IGF-1 LR3 is a potent IGF-1 analog with extended half-life and reduced IGFBP binding. It promotes muscle growth, fat metabolism, tissue repair, and recovery through enhanced protein synthesis and insulin sensitivity.
IGF-1 LR3
Also known as: Long R3 Insulin-like Growth Factor-1; LR3 IGF-1
Overview
Benefits
- Muscle development
- Enhanced recovery
- Fat loss
- Metabolic health
- Bone strength
- Anti-aging
Consider This Peptide If You Want To
- Enhance muscle growth, strength, and recovery
- Support tissue regeneration and performance
Dosage & Administration
Dosage Guidelines
Recommended Dosage
• Amount:20 mcg
• Frequency:daily
• Duration:3 weeks
• Rest Period:3 weeks
• Time of Day:morning
• Ingestion:subcutaneous
Administration Routes:Subcutaneous
Research Findings on Dosage:
• Subcutaneous Injection:
◦ Commonly Reported Dosage: 20-60 mcg (can be injected multiple times daily), 5 days on, 2 days off
◦ Duration: 3-6 week cycles followed by a 3-6 week break
• Administration Notes:
◦ IGF-1 LR3 operates independently of the body's endogenous growth hormone release. Therefore, it is not necessary to take on an empty stomach.
◦ Taking post-workout with food will yield the greatest muscle-building effects.
Mechanism of Action
Mechanism of Action
How this peptide works in the body
Anabolic Growth Pathways:
IGF-1 LR3 binds to insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR), triggering mitogenic and anti-apoptotic signaling cascades. This activation stimulates the mechanistic target of rapamycin (mTOR) pathway, driving muscle hypertrophy and hyperplasia by promoting protein synthesis and cellular growth. Additionally, it activates muscle satellite cells, leading to increased muscle mass, repair, and regeneration.
Metabolic Regulation:
IGF-1 LR3 enhances insulin sensitivity by upregulating glucose transporter (GLUT-4) expression, facilitating glucose uptake into muscle cells and reducing circulating blood sugar levels. This effect optimizes energy metabolism and supports fat oxidation. Simultaneously, IGF-1 LR3 inhibits adipocyte differentiation and suppresses lipogenesis, while enhancing lipolysis, leading to fat loss and improved body composition.
Bone and Tissue Repair:
IGF-1 LR3 stimulates osteoblast proliferation and differentiation, supporting bone mineralization and skeletal strength. It also enhances collagen synthesis and reduces inflammation, accelerating wound healing, tendon repair, and overall tissue regeneration.
Consider Stacking With
- BPC-157
- TB-4
- AOD-9604
- PEG-MGF
- 5-Amino-1MQ
- Semaglutide/Tirzepatide
- Kisspeptin-10
Side Effects & Cautions
Common Side Effects
- Injection site redness, itching, swelling
- Joint pain or stiffness
- Peripheral edema
Cautions
- Receptor desensitization with prolonged use
- Avoid in active cancer or diabetes
Research & References
Research Highlights
Muscle Growth and Recovery: Studies show enhanced muscle fiber proliferation and increased protein synthesis following IGF-1 LR3 administration.
Fat Loss Mechanism: Research demonstrates improved lipid profiles and decreased fat storage through IGF-1 receptor modulation.
Bone Density: Clinical models reveal significant improvements in bone mineral density with IGF-1 analog treatments.
Tissue Regeneration: Animal studies indicate accelerated wound healing and tissue repair.
References
Clemmons, D. R. (1998). "Role of insulin-like growth factor binding proteins in controlling IGF actions." Molecular and Cellular Endocrinology
Fryburg, D. A., et al. (1995). "Insulin and insulin-like growth factor-I enhance human skeletal muscle protein anabolism during hyperaminoacidemia by different mechanisms." The Journal of Clinical Investigation
Yakar, S., et al. (1999). "Normal growth and development in the absence of hepatic insulin-like growth factor I." Proceedings of the National Academy of Sciences
Velloso, C. P. (2008). "Regulation of muscle mass by growth hormone and IGF-I." British Journal of Pharmacology
Barton-Davis, E. R., et al. (1998). "Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function." Proceedings of the National Academy of Sciences