Side-by-side · Research reference
MGFvsProstamax
Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.
AAnimal-StrongHUMAN-REVIEWED14/55 cited
BAnimal-MechanisticHUMAN-REVIEWED11/38 cited
MGF
IGF-1Ec Splice Variant · Muscle-Specific
SQ · Research context only
Prostamax
Khavinson Bioregulator · Tissue-Specific Peptide
4 AAPeptide length
SQ · Protocol per Khavinson tradition
01Mechanism of Action
Parameter
MGF
Prostamax
Primary target
Satellite cells (Pax7+) in skeletal muscleMoore 2018
Chromatin in prostatic cells — pericentromeric heterochromatin regions
Pathway
Mechanical stress → IGF-1Ec mRNA upregulation → Local E-domain peptide release → Satellite cell activation
Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012
Downstream effect
Satellite cell proliferation, myoblast differentiation, muscle fiber repair
Increased sister chromatid exchange, Ag-NOR activation, reduced C-heterochromatin condensation; tissue-specific regenerative stimulation in prostate organotypic culturesDzhokhadze 2012Zakutskiĭ 2006
Feedback intact?
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—
Origin
Alternative splicing of IGF-1 gene (exons 4-6) produces IGF-1Ec precursor; E-domain cleaved post-translationallyArmakolas 2016Vassilakos 2017
Synthetic tetrapeptide modeled on naturally occurring protein-derived bioregulators isolated between lysine-arginine motifs in long-lived speciesKhavinson 2017
Antibody development
—
—
02Dosage Protocols
Parameter
MGF
Prostamax
Synthetic peptide
24-amino-acid E-domain sequence
Corresponds to human IGF-1Ec exons 4-6 region.
—
Rodent cardiac model
200 μg/kg via peptide-eluting microstructures
Post-MI injection; improved ejection fraction by 8 weeks.
—
Acute delivery (mouse MI)
Single bolus within 12 hrs post-infarctionShioura 2014
Delayed decompensation; no human protocol established.
—
Human evidence
None — no published clinical trials
All dosing extrapolated from animal models.
—
Detection in doping
Full-length MGF detected via LC-MS in illicit productsThevis 2014
WADA-prohibited since 2005; no therapeutic indication.
—
Evidence basis
Animal models + in vitro only
Animal / organotypic cultureZakutskiĭ 2006Dzhokhadze 2012
No randomized controlled trials in humans.
Effective concentration (in vitro)
—
0.05 ng/mLZakutskiĭ 2006
Organotypic culture model; demonstrated tissue-specific stimulation.
Human clinical dose
—
Not established
No published human trials; dosing extrapolated from Russian clinical tradition (not peer-reviewed).
Age groups studied
—
Young (3-week) and aged (18-month) rats; elderly humans (75–86 years) in vitroZakutskiĭ 2006Dzhokhadze 2012
Duration
—
Not specified
Khavinson protocols typically 10–20 days per cycle; no long-term safety data.
04Side Effects & Safety
Parameter
MGF
Prostamax
Human safety data
None — no clinical trials published
Absent — no published Phase 1/2/3 trials
Theoretical IGF-1 axis risk
Chronic IGF-1Ec overexpression linked to cancer progression (prostate, colorectal, breast)
—
Tumor promotion
IGF-1Ec overexpressed in osteosarcoma, colorectal polyps with dysplasia, endometrial cancer
—
Antibody development
Unknown — no longitudinal human exposure data
—
Local injection reaction
Presumed similar to other peptides (erythema, induration) — no direct evidence
—
Dysregulated expression with age
Older adults (70+ yrs) show blunted IGF-1Ec response post-exercise vs youngMoore 2018
—
Published adverse events
—
None reported in available literature
Genotoxicity signals
—
Increased sister chromatid exchange (SCE) — marker of DNA recombination/repair; unclear long-term implications
Metal ion interactions
—
Modulates Cu(II) and Cd(II) chromatin effects; unknown clinical relevance
Absolute Contraindications
MGF
- ·Active malignancy or history of IGF-1-sensitive cancers (prostate, colorectal, breast, osteosarcoma)
- ·No established therapeutic use — investigational only
Prostamax
- ·Active prostate malignancy — epigenetic modulation effects unknown in cancer
Relative Contraindications
MGF
- ·Family history of IGF-1-axis malignancies
- ·Use outside research setting
Prostamax
- ·History of prostate cancer — theoretical concern re: transcriptional activation
- ·Undiagnosed prostatic nodules or elevated PSA
05Administration Protocol
Parameter
MGF
Prostamax
1. No validated protocol
MGF (E-domain peptide) has no approved clinical protocol. All published data derive from animal models or in vitro experiments.
Subcutaneous or intramuscular — per Khavinson bioregulator tradition. No published human pharmacokinetic data.
2. Synthetic peptide form
Commercially available MGF corresponds to the 24-amino-acid human E-domain (hEc). Rodent E-domain (Eb) is structurally distinct and not interchangeable.
If lyophilised: reconstitute with sterile water per manufacturer protocol (not standardized in literature).
3. Animal delivery models
Rodent studies used peptide-eluting polymeric microstructures (cardiac) or direct intramuscular injection. Routes and doses non-translatable to humans.Peña 2015Shioura 2014
Typically daily or every-other-day in Russian clinical tradition; duration 10–20 days per cycle.
4. WADA prohibition
MGF peptides prohibited in sport since 2005. Detection via LC-MS established for full-length MGF products.Thevis 2014
No established biomarkers. Theoretical: PSA, prostate imaging, symptom scores (IPSS for BPH).
5. Research context only
Any human use falls outside approved medical practice and regulatory frameworks. No safety or efficacy data exist.
All protocols derived from non-peer-reviewed Russian clinical practice; Western regulatory approval absent.
06Stack Synergy
MGF
+ BPC-157
Multi-pathwayMGF activates satellite cells for muscle fiber repair; BPC-157 promotes angiogenesis, collagen synthesis, and tendon healing via distinct pathways (VEGF, FAK, integrin signaling). Theoretical synergy in post-injury contexts combines myogenic (MGF) and stromal (BPC-157) repair mechanisms. Both lack human validation.
- MGF
- No established dose
- BPC-157
- 250–500 mcg SQ near injury site
- Context
- Animal models only
- Primary benefit
- Theoretical multi-tissue repair (muscle + tendon/ligament)
+ TB-500
ModerateTB-500 (thymosin beta-4 fragment) enhances actin polymerization, cell migration, and angiogenesis—complementary to MGF satellite cell activation. Both upregulated post-injury; combined use presumed additive for muscle regeneration in preclinical models.
- MGF
- No established dose
- TB-500
- 2–5 mg SQ weekly
- Context
- Animal models only
- Primary benefit
- Satellite cell activation + enhanced migration/angiogenesis
Prostamax
— no documented stacks