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Bioregulator Peptides Explained: Comparison by Tissue Target
The table below summarises the primary bioregulator peptides studied in clinical and preclinical research, organised by the tissue they target and the mechanisms involved. Thymalin Thymus gland Immune system (T-cells, thymic tissue) Upregulates IL-2, interfero
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- The table below summarises the primary bioregulator peptides studied in clinical and preclinical research, organised by the tissue they target and the mechanisms involved.
- Thymalin
- Thymus gland
- Immune system (T-cells, thymic tissue)
- Upregulates IL-2, interferon-gamma, and T-cell receptor gene transcription
- Immune senescence, post-infection recovery, cancer adjuvant therapy
- Most extensively studied bioregulator; reproducible immune marker improvements in elderly populations (Russian trials, limited Western replication)
- Epithalamin
- Pineal gland
- Circadian rhythm regulation, melatonin production
- Increases AANAT gene expression (rate-limiting enzyme in melatonin synthesis)
- Aging, sleep disorders, cancer prevention (melatonin's oncostatic effects)
- Strongest mortality reduction signal in long-term trials (6+ years); mechanism well-characterised but requires independent validation
- Cortagen
- Vascular tissue
- Cardiovascular endothelium, blood vessels
- Enhances eNOS gene expression, increases nitric oxide bioavailability
- Hypertension, atherosclerosis, endothelial dysfunction
- Preclinical data robust; human trials limited to Russian centres; mechanism aligns with known NO pathways
- Vilon
- Gastrointestinal mucosa
- GI tract epithelium, mucosal repair
- Promotes epithelial cell proliferation gene transcription (EGF, TGF-beta pathways)
- Gastric ulcers, inflammatory bowel conditions, mucosal aging
- Early-stage research; tissue-repair mechanism plausible but clinical evidence less developed than thymic or pineal peptides
- Tissue matching is the governing rule: peptides target the system from which they were isolated. A vascular peptide won't produce immune effects, and a thymus peptide won't influence circadian genes. This isn't receptor promiscuity. It's DNA-binding specificity driven by amino acid sequence complementarity to gene promoters.