IGF-1 LR3

Insulin-like growth factor 1 LR3 (IGF-1 LR3) from PeptideShop comes in vials of 3 mg and has to be reconstituted prior use. This peptide is synthetic and chemically altered to have a longer-half life, be more effective, and essentially increase its biological activity. 

So, the story of IGF-1 LR3 begins with IGF.

It’s one of the primary growth hormone (GH) mediators , a hormone that promotes cell growth and differentiation during the formative childhood years, and continues to have an anabolic effect in adulthood.

IGF-1 peptide is a 70 amino acid long chain, structurally similar to insulin and, more importantly, capable of binding to the insulin receptors within the body. Once GH is secreted in the anterior pituitary gland, IGF-1 also gets released into the bloodstream and reaches basically every cell in the human body.

There, along with additional chemical compounds, promotes cellular growth and survival, while preventing cell apoptosis (a kind of cellular death). As such, IGF-1 became greatly important due to its role in tissue homeostasis.

IGF-1 LR3 and Cell Division

Just like naturally produced IGF-1, IGF-1 LR3 is also considered to be a potent cell division and proliferation stimulant. It mostly targets bone and muscle cells, cells of the connective tissue, but also the building blocks of lungs and blood vessels. 

But, unlike IGF-1, the LR3 variant remains in the bloodstream longer (due to its altered structure), making it a more potent stimulant; in fact, in vitro studies showed that one dosage of IGF-1 LR3 is three times more potent, as compared to IGF-1 in a similar dosage. 

Speaking of medical studies, they showed that IGF-1 does not lead to mear cell hypertrophy (cell enlargement), it actually boosts cell division. For this very reason, it became an interesting compound. Of course, we still need more scientific studies with human test subjects to evaluate the full effects on the body.

IGF-1 LR3 And Fat Metabolism 

In the previous section, we mentioned IGF-1’s benefits on muscle cells, and now we’re going to take a closer look at its fat metabolism properties. As studies have shown, fat binds to both IGF-1 and Insulin receptors in the body; this binding action increases blood glucose uptake in cells through the body, resulting in overall dropped sugar blood levels. This action then indirectly leads to the breakdown of adipose tissue in the liver.

Of course, this reduction in blood glucose levels is what’s interesting in diabetes research and scientists are now trying to figure out how to best use IGF-1 LR3’s action in the fight to manage diabetes more effectively.

IGF-1 LR3 And Myostatin Regulation

Myostatin is a protein found exclusively in the skeletal muscles (muscles used for movement), which regulates hypertrophy and muscle cell differentiation. This is especially important in healing injuries.

But in an event of a disease (various types of muscle dystrophies) where a person experiences muscle loss, IGF-1 LR3 is seen as a myostatin stimulator, with the potential to turn the disease outcome around - slow down muscle loss, and help the patient maintain their strength and mobility.

Though we don’t yet have any definitive results from human studies, studies on mice showed promising results. Thanks to its longer half life, IGF-1 LR3 was able to counteract the negative effects of the disease - stimulate myostatin, protect muscle cells and even prevent cell death. 

IGF-1 LR3 And Longevity

Knowing that IGF-1 LR3 helps with wound healing, researchers turned their attention to longevity and long-term cell damage protection. Once again, we don’t have many human studies dealing with this problem, but studies done on cow and pig test subjects showed that administering this peptide can offset cellular aging.

A related mice study was aimed at finding out if LR3-based therapy can slow down the progression of diseases such as dementia, muscle atrophy and kidney disease. We are still waiting for the results of this study, but the initial findings are promising.

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7913862/

https://pubmed.ncbi.nlm.nih.gov/24575400/

https://pubmed.ncbi.nlm.nih.gov/22522510/