It has a cyclic structure, lipophilic nature, and is enzymatically stable which makes it a more favourable candidate for manipulating the binding-release process between IGF-1 and its binding protein, thereby normalising IGF-1 function.

[18] Studies have shown the importance of the GH-IGF-1 axis in directing development and growth, where mice with a IGF-1 deficiency had a reduced body- and tissue mass.

The levels of IGF-1 in the body vary throughout life, depending on age, where peaks of the hormone is generally observed during puberty and the postnatal period.

After puberty, when entering the third decade of life, there is a rapid decrease in IGF-1 levels due to the actions of GH.

Growth hormone is made in the anterior pituitary gland, released into the bloodstream, and then stimulates the liver to produce IGF-1.

Its primary action is mediated by binding to its specific receptor, IGF1R, which is present on the surface of many cell types in many tissues[further explanation needed].

They control vital brain functions, such as survival, growth, energy metabolism, longevity, neuroprotection and neuroregeneration.

[28] Together they play an essential role in proliferation, survival, regulation of cell growth and affect almost every organ system in the body.

[30] A splice variant of IGF-1 sharing an identical mature region, but with a different E domain is known as mechano-growth factor (MGF).

[37][35] The genetic origins of these individuals have been traced back to Mediterranean, South Asian, and Semitic ancestors, with the latter group comprising the majority of cases.

People with LS are unresponsive to growth hormone therapy; the disease is instead treated mainly with recombinant IGF-1, Mecasermin.

[38] Acromegaly is a syndrome caused by the anterior pituitary gland producing excess growth hormone (GH).

[44] IGF-1 levels can be analyzed and used by physicians as a screening test for growth hormone deficiency (GHD),[45] acromegaly and gigantism.

[49][50] Low serum IGF-1 levels have been suggested as a biomarker for predicting fibrosis, but not steatosis, in people with metabolic dysfunction–associated steatotic liver disease.

[67] On the other hand, a high IGF-1 bioavailability in people with diabetes may delay or prevent diabetes-associated complications, as it improves impaired small blood vessel function.

[68] Low serum IGF‐1 levels can be considered an indicator of liver fibrosis in type 2 diabetes mellitus patients.