Side-by-side · Research reference

IGF-DESvsProstamax

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

AAnimal-StrongHUMAN-REVIEWED8/60 cited

BAnimal-MechanisticHUMAN-REVIEWED11/38 cited

IGF-DES

IGF-1 Analogue · Truncated N-Terminal

~10×Potency vs IGF-1

ReducedIGFBP binding

ResearchStatus

Injection (local or systemic) · Research protocols onlyBredehöft 2008

Prostamax

Khavinson Bioregulator · Tissue-Specific Peptide

0.05 ng/mLActive concentrationZakutskiĭ 2006

2.5×SCE frequency increaseDzhokhadze 2012

4 AAPeptide length

SQ · Protocol per Khavinson tradition

01Mechanism of Action

Parameter

IGF-DES

Prostamax

Primary target

IGF-1 receptor (IGF1R)Shields 2007

Chromatin in prostatic cells — pericentromeric heterochromatin regions

Pathway

IGF1R activation → PI3K/Akt & MAPK signaling → protein synthesis, proliferation

Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012

Downstream effect

Enhanced muscle protein synthesis, myoblast differentiation, reduced apoptosis, cell proliferation

Increased sister chromatid exchange, Ag-NOR activation, reduced C-heterochromatin condensation; tissue-specific regenerative stimulation in prostate organotypic culturesDzhokhadze 2012 Zakutskiĭ 2006

Feedback intact?

Unknown — no human endocrine feedback data

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Origin

Synthetic truncation of native IGF-1 — removal of N-terminal Gly-Pro-Glu tripeptideBredehöft 2008

Synthetic tetrapeptide modeled on naturally occurring protein-derived bioregulators isolated between lysine-arginine motifs in long-lived speciesKhavinson 2017

Antibody development

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02Dosage Protocols

Parameter

IGF-DES

Prostamax

Research dose range

10–100 ng/mL (in vitro); μg doses (animal models)

Highly context-dependent; no standardized human protocol.

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Route

Subcutaneous or intramuscular (local injection favored)

Local delivery maximizes tissue-specific uptake.

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Frequency

Variable — daily to multiple times daily in research

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Evidence basis

Animal models + in vitro only

Animal / organotypic cultureZakutskiĭ 2006 Dzhokhadze 2012

No randomized controlled trials in humans.

Human data

None — no clinical trials

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Half-life

Shorter than IGF-1 due to reduced IGFBP binding

Rapid tissue uptake, limited systemic circulation.

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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

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Young (3-week) and aged (18-month) rats; elderly humans (75–86 years) in vitroZakutskiĭ 2006 Dzhokhadze 2012

Duration

—

Not specified

Khavinson protocols typically 10–20 days per cycle; no long-term safety data.

03Metabolic / Fat Loss Evidence

Parameter

IGF-DES

Prostamax

Primary mechanism

Indirect via muscle hypertrophy → metabolic rate elevation

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Direct lipolysis

Minimal evidence — IGF-1 axis primarily anabolic, not lipolytic

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Prostate model

Inhibited BPH cell proliferation when combined with vitamin D3 analogueCrescioli 2002

Context-specific anti-proliferative effect, not fat loss.

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04Side Effects & Safety

Parameter

IGF-DES

Prostamax

Hypoglycemia risk

Theoretical — IGF-1 axis enhances glucose uptake

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Mitogenic risk

Chronic IGF-1 receptor activation may promote cell proliferation, potential tumor growthCrescioli 2002

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Injection site reaction

Expected — erythema, irritation, local swelling

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Edema / Fluid retention

Possible via sodium retention (IGF-1 axis effect)

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Human safety data

Absent — no human trials, all effects theoretical or extrapolated

Absent — no published Phase 1/2/3 trials

Unknown long-term effects

No chronic dosing studies in humans; endocrine, metabolic consequences unknown

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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

IGF-DES

·Active malignancy or history of cancer (mitogenic risk)
·Pregnancy / lactation (no safety data)
·Hypoglycemia disorders

Prostamax

·Active prostate malignancy — epigenetic modulation effects unknown in cancer

Relative Contraindications

IGF-DES

·Diabetes mellitus (unpredictable glucose effects)
·Renal or hepatic impairment (clearance unknown)
·Edema-prone conditions (heart failure, nephrotic syndrome)

Prostamax

·History of prostate cancer — theoretical concern re: transcriptional activation
·Undiagnosed prostatic nodules or elevated PSA

05Administration Protocol

Parameter

IGF-DES

Prostamax

1. Research context only

Des(1-3)IGF-1 has no approved human protocol. All administration details are derived from animal or in vitro research and should not be construed as medical guidance.

Subcutaneous or intramuscular — per Khavinson bioregulator tradition. No published human pharmacokinetic data.

2. Reconstitution (if lyophilized)

Sterile water or bacteriostatic water per research protocol. Gently swirl; do not shake. Store reconstituted peptide at 2–8 °C.

If lyophilised: reconstitute with sterile water per manufacturer protocol (not standardized in literature).

3. Injection site

Subcutaneous (abdomen, thigh) or intramuscular (deltoid, vastus lateralis). Local injection to target tissue (e.g., muscle group) may enhance regional uptake.

Typically daily or every-other-day in Russian clinical tradition; duration 10–20 days per cycle.

4. Timing

Frequency and timing vary by research design. Post-exercise or fasted state may theoretically enhance muscle uptake.

No established biomarkers. Theoretical: PSA, prostate imaging, symptom scores (IPSS for BPH).

5. Needle gauge

27–31G insulin syringe for subcutaneous; 25–27G for intramuscular.

All protocols derived from non-peer-reviewed Russian clinical practice; Western regulatory approval absent.

6. Monitoring

Glucose monitoring essential (hypoglycemia risk). No established IGF-1 or safety labs for human use.

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06Stack Synergy

IGF-DES

+ BPC-157

Moderate

View BPC-157 →

Des(1-3)IGF-1 promotes myoblast differentiation and protein synthesis, while BPC-157 enhances tissue repair, angiogenesis, and collagen synthesis. Both act on distinct pathways (IGF1R vs gastric pentadecapeptide mechanisms) to support muscle recovery and connective tissue integrity. Synergy is mechanistic but lacks direct co-administration studies.

Des(1-3)IGF-1: Research dose post-workout (local IM)
BPC-157: 250–500 mcg SQ, daily or twice daily
Frequency: Daily or per research protocol
Primary benefit: Accelerated muscle repair, enhanced hypertrophy, connective tissue support

+ TB-500

Moderate

View TB-500 →

TB-500 (Thymosin Beta-4 fragment) promotes cell migration, angiogenesis, and wound healing via actin regulation. Des(1-3)IGF-1 drives protein synthesis and myoblast proliferation. Combined, these peptides may synergistically enhance muscle recovery, repair, and hypertrophy through complementary anabolic and regenerative pathways. No direct human co-administration data.

Des(1-3)IGF-1: Research dose post-workout (local IM)
TB-500: 2–5 mg SQ, 2× weekly
Frequency: Per research cycle
Primary benefit: Muscle hypertrophy, injury recovery, vascular support

Prostamax

— no documented stacks