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Specimen Atlas of Research Peptides81 plates · MIT
Side-by-side · Research reference

IGF-1 LR3vsVilon

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-StrongHUMAN-REVIEWED13/49 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
Vilon
Khavinson Bioregulator · Dipeptide
2 AADipeptide
T-helperStimulatesLinkova 2011
MouseModel basisKhavinson 2002
Literature lacks standardised clinical route

01Mechanism of Action

Parameter
IGF-1 LR3
Vilon
Primary target
IGF-1 receptor (IGF-1R)McTavish 2009
Immune cell differentiation pathways, chromatin modification
Pathway
IGF-1R → IRS-1 → PI3K/Akt → Cell proliferation, protein synthesis, anti-apoptosisMuhlbradt 2009
Vilon → Thymocyte sphingomyelinase activation → T-helper & cytotoxic T-cell differentiation; epigenetic suppression of aging markers (CCL11, HMGB1)
Downstream effect
Enhanced cell proliferation, muscle anabolism, inhibition of apoptosis, increased telomerase activity
Enhanced T-cell differentiation (CD4+, CD8+, B-cells), thymocyte proliferation, modulated IL-1β comitogenic activity, proposed chromatin decondensation in aged lymphocytesLinkova 2011Khavinson 2002Lezhava 2023
Feedback intact?
No — exogenous IGF analogue bypasses GH-mediated regulation
Unknown — no HPA/HPG axis data
Origin
Synthetic 83-AA analogue: 13-AA N-terminal extension + Arg substitution at position 3
Synthetic dipeptide derived from Khavinson thymic peptide extraction studies (Thymalin fraction)Morozov 1997
Antibody development

02Dosage Protocols

Parameter
IGF-1 LR3
Vilon
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.
Evidence basis
Animal / in vitro only
Mouse / in vitro only
Human use
Not FDA-approved; no published human trials
Standard dose
No clinical standard — literature lacks human dosing
Russian practice: often combined with other Khavinson peptides; no FDA/EMA trials.
Animal model dose
In vitro: 0.01–10 μg/mL culture medium (mouse thymocytes)
Not translatable to human mg/kg without pharmacokinetic data.
Frequency
Unknown — literature does not specify chronic administration protocols
Duration
Not characterised in humans
Route
Likely SQ or oral (Khavinson school uses both); no published ROA validation
Half-life
Not published — dipeptides typically <10 min plasma t½

03Metabolic / Fat Loss Evidence

Parameter
IGF-1 LR3
Vilon
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
Vilon
Hypoglycemia risk
Theoretical — IGF-1 analogues can lower blood glucose
Excessive cell proliferation
Mitogenic signaling; theoretical tumor promotion risk
Telomerase activation
2–10-fold increase in prostate cancer cells (PC-3, DU-145, LAPC-4)Wetterau 2003
Critically involved in cancer cell immortalization.
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
Human safety data
Absent from PubMed-indexed literature
Theoretical risk
Immune hyperactivation in autoimmune-prone individuals (T-cell differentiation enhancement)
Antibody formation
Not reported; dipeptides generally low immunogenicity
Animal models
No adverse effects noted in mouse thymocyte or pineal lymphoid cultures
Absolute Contraindications
IGF-1 LR3
  • ·Active malignancy or history of cancer
  • ·Not approved for human use
Vilon
  • ·Active autoimmune disease (theoretical — no clinical data)
Relative Contraindications
IGF-1 LR3
  • ·Diabetes or glucose intolerance
  • ·Family history of cancer
Vilon
  • ·Pregnancy / lactation (no safety data)
  • ·Acute infection with cytokine storm risk (immune modulation unknown)

05Administration Protocol

Parameter
IGF-1 LR3
Vilon
1. Research use only
IGF-1 LR3 is not FDA-approved for human use. All administration data derives from animal or in vitro studies.
No clinical protocols exist in Western peer-reviewed literature. Russian gerontological practice may use 1–10 mg ranges, but dosing is empirical.
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
Subcutaneous injection (common for Khavinson peptides) or oral (some bioregulators reportedly active orally due to small size). No validated ROA.
3. Reconstitution (research)
Lyophilised powder reconstituted in sterile water or buffered saline per manufacturer protocol. Store at 2–8 °C after reconstitution.
Unknown — no circadian or meal-timing data. Khavinson school often recommends morning administration.
4. Stability
Enhanced stability vs native IGF-1 due to reduced IGFBP binding; exact half-life in vivo not fully characterized in humans.
Likely lyophilised powder, refrigerated. Reconstitution protocols not published.

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)
Vilon
+ Epitalon
Moderate
View Epitalon

Both are Khavinson bioregulators targeting aging pathways. Epitalon (Ala-Glu-Asp-Gly) acts on telomerase and pineal function; Vilon on immune differentiation and chromatin decondensation. Combined in Russian gerontological protocols for multi-system aging intervention. Lezhava et al. (2023) tested both on aged lymphocyte chromatin, showing distinct epigenetic effects. Complementary, not synergistic in strict pharmacological sense.

Vilon
Empirical — no standard
Epitalon
Empirical — often 10 mg cycles
Frequency
Sequential or concurrent (literature ambiguous)
Primary benefit
Multi-system aging modulation (immune + pineal/circadian)
+ Thymalin
Weak
View Thymalin

Thymalin is the parent polypeptide complex from which Vilon was isolated. Both target immune differentiation, but Thymalin is a complex mixture (multiple peptides), whereas Vilon is a purified dipeptide. Morozov & Khavinson (1997) described Vilon as a synthetic successor designed to replicate Thymalin's immunomodulatory effects with greater specificity. Redundant in practice; no published combination studies.

Vilon
No standard
Thymalin
10–100 mg IM (polypeptide complex)
Primary benefit
Redundant — both target T-cell differentiation