NOT FOR HUMAN CONSUMPTION

Prostamax (Lys-Glu-Asp-Pro) 

1. Identity and Classification

• Molecular structure: A synthetic tetrapeptide composed of the amino acids Lysine (K), Glutamic acid (E), Aspartic acid (D), and Proline (P). Its abbreviation is KEDP.

• Peptide class: Bioregulatory short-chain peptide.

• Origin: Developed in the 1980s–1990s by the St. Petersburg Institute of Bioregulation and Gerontology, led by Prof. Vladimir Khavinson. Prostamax is part of the “Cytomedin” peptide family focused on organ-specific genetic reactivation.

• Commercial availability: Sold by peptide vendors in lyophilized vials (typically 20 mg) or prefilled injection pens (usually 2 mg in 20 units), labeled strictly for “research use only”.

2. Proposed Mechanisms of Action

2.1. Chromatin Modulation and Epigenetic Regulation

Prostamax is believed to function by binding to condensed chromatin structures, particularly in aged or dysfunctional cells of the prostate and immune tissues. This interaction may trigger:

• Decondensation of heterochromatin, re-opening silenced gene regions (especially in nucleolar organizing regions).

• Reactivation of ribosomal RNA genes, leading to increased ribosome biogenesis, which boosts protein synthesis.

• Restoration of “youthful” transcriptional activity, similar to other Khavinson peptides (e.g., Epitalon, Vilon).

These effects have been observed primarily through melting curve analysis of chromatin, and in vitro assays on lymphocytes and prostate cells.

2.2. Anti-inflammatory Action in Prostate Tissue

In animal studies, Prostamax has demonstrated a significant anti-inflammatory effect in models of chronic prostatitis. Mechanisms include:

• Suppression of lymphocytic infiltration and cytokine-mediated damage.

• Reduction of vascular congestion, fibrosis, and stromal edema.

• Restoration of epithelial structure in prostate acini.

These histological changes suggest tissue remodeling and immune modulation, though specific cytokine profiles have not been characterized.

2.3. Enhancement of Sexual and Reproductive Function (Animal Data)

• A notable outcome in the 2013 rat study was an observed increase in mating behavior in males with prostatitis treated with Prostamax.

• The peptide may support spermatogenesis, improve testicular microcirculation, and reduce oxidative stress—though such mechanisms remain speculative.

2.4. Immune Modulation

Because lymphocytes also exhibit chromatin decondensation under Prostamax treatment (similar to observations with Epitalon and Livagen), the peptide is theorized to:

• Enhance T- and B-lymphocyte transcriptional activity.

• Improve immune cell proliferation and resilience.

• Counteract immune senescence through reactivation of silenced ribosomal genes.

No flow cytometry or cytokine data are available to confirm these effects.

3. Preclinical and Experimental Evidence

3.1. 2013 Rat Model of Chronic Aseptic Prostatitis

• Study type: Controlled, comparative study with 4 groups: control, untreated prostatitis, Serenoa repens (saw palmetto) treated, and Prostamax-treated.

• Key outcomes:

  • Dramatic reduction in prostate tissue inflammation, necrosis, and atrophy in Prostamax group.

  • Restoration of glandular architecture.

  • Increased sexual activity and lower systemic inflammation.

• Conclusion: Prostamax outperformed both placebo and Serenoa repens in structural and behavioral markers of prostatitis.

• Limitations:

  • Single-species, short-duration study.

  • No blinded scoring or cytokine assays.

  • Not replicated in peer-reviewed Western studies.

3.2. Epigenetic Profiling Studies

• Chromatin-binding studies used thermal denaturation profiles to track decondensation in lymphocytes from elderly donors exposed to KEDP.

• Showed greater chromatin mobility and open configuration, consistent with higher transcriptional readiness.

• Similar profiles seen in other Khavinson peptides, suggesting class-wide genomic activation mechanisms.

3.3. Absence of Human Clinical Trials

• As of July 2025:

  • No clinical trials registered on ClinicalTrials.gov or EU Clinical Trials Register.

  • No human pharmacokinetic or toxicology data published.

  • Anecdotal reports exist in biohacking and peptide forums, but these are uncontrolled and subject to placebo bias.

4. Dosing Protocols (for research)

Commonly Reported Regimens

• Reconstitution: Peptide powder is diluted with bacteriostatic water. Refrigeration at 2–8 °C required after mixing.

• No pharmacokinetic guidance exists for absorption, distribution, metabolism, or excretion in humans.

5. Safety Profile and Side Effects

5.1. Animal Toxicology

• Limited toxicology studies suggest low acute toxicity.

• No adverse histological effects reported in rats at therapeutic doses.

• Chronic or cumulative toxicity not studied.

5.2. Human Safety — Unknown

• No formal adverse event records.

• No studies on mutagenicity, carcinogenicity, or teratogenicity.

• Theoretically, reactivating silenced gene regions could unintentionally derepress proto-oncogenes, especially in older individuals with somatic mutations.

5.3. Anecdotal User Reports

Some reported effects include:

• Mild fatigue, transient dizziness, or minor injection site reactions.

• A few accounts of subjective improvement in urinary comfort and libido.

• No validated biomarkers or structured follow-up.

6. Regulatory Status and Availability

• Not approved by FDA, EMA, or any health authority.

• Marketed for laboratory use only; therapeutic claims are legally restricted.

• Found via:

  • Specialized research peptide sites (e.g., Core Peptides, Peptide Sciences).

  • Capsule form in Russian “Cytogen” product lines (gray market availability).

• No batch standardization or verified GMP certification in most suppliers.

• Legal ambiguity: Self-administration constitutes unregulated experimentation.

7. Summary of Scientific Validity

8. Final Evaluation and Research Outlook

What Prostamax Might Offer (Hypothetically):

• Restoration of youthful transcriptional activity in prostate and immune tissues.

• Reduction of chronic prostatic inflammation and fibrosis.

• Potential support for reproductive health in aging males.

• Chromatin remodeling with systemic “anti-aging” potential.

What Is Still Missing:

• Clinical validation of efficacy and safety in humans.

• Pharmacological profiling (bioavailability, half-life, metabolism).

• Controlled trials comparing to existing BPH/prostatitis treatments.

• Toxicology, long-term safety, and cancer-risk studies.

Bottom Line:

Prostamax is a biologically intriguing experimental peptide with early-stage evidence of epigenetic and anti-inflammatory effects in prostate tissues. However, its use in humans is entirely unsupported by clinical science, and potential risks—especially with chronic or unsupervised use—are unquantified.

Any use beyond laboratory research is experimental, unregulated, and ethically complex. Researchers interested in this peptide should approach it with rigorous scientific controls and clear safety oversight.