifically affected MMP-14, an enzyme involved in extracellular-matrix remodeling. This provides direct EDL-specific biological evidence.
Kidney tissue renewal
A separate 2015 study examined kidney tissue cultures from young and old rats. The complete calf-kidney polypeptide complex produced the strongest effects on Ki-67, p53, and cellular renewal. Both T-31/AED and T-35/EDL also stimulated proliferation and reduced apoptosis, although less strongly than the complete peptide complex. This is another useful evidence-identity lesson: kidney polypeptide extract ≠ EDL alone. The extract's stronger effect shouldn't be credited entirely to Ovagen.
Acute kidney injury
T-35/EDL has also been investigated in experimental kidney-injury models. One study examined organ-specific peptides during kidney injury produced by rhabdomyolysis. Researchers evaluated processes involving tubular-cell toxicity, oxidative stress, energy imbalance, and acute renal dysfunction. T-31 and T-35 were among the kidney-associated peptides investigated. This moves EDL beyond cell culture into whole-animal renal injury research. It still remains preclinical.
Extracellular-matrix remodeling
The 2014 kidney-cell experiment identified MMP-14 as a particular target responsive to T-35/EDL. MMP-14 participates in extracellular-matrix remodeling, cell migration, and tissue remodeling. That provides a more specific experimentally observed molecular effect than vague claims that Ovagen simply “rejuvenates the kidney.”
Cell proliferation and apoptosis
EDL has been investigated for effects on the balance between cell proliferation and programmed cell death. In kidney tissue culture, T-35 stimulated proliferation and reduced apoptosis relative to untreated aging tissue, although its effects were less pronounced than the complete kidney-derived peptide preparation. These are tissue-culture findings. They don't establish kidney regeneration in living humans.
Ovarian biology
Despite the name, direct ovarian evidence was not identified. Current evidence reviews likewise find no published EDL study involving ovarian tissue or ovarian function. Therefore Aminodex should not describe Ovagen as an ovarian peptide merely because the name suggests it. That's exactly the sort of circular evidence problem we're trying to eliminate.
Liver biology
Ovagen is also marketed in some places as a liver bioregulator. But the identifiable primary EDL literature reviewed for this profile centers on the kidney, not liver disease. Therefore: “Ovagen supports liver regeneration” currently exceeds the direct published evidence.
How Does It Work?
No established classical receptor is known. The direct experimental findings support effects involving EDL / T-35 changes in kidney-cell signaling, MMP-14 regulation, changes in proliferation/apoptosis under experimental conditions, and potential alteration of tissue-remodeling processes. Broader Khavinson-family hypotheses propose cellular uptake, gene regulation, peptide-DNA interactions, and epigenetic regulation. Those broader mechanisms shouldn't be presented as definitively established for Ovagen.
What Does the Research Show?
Human research
No peer-reviewed human administration study of Ovagen/EDL was identified. No established human pharmacokinetic trial, safety study, renal trial, liver trial, or ovarian trial was found in the literature reviewed here. Human evidence maturity: NONE ESTABLISHED.
Animal research
Limited but direct. T-35/EDL has been investigated in experimental kidney injury, including rhabdomyolysis-associated renal injury. Other renal-injury research reported in this literature includes toxic and ischemic kidney models, but each paper should be individually identity-checked before inclusion.
In-vitro research
This is currently the strongest evidence category. Direct EDL/T-35 research includes aging primary kidney-cell cultures, organotypic kidney cultures, extracellular-matrix remodeling, and proliferation/apoptosis endpoints.
Notable Studies
Peptides Regulate Expression of Signaling Molecules in Kidney Cell Cultures During In Vitro Aging
in-vitroResearchers investigated a calf-kidney polypeptide complex plus T-31/AED and T-35/EDL in aging primary kidney-cell cultures. They examined Ki-67, p53, MMP-14 and IL-8. The kidney complex and T-31 primarily influenced cellular-renewal processes, while MMP-14 was identified as a target of T-35/EDL.
Limitations: Cell culture only. It doesn't demonstrate improved renal function, kidney regeneration or clinical benefit in humans.
View publication →Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals
in-vitroResearchers compared a calf-kidney polypeptide complex with short peptides T-31/AED and T-35/EDL in kidney explants from young and old rats. The short peptides stimulated proliferation and reduced apoptosis, although their effects were weaker than the complete kidney-derived polypeptide preparation.
Limitations: Ex-vivo rat kidney tissue. It doesn't establish systemic pharmacology or therapeutic efficacy in living animals or humans.
View publication →Main Mechanisms of Rhabdomyolysis-Caused Kidney Injury and Their Correction by Organospecific Peptides
animalResearchers investigated kidney-associated T-31 and T-35 peptides and Epitalon in experimental rhabdomyolysis-associated kidney injury. The study examined tubular toxicity, oxidative stress, energy imbalance and functional renal disturbance, providing direct whole-animal evidence that the kidney-associated short peptides had biological effects in an acute renal-injury model.
Limitations: Rodent experimental disease model; article published in Russian; does not establish human nephroprotection or long-term safety.
View publication →What We Still Don't Know
Human pharmacokinetics; human bioavailability; human safety; effective human exposure; primary molecular target; whether kidney effects occur after systemic human exposure; whether it improves human renal function; whether it protects against acute kidney injury; whether it changes chronic kidney disease progression; whether it has meaningful liver effects; whether it has meaningful ovarian effects; whether tissue specificity exists in vivo; long-term toxicity; reproductive effects; whether findings independently replicate; whether research-market “Ovagen” reliably contains EDL.
Related Compounds
Recent publications
Latest titles from PubMed, not reviewed by Aminodex. Not an endorsement. See all on PubMed ↗
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Sources & References
- Khavinson VKh, Linkova NS, Polyakova VO, et al. Peptides regulate expression of signaling molecules in kidney cell cultures during in vitro aging. Bulletin of Experimental Biology and Medicine. 2014;157(2):261–264.
- Chalisova NI, Linkova NS, Nichik TE, et al. Peptide Regulation of Cells Renewal Processes in Kidney Tissue Cultures from Young and Old Animals. Bulletin of Experimental Biology and Medicine. 2015;159(1):124–127.
- Zamorskiĭ II, Shchudrova TS. Main mechanisms of rhabdomyolysis-caused kidney injury and their correction by organospecific peptides. Biofizika. 2014;59(5):1023–1026.
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