IGF-1 LR3 1 mg

What is IGF1-LR3?

IGF1-LR3 is an extended and re-engineered form of insulin-like growth factor-1 that has been altered to stay active in the body far longer than the naturally occurring hormone. It belongs to the IGF family of peptides that coordinate growth, cell replication, and communication between tissues. Compared with standard IGF-1, this version binds weakly to the usual carrier proteins in the blood, so it is cleared much more slowly and can signal cells for an extended period. The longer activity is achieved by adding a stretch of extra amino acids to the N-terminal end of the original molecule and by replacing the third amino acid with arginine, which together produce a substantially prolonged half-life.

IGF1-LR3 Structure

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

IGF1-LR3 Research

Role in Cellular Growth

IGF1-LR3 is a strong promoter of both cell multiplication and maturation, acting on many tissues including skeletal muscle, bone, liver, skin, lung, kidney, blood cells, and the nervous system. It can be viewed as a coordination signal that encourages young cells to divide and then progress toward their fully specialized roles. Because this variant remains in circulation much longer than unmodified IGF-1, the same nominal amount of peptide produces a much greater overall period of receptor activation. In experimental models, its activity is associated mainly with an increase in cell number within a tissue (hyperplasia) rather than simple enlargement of existing cells, which is particularly relevant for research on muscle and connective tissue development.

Influence on Glucose and Fat Use

IGF1-LR3 interacts with both IGF receptors and insulin receptors, which gives it a pronounced effect on how cells handle blood sugar and stored fats. By encouraging glucose transport from the bloodstream into muscle, liver, and nerve cells, it lowers circulating glucose levels and shifts the body toward using internal energy reserves. As blood sugar falls, fat cells and the liver respond by releasing stored fuels through the breakdown of glycogen and triglycerides, leading to greater energy expenditure and a reduction in fat stores under experimental conditions.

Because it improves cellular uptake of glucose, IGF1-LR3 can reduce the amount of insulin required to maintain a given level of blood sugar in research models. This insulin-sparing effect has prompted interest in how IGF-related pathways might be leveraged to better understand insulin resistance and the progression of metabolic disorders.

Interaction with Myostatin

Myostatin is a regulatory protein that limits muscle growth and helps ensure that repair and enlargement do not proceed unchecked. While this control is important for balance, excessive myostatin activity contributes to muscle wasting in a number of settings. IGF1-LR3 has been shown in animal and cell studies to counter some of myostatin’s actions, supporting muscle cell survival and reducing programmed cell death in stressed or diseased muscle tissue.

In models of severe muscle loss, IGF1-LR3 activates key muscle regulatory factors such as MyoD, which are normally turned on by resistance exercise or tissue damage. Through this pathway, the peptide supports the formation of new muscle fibers and protects existing ones, making it a valuable research tool for exploring strategies to preserve muscle mass during immobilization or in inherited muscle disorders.

IGF1-LR3 in Aging Studies

Because IGF signaling is deeply involved in tissue repair, maintenance, and adaptation, IGF1-LR3 has become a focus of research into healthy aging and functional decline. Studies in large and small animal models are examining whether carefully controlled IGF1-LR3 exposure can help maintain organ function, preserve muscle, and support cognitive performance as organisms grow older. Findings from this work build on earlier evidence that balanced growth hormone and IGF pathways can influence both lifespan and the quality of life during later years, particularly by moderating the accumulation of cellular damage.

Connections to Glucocorticoid Use

Glucocorticoid medications are widely used to control inflammation and immune activity, yet long-term treatment often causes muscle loss, fat gain, and weakened bones. IGF1-LR3 is being investigated as a way to offset some of these catabolic effects in experimental systems. By promoting protein synthesis and survival in muscle and bone cells, it may help dampen tissue breakdown associated with prolonged glucocorticoid exposure and support better structural integrity while anti-inflammatory therapy is ongoing.

In animal studies, IGF1-LR3 has shown minimal to moderate reported adverse effects, poor effectiveness when given orally, and strong activity following subcutaneous administration. Research protocols use species- and context-specific dosing that cannot be directly converted to human use. At present, IGF1-LR3 is intended solely for controlled laboratory and educational investigations and is not approved for human consumption or unsupervised application.