IGF-1 LR3 (Long R3)

What is IGF1-LR3?

IGF1-LR3 is a modified version of insulin-like growth factor-1 (IGF-1). The full name of the peptide is insulin-like growth factor-1 long arginine 3. All IGF-1 derivatives play prominent roles in cell division, cell proliferation, and cell-to-cell communication. Though it has similar effects, IGF1-LR3 does not adhere to IGF-binding proteins as strongly as IGF-1. This results in IGF1-LR3 remaining in the bloodstream 120 times longer than IGF-1.

This extended half-life is a result of its structural changes. The peptide is created by adding 13 amino acids to the N-terminal end of IGF-1 and by converting the glutamic acid at position 3 of IGF-1 to an arginine residue. This modification makes IGF1-LR3 a much more potent molecule, providing approximately three times as much cell activation as a similar dose of IGF-1.

IGF1-LR3 Structure

Chemical Details

• Formula: C403H627N111O129S
• Molecular Weight: 9117.5 g/mol
• Purity (HPLC): Typically greater than 98%
• Sequence: M-P-L-S-E-R-K-D-V-S-T-P-P-V-L-K-P-G-A-F-L-R-L-S-H-I-E-D-L-G-R-L-V-C-E-A-G-V-C-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

IGF1-LR3 Research

Cell Division

Like IGF-1, IGF1-LR3 is a potent stimulus for cell division and proliferation. Its primary effects are on connective tissue like muscle and bone, but it also promotes cell division in liver, kidney, nerve, skin, lung, and blood tissues. IGF-1 is best thought of as a maturation hormone because it not only promotes cell proliferation, but differentiation as well. IGF-1 causes cells to mature, in other words, so that they can carry out their specialized functions.

Unlike IGF-1, IGF1-LR3 remains in the bloodstream for long periods of time. This property makes IGF1-LR3 a much more potent molecule. A dose of IGF1-LR3 provides approximately three times as much cell activation as a similar dose of IGF-1. Importantly, IGF1-LR3 and all IGF-1 derivatives do not promote cell enlargement (hypertrophy), but rather promote cell division and proliferation (hyperplasia). In general, this is beneficial for the maturation process because it causes muscle cells to get larger and increases the total number of muscle cells.

Fat Metabolism and Diabetes

IGF1-LR3 boosts fat metabolism in an indirect manner by binding to both the IGF-1R receptor and the insulin receptor. These actions increase glucose uptake from the blood by muscle, nerve, and liver cells. This results in an overall decrease in blood sugar levels, which then triggers the reduction of adipose tissue as well as reduced levels of insulin, fatty acids, and triglycerides. Overall, this produces a net decrease in adipose tissue and a net energy consumption (i.e., net catabolism).

Given its role in reducing blood sugar levels, it should come as no surprise that IGF1-LR3 reduces insulin levels as well as the need for insulin administration in diabetic mice. In some cases, this translates into a 10% decrease in insulin requirements to maintain the same blood sugar levels. This fact may help scientists understand how to decrease insulin doses in individuals who have decreased insulin sensitivity and may even offer insight to prevention of diabetes in the first place.

IGF1-LR3 Longevity Research

IGF-1 appears to play a role in repair and maintenance throughout the body, making it a protective molecule against cell damage and the effects of aging. Research in cows and information from human populations seem to suggest that low-level elevation in IGF-1 activity may counteract the effects of cellular aging. Ongoing research in mice seeks to determine if IGF1-LR3 might even prolong lifespan and slow the progression of age-related conditions such as dementia, muscle atrophy, and kidney disease. This research reveals that IGF-1 administration can prolong life and reduce disability [3], [4], [5].

Impairs Myostatin

Myostatin (a.k.a. growth-differentiation factor 8) is a muscle protein that partially inhibits muscle growth. Inhibiting myostatin could be of benefit in general health, aging, and disease. The ability to stop myostatin from functioning could be beneficial in conditions like muscular dystrophy where the goal is to prevent or even reverse muscle atrophy in patients. It also has the potential to help men and women who suffer muscle loss during prolonged immobility. In these cases, inhibiting this natural enzyme could help to slow muscle breakdown, maintain strength, and stave off morbidity.

In mouse models of DMD, it has been found that IGF1-LR3 and other IGF-1 derivatives are capable of counteracting the negative effects of myostatin to protect muscle cells and prevent apoptosis. IGF1-LR3, thanks to its long half-life, is particularly effective in counteracting myostatin and appears to work by activating a muscle protein called MyoD [1]. MyoD is a protein normally expressed during development, but is also activated following muscle damage and is responsible for muscle hypertrophy.

Glucocorticoid Signaling

Glucocorticoids, secreted primarily by the adrenal glands, are important clinical drugs used to control pain and reduce inflammation in cases such as infection, sepsis, injury, and cancer. Unfortunately, glucocorticoids have a number of undesirable side effects that include deterioration of bone density. There is some interest in using IGF1-LR3 to reduce the side effects of glucocorticoids and thus allow for more effective therapy [6].

IGF1-LR3 exhibits minimal to moderate side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. IGF1-LR3 for sale at Peptide Sciences is limited to educational and scientific research only, not for human consumption.

Article Author

The referenced literature underwent research, compilation, and organization by Dr. E. Logan, M.D. Dr. E. Logan possesses a doctorate qualification from Case Western Reserve University School of Medicine alongside a B.S. in molecular biology.

Scientific Journal Author

Dr. Anastasios Philippou, Ph.D. focused on Experimental Physiology at the National & Kapodistrian University of Athens Medical School. His extensive studying and documented research pertaining to the effects of muscle regeneration, the role of IGF-1 in skeletal muscle physiology, the expression of IGF-1 isoforms after exercise induced muscle damage in humans, characterization of the MGF E peptide actions in vitro, and epigenetic regulation of gene expression induced by physical exercise are most impressive.

Dr. Anastasios Philippou, Ph.D. is being referenced as one of the leading scientists involved in the research and development of IGF1-LR3. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this doctor. The purpose of citing this doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Anastasios Philippou, Ph.D. is listed in [7] and [8] under the referenced citations.

Referenced Citations

Citation #

Source Summary

URL/Reference

[1]

Adipose Tissue-Derived Stem Cell Secreted IGF-1 Protects Myoblasts from the Negative Effect of Myostatin

[suspicious link removed]

[2]

Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis

N. Li, et al. Endocrinology, 2016

[3]

Human growth hormone and human aging

E. Corpas, et al. Endocr. Rev., 1993

[4]

Diverse roles of growth hormone and insulin-like growth factor-1 in mammalian aging: progress and controversies

W. E. Sonntag, et al. J. Gerontol. A. Biol. Sci. Med. Sci., 2012

[5]

IGF hGH/IGF system: metabolism outline and physical exercise.

https://www.ncbi.nlm.nih.gov/pubmed/22714057

[6]

Implications of glucocorticoid therapy in idiopathic inflammatory myopathies

B. Y. Hanaoka, et al. Nat. Rev. Rheumatol., 2012

[7]

Musculoskeletal Neuronal Interact, 2007

A Philippou, et al. [Semantic Scholar]

[8]

In vivo, 2009

A Philippou, et al. [liter Journals]