OVERVIEW

IGF-1 LR3 (Insulin-Like Growth Factor-1 Long R3) is a synthetic modified form of IGF-1, designed to extend its biological activity by preventing binding to IGF-binding proteins. This modification makes IGF-1 LR3 up to 120 times longer-lasting than standard IGF-1, significantly enhancing its effects on cell growth, metabolism, and muscle repair.

Research suggests IGF-1 LR3 may:

• Stimulate cell division and tissue growth, affecting muscles, bones, nerves, and vital organs.
• Enhance fat metabolism, leading to reduced adipose tissue and improved glucose regulation.
• Support muscle repair and hypertrophy, by counteracting myostatin’s inhibitory effects.
• Promote longevity and cellular maintenance, by reducing age-related tissue degeneration.
• Protect against glucocorticoid-induced muscle loss, supporting muscle preservation in individuals undergoing corticosteroid therapy.

Due to these properties, IGF-1 LR3 has been explored in muscle-wasting conditions, diabetes research, and anti-aging therapies.

RESEARCH

IGF-1 LR3 and Cell Growth

• IGF-1 LR3 is a potent stimulator of cell division and proliferation.
• Primarily affects muscles and bones, but also influences liver, kidney, nerve, skin, lung, and blood tissues.
• Longer circulation time compared to IGF-1, making it more effective in promoting cell maturation and tissue regeneration.
• Potential application: Regenerative medicine and muscle recovery.

IGF-1 LR3 and Fat Metabolism

• IGF-1 LR3 binds to insulin receptors, enhancing glucose uptake in muscle, liver, and nerve cells.
• This leads to lower blood sugar levels, triggering fat breakdown and a net decrease in adipose tissue.
• Potential application: Obesity management and diabetes therapy.

IGF-1 LR3 and Muscle Growth (Myostatin Inhibition)

• Myostatin is a natural inhibitor of muscle growth—IGF-1 LR3 blocks its effects, allowing enhanced muscle repair and hypertrophy.
• Research suggests IGF-1 LR3 may be beneficial for conditions such as Duchenne Muscular Dystrophy (DMD) and muscle atrophy due to immobility or chronic illness.
• Potential application: Muscle-wasting disorder treatment and sports performance research.

IGF-1 LR3 and Longevity Research

• IGF-1 LR3 supports tissue repair and maintenance, offering protective benefits against age-related decline.
• Studies in livestock models (cows and pigs) suggest IGF-1 LR3 can counteract cellular aging effects.
• Ongoing research in mice explores IGF-1 LR3’s role in preventing dementia, muscle loss, and kidney disease.
• Potential application: Anti-aging and age-related disease prevention.

IGF-1 LR3 and Glucocorticoid Protection

• Glucocorticoids are commonly used anti-inflammatory drugs, but long-term use can cause muscle wasting, fat gain, and bone density loss.
• IGF-1 LR3 counteracts these negative effects, allowing for more effective corticosteroid therapy with reduced side effects.
• Potential application: Muscle preservation in patients undergoing glucocorticoid therapy.

STRUCTURE

• Molecular Formula: C₄₀₀H₆₂₅N₁₁₁O₁₁₅S₉
• Molecular Weight: 9117.5 g/mol
• Amino Acid Sequence:
  MFPAMPLSSL FVNGPRTLCG AELVDALQFV CGDRGFYFNK PTGYGSSSRR APQTGIVDEC CFRSCDLRRL EMYCAPLKPA KSA
• CAS Registry Number: 946870-92-4

CITATIONS

1. Adipose Tissue-Derived Stem Cell Secreted IGF-1 Protects Myoblasts from the Negative Effect of Myostatin. Hindawi Journal.
2. N. Li, Q. Yang, R. G. Walker, T. B. Thompson, M. Du, and B. D. Rodgers. Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis. Endocrinology (2016).
3. E. Corpas, S. M. Harman, and M. R. Blackman. Human growth hormone and human aging. Endocr. Rev. (1993).
4. W. E. Sonntag, A. Csiszar, R. deCabo, L. Ferrucci, and Z. Ungvari. Diverse roles of growth hormone and insulin-like growth factor-1 in mammalian aging: progress and controversies. J. Gerontol. A. Biol. Sci. Med. Sci. (2012).
5. IGF-I/IGFBP system: metabolism outline and physical exercise. NCBI.
6. B. Y. Hanaoka, C. A. Peterson, C. Horbinski, and L. J. Crofford. Implications of glucocorticoid therapy in idiopathic inflammatory myopathies. Nat. Rev. Rheumatol. (2012).
7. A. Philippou, A. Halapas, M. Maridaki, M. Koutsilieris. Expression of IGF-1 isoforms after exercise-induced muscle damage in humans. J. Musculoskelet Neuronal Interact. (2007).
8. A. Philippou, E. Papageorgiou, G. Bogdanis, A. Halapas. Characterization of the MGF E peptide actions in vitro. In Vivo (2009).