IGF-1LR3

IGF-1 LR3 (Receptor Grade) is a synthetic variant of the naturally occurring insulin-like growth factor 1 (IGF-1). This modified form includes an extended N-terminal sequence and a substitution at the third amino acid position, enhancing its stability and potency. Due to these modifications, IGF-1 LR3 exhibits a significantly prolonged half-life compared to standard IGF-1, making it more effective in various research applications.

IGF1-LR3 Research

Cell Division and Proliferation

IGF1-LR3, similar to IGF-1, is a powerful stimulator of cell division and proliferation, primarily targeting connective tissues such as muscle and bone. It also promotes cell growth in the liver, kidney, nerve, skin, lung, and blood tissues. Unlike IGF-1, which acts for a shorter time, IGF1-LR3 remains in the bloodstream longer, making it approximately three times more potent in activating cells. It induces cell proliferation (hyperplasia), not cell enlargement (hypertrophy), meaning it increases the number of cells rather than their size—resulting in more muscle cells rather than bigger muscle cells.

Fat Metabolism and Diabetes

IGF1-LR3 enhances fat metabolism indirectly by binding both to IGF-1 and insulin receptors, increasing glucose uptake by muscle, nerve, and liver cells. This reduces blood sugar levels, triggering fat and liver tissues to break down glycogen and triglycerides, leading to fat loss and increased energy expenditure. Due to these effects, IGF1-LR3 reduces insulin levels and the need for external insulin in diabetic individuals, often lowering insulin requirements by about 10%. This may offer insights into reducing insulin doses and preventing type 2 diabetes.

Myostatin Inhibition

Myostatin, a protein that inhibits muscle growth and differentiation, plays a key role in preventing excessive muscle growth and aiding proper healing. However, inhibiting myostatin can be beneficial in muscle-wasting conditions like Duchenne muscular dystrophy (DMD) or prolonged immobilization. IGF1-LR3 and its derivatives counteract myostatin’s negative effects by activating MyoD—a protein essential for muscle growth triggered by exercise or injury—thus protecting muscle cells and preventing apoptosis.

Longevity Research

IGF1-LR3 supports tissue repair and maintenance, protecting against cellular damage and aging. Studies in livestock suggest IGF1-LR3 may mitigate cellular aging effects. Ongoing mouse research explores its potential in preventing conditions such as dementia, muscle loss, and kidney disease, showing it can extend lifespan and reduce disability.

Glucocorticoid Signaling

Glucocorticoids are widely used anti-inflammatory drugs but cause side effects including muscle wasting, fat gain, and bone loss. IGF1-LR3 is being investigated for its ability to reduce these side effects, potentially allowing for safer, more effective glucocorticoid therapies.

Research Applications

IGF-1 LR3 is primarily utilized in scientific studies focusing on:

• Cellular Growth and Repair: Investigating its role in promoting cell division and tissue regeneration.
• Muscle Hypertrophy: Exploring its potential to stimulate muscle growth and counteract muscle wasting conditions.
• Neuroprotection: Assessing its effects on neuronal health and potential therapeutic applications in neurodegenerative diseases.
• Endocrine Research: Studying its interactions with growth hormone pathways and insulin signaling.

These applications are part of ongoing research aimed at understanding the broader implications of IGF-1 LR3 in various biological processes.

Product Specifications

• Form: Lyophilized (freeze-dried) powder for reconstitution.geneproteins.com
• Purity: 99% or higher, ensuring high-quality material for research purposes.
• Packaging: Each package contains 10 vials, each with 100 micrograms of IGF-1 LR3.

This product is intended strictly for laboratory research and is not approved for human consumption.

References

• “Adipose Tissue-Derived Stem Cell Secreted IGF-1 Protects Myoblasts from the Negative Effect of Myostatin,” Hindawi. [Online] Available: https://www.hindawi.com/journals/bmri/2014/129048/ [Accessed May 16, 2019]
• Li N, Yang Q, Walker RG, Thompson TB, Du M, Rodgers BD. “Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis.” Endocrinology, 2016;157(1):282-291.
• Corpas E, Harman SM, Blackman MR. "Human growth hormone and human aging." Endocrine Reviews, 1993;14(1):20-39.
• Sonntag WE, Csiszar A, deCabo R, Ferrucci L, Ungvari Z. “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;67(6):567-598.
• “IGF-/IGFBP system: metabolism outline and physical exercise,” PubMed - NCBI. Available: https://www.ncbi.nlm.nih.gov/pubmed/22714057 [Accessed May 16, 2019]
• Hanaoka BY, Peterson CA, Horbinski C, Crofford LJ. “Implications of glucocorticoid therapy in idiopathic inflammatory myopathies.” Nat Rev Rheumatol, 2012;8(8):448-457.
• Philippou A, Halapas A, Maridaki M, Koutsilieris M. “Role of IGF-1 in muscle regeneration.” J Musculoskelet Neuronal Interact, 2007. [Semantic Scholar] 
• Philippou A, Papageorgiou E, Bogdanis G, Halapas A. “In vivo studies on IGF-1 and muscle hypertrophy.” [Journal, 2009]