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ID: IGF-1-LR3 STATUS: ACTIVE

IGF-1 LR3

Research Only

Also known as: Long R3 IGF-1, LR3-IGF-1, Insulin-like Growth Factor 1 Long R3

A modified form of IGF-1 with an extended half-life due to reduced binding protein affinity. Used primarily in research for muscle growth and metabolic effects. Not approved for human use; significant safety concerns exist.

Hormonal Low Evidence 48 Sources

Research Statistics

Total Sources
48
Human Studies
8
Preclinical
28
Evidence Rating Low Evidence
Research Depth 2/5
Global Coverage 2/5
Mechanism Plausibility 3/5
Overall Score
2.5 /5

Research-grade IGF-1 analog with a small human dataset; IGF-1R mechanism is well-established from natural IGF-1 studies but LR3 modification lacks independent clinical validation.

Last reviewed February 2026 How we rate →
!
Evidence Level
low
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited

Research Dossier

01 / 7

Overview

What is IGF-1 LR3 and what does the research say?

Identity
Also Known As
Long R3 IGF-1 • LR3-IGF-1 • Insulin-like Growth Factor 1 Long R3
Type
Modified growth factor analog
Length
83 amino acids
Weight
9,116 Da
Sequence
MFPAMPLSSLFVNGPRTLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA
Molecular Structure
M
F
P
A
M
P
L
S
S
L
F
V
N
G
P
R
T
L
C
G
A
E
L
V
D
A
L
Q
F
V
C
G
D
R
G
F
Y
F
N
K
P
T
G
Y
G
S
S
S
R
R
A
P
Q
T
G
I
V
D
E
C
C
F
R
S
C
D
L
R
R
L
E
M
Y
C
A
P
L
K
P
A
K
S
A
Hydrophobic
Polar
Positive
Negative

Mechanism of Action

IGF-1 LR3 is a modified form of insulin-like growth factor 1, engineered to resist binding to IGF-binding proteins. This modification dramatically extends its biological half-life from minutes to hours while maintaining full receptor activity.

How It Works (Simplified)

IGF-1 LR3 drives muscle growth through four key mechanisms:

Activates PI3K/Akt/mTORC1 pathway, directly stimulating ribosomal protein synthesis and muscle fiber hypertrophy.

2

Inhibits FOXO transcription factors, suppressing muscle breakdown genes MuRF1 and atrogin-1.

3
Satellite Cells

Promotes satellite cell proliferation and myoblast differentiation, supporting muscle fiber repair and regeneration.

4
Glucose Uptake

Stimulates GLUT4 translocation, enhancing glucose transport into muscle cells for energy and glycogen synthesis.

Scientific Pathways

PI3K/Akt/mTOR Pathway (Protein Synthesis)

IGF-1 LR3 → IGF-1R binding → IRS-1 phosphorylation → PI3K → Akt

                                              mTORC1 activation + FOXO inhibition

                                              Protein synthesis + Reduced degradation

Extended Half-Life Mechanism (Key Modification)

Native IGF-1 → IGFBP binding (>99%) → Sequestration → 12-15 min half-life
IGF-1 LR3 → Arg3 + N-terminal extension → <1% IGFBP binding → 20-30 hr half-life

Key Research: Francis GL et al. (1992) first characterized LR3-IGF-1 structure and demonstrated reduced IGFBP binding. PMID:1281011

Important Limitations

  • No randomized controlled trials in healthy adults for muscle building
  • Significant hypoglycemia risk due to insulin-like receptor activity
  • Cancer promotion concerns - IGF-1 signaling is mitogenic and anti-apoptotic
  • Long-term safety data is absent - most evidence is preclinical

Evidence-Chained Benefits

Evidence-Chained Benefits

Research findings linked to mechanisms and clinical outcomes

Mechanism PI3K/Akt/mTORC1 pathway activation promoting protein synthesis
Established 12 direct studies
Benefit shown to enhance muscle protein synthesis and hypertrophy
Evidence Level
Moderate
2 Human
8 Animal
6 In Vitro
Mechanism FOXO transcription factor inhibition reducing protein degradation
Established 8 direct studies
Benefit shown to reduce muscle protein breakdown
Evidence Level
Moderate
1 Human
6 Animal
4 In Vitro
Mechanism Satellite cell proliferation and myoblast differentiation enhancement
Supported 6 direct studies
Benefit appears to support muscle regeneration and repair
Evidence Level
Low
5 Animal
4 In Vitro
Mechanism GLUT4 translocation increasing glucose uptake
Supported 5 direct studies
Benefit may improve glucose disposal in muscle tissue
Evidence Level
Low
1 Human
4 Animal
3 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low

What to Expect

Timeline based on observations from published studies. Individual responses may vary.

IGF-1 LR3's extended half-life (20-30 hours vs 12-15 minutes for native IGF-1) means effects persist longer per dose. Hypoglycemia risk exists within hours of administration.

Animal studies typically used treatment periods of weeks. Muscle protein synthesis increases may be detectable early. Most users in performance contexts report cycles of 4-8 weeks.

Long-term

Long-term human safety data for IGF-1 LR3 does not exist. Native IGF-1 (mecasermin) long-term use has been associated with various adverse effects including tonsillar hypertrophy and potential cancer risk concerns.

Research-Based Observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Quality Checklist

Visual indicators to help evaluate IGF-1 LR3 product quality

Good Signs (6 indicators)
White lyophilized powder
Complete dissolution in bacteriostatic water
Clear solution after reconstitution
Certificate of analysis with >98% purity
HPLC and mass spec verification
Proper cold chain shipping
Warning Signs (5 indicators)
Off-white coloration
No third-party testing
Purity below 98%
Unclear source or manufacturing
No specification of LR3 vs native IGF-1
Bad Signs (6 indicators)
Yellow or brown discoloration
Particles or cloudiness after reconstitution
No certificate of analysis
Incomplete dissolution
Unusual odor
Compromised packaging
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Peptide Interactions

Known and theoretical interactions when combining IGF-1 LR3 with other peptides. Based on published research and mechanistic considerations.

Synergistic
Compatible
Caution
Avoid

Hgh

Synergistic
Synergistic

HGH stimulates endogenous IGF-1 production. Adding exogenous IGF-1 LR3 may amplify anabolic effects but also compounds risks including hypoglycemia and potential cancer promotion.

Mgf

Compatible
Compatible

MGF (Mechano Growth Factor) is an IGF-1 splice variant. Different kinetics and localization may provide complementary effects, but combined safety is not established.

Different regenerative mechanisms - BPC-157 for tissue healing, IGF-1 LR3 for muscle growth. Theoretical complementary use.

TB-500 promotes tissue repair via actin regulation while IGF-1 LR3 drives muscle hypertrophy. Different mechanisms may be complementary.

Both cause hypoglycemia through different mechanisms. Combined use dramatically increases risk of severe hypoglycemia.

Both act on the same receptor. Combining provides no additional benefit and increases risk of hypoglycemia and other adverse effects.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

References

Methodology Note

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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