Side-by-side · Research reference

IGF-1 LR3vsProstamax

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

AAnimal-StrongHUMAN-REVIEWED10/58 cited

BAnimal-MechanisticHUMAN-REVIEWED11/38 cited

IGF-1 LR3

IGF-1 Analogue · Research

3–10×Potency vs IGF-I

Low IGFBPBinding affinity

ResearchStatus

Research only · SQ typical in animal models

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-1 LR3

Prostamax

Primary target

IGF-1 receptor (IGF-1R)McTavish 2009

Chromatin in prostatic cells — pericentromeric heterochromatin regions

Pathway

IGF-1R → IRS-1 → PI3K/Akt → Cell proliferation, protein synthesis, anti-apoptosisMuhlbradt 2009

Epigenetic modulation → heterochromatin decondensation → transcriptional derepressionDzhokhadze 2012

Downstream effect

Enhanced cell proliferation, muscle anabolism, inhibition of apoptosis, increased telomerase activity

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

Feedback intact?

No — exogenous IGF analogue bypasses GH-mediated regulation

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Origin

Synthetic 83-AA analogue: 13-AA N-terminal extension + Arg substitution at position 3

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

Antibody development

—

02Dosage Protocols

Parameter

IGF-1 LR3

Prostamax

Research dose (animal models)

Variable by protocol and species

In vivo murine atherosclerosis studies used sustained delivery.

—

In vitro typical concentration

10–1000 ng/mLThomas 2007

Dose-dependent effects on follicle growth and estradiol production.

—

Half-maximal stimulation

0.6 nM LR3 vs 1.5 nM native IGF-1Price 2004

2.5-fold greater potency in lung fibroblast proliferation.

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Evidence basis

Animal / in vitro only

Animal / organotypic cultureZakutskiĭ 2006 Dzhokhadze 2012

No randomized controlled trials in humans.

Human use

Not FDA-approved; no published human trials

—

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 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-1 LR3

Prostamax

Mechanism

IGF-1R activation → lipolytic signaling; secondary to anabolic effects

—

Direct lipolytic evidence

Minimal — primarily anabolic/anti-apoptotic in literature

—

Atherosclerotic plaque effects

Reduced stenosis and core size in ApoE-KO micevon 2011

Plaque stabilization via vSMC phenotype modulation, not direct fat loss.

—

Human data

None published

—

04Side Effects & Safety

Parameter

IGF-1 LR3

Prostamax

Hypoglycemia risk

Theoretical — IGF-1 analogues can lower blood glucose

—

Excessive cell proliferation

Mitogenic signaling; theoretical tumor promotion risk

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Telomerase activation

2–10-fold increase in prostate cancer cells (PC-3, DU-145, LAPC-4)Wetterau 2003

Critically involved in cancer cell immortalization.

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Oocyte degeneration

Increased oocyte degeneration at high doses (≥1000 ng/mL) in bovine folliclesThomas 2007

—

Unregulated anabolism

Bypasses physiological GH/IGF-1 feedback; no pulsatility control

—

Unknown human safety profile

No published human trials; safety data absent

—

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

Human safety data

—

Absent — no published Phase 1/2/3 trials

Absolute Contraindications

IGF-1 LR3

·Active malignancy or history of cancer
·Not approved for human use

Prostamax

·Active prostate malignancy — epigenetic modulation effects unknown in cancer

Relative Contraindications

IGF-1 LR3

·Diabetes or glucose intolerance
·Family history of cancer

Prostamax

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

05Administration Protocol

Parameter

IGF-1 LR3

Prostamax

1. Research use only

IGF-1 LR3 is not FDA-approved for human use. All administration data derives from animal or in vitro studies.

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

2. Typical research route

Subcutaneous or intraperitoneal injection in animal models. In vitro: added directly to culture medium at concentrations of 10–1000 ng/mL.Thomas 2007

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

3. Reconstitution (research)

Lyophilised powder reconstituted in sterile water or buffered saline per manufacturer protocol. Store at 2–8 °C after reconstitution.

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

4. Stability

Enhanced stability vs native IGF-1 due to reduced IGFBP binding; exact half-life in vivo not fully characterized in humans.

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

5. Note

—

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

06Stack Synergy

IGF-1 LR3

+ GHRP-6

Multi-pathway

View GHRP-6 →

GHRP-6 stimulates endogenous GH release, which drives hepatic IGF-1 synthesis. IGF-1 LR3 provides exogenous, IGFBP-resistant IGF signaling. Combining upstream GH stimulation with downstream IGF receptor activation creates a dual-pathway anabolic effect. However, this bypasses natural feedback and carries compounded mitogenic risk.

GHRP-6: 100–200 mcg SQ · 2–3× daily
IGF-1 LR3: Research doses variable · post-workout typical in animal models
Note: Research context only — no human protocols exist
Primary benefit: Theoretical maximal anabolic signaling (GH + IGF axes)

+ Ipamorelin

Multi-pathway

View Ipamorelin →

Ipamorelin (selective GHRP) stimulates pulsatile GH release without cortisol/prolactin elevation. IGF-1 LR3 directly activates IGF-1R independent of GH. This stack targets both upstream (GH secretion) and downstream (IGF receptor) nodes but eliminates physiological feedback, raising safety concerns around unchecked proliferation.

Ipamorelin: 200–300 mcg SQ · evening
IGF-1 LR3: Research doses only · timing variable
Caution: No human data; animal/in vitro only
Primary benefit: Dual-axis anabolic signaling (theoretical)

Prostamax

— no documented stacks