DES(1-3)IGF is a truncated form of IGF-1 with the tri-peptide structure Glycine-Proline-Glutamine cleaved from the N-terminus. It has been isolated from and detected in numerous in vivo sources, including the human brain, bovine colostrum, and porcine uterus. In vitro studies demonstrate that at equal doses DES(1-3)IGF is ten times more potent than IGF-1 at stimulating hypertrophy and proliferation in cultured cells. It is likely generated through post-translational modification in the sequence of circulating mature IGF-1 via protease action.
The clearance rate from plasma of DES(1-3)IGF is four times faster than IGF-1, although the metabolic effects last for three to five times those of IGF-1. This is likely because DES(1-3)IGF remains in higher concentrations, post-clearance, in the extracellular space of target tissues than does IGF-1.
DES(1-3)IGF holds promise for inflammatory bowel disease treatment, as it has been demonstrated in vivo to bind preferentially to gut tissue; it also, like other forms of IGF-1, should prove useful in treating catabolic states such as those from wasting diseases.
Des(1-3)IGF has not been tested clinically yet as success with IGF-I is considered essential before the extra expense of a more potent variant can be justified. Perhaps the more selective action of des(l-3)IGF-I on gut tissue warrants the evaluation of this growth factor as treatment for inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis, which have no other effective therapies.
DES(1-3)IGF has been shown to stimulate proliferation in cultured myoblasts. It binds to the same type I IGF receptor as IGF-1, but has a mere 1% binding affinity for the IGF binding proteins (IGFBP) found to be excreted by nearly all mammalian cells; thus, a much lower amount of DES(1-3)IGF is as biologically active as a higher dose of IGF-1.
Across a broad range of rat models (normal adult, diabetic, dexamethasone-treated, GH deficient, partial gut removal, chronic renal failure), DES(1-3)IGF demonstrated a robust and consistent one 1-3 times greater effect on body growth than IGF-1:
Growth effects of des( lL3)1GF-I in rats occur in most tissues, although carcass fat is reduced and there is a trend for muscle weight to increase proportionately less than body weight. The selective increase in gut tissues is particularly striking as it occurs even in diabetes, where the condition itself stimulates gut growth and where insulin treatment has the opposite effect. Responses are demonstrated throughout the alimentary tract and are accompanied by improvements in nutrient uptake .
Ballard speculates that the reason DES(1-3)IGF is more effective at gut healing than IGF-1 is due to the presence of many more than usual IGF binding proteins, which render IGF-1 ineffective. Interestingly, the presence binding proteins in some cases have been demonstrated to increase the effectiveness of local wound healing.
DES(1-3)IGF is has not yet been seriously considered for treatment of human diseases, even though it holds promise according to research done on animal models, and exhibits some clinical differences from other available IGF forms. In the future, as peptides are administered for therapy, the trend may change; DES(1-3)IGF has some unique advantages over other forms of IGF, primarily due to a lack of affinity for IGF binding proteins. It should be noted that IGF binding proteins mediate some of the actions (both in terms of upregulation, and downregulation, depending on environment, circumstance, and type of IGFBP) of IGF-1; although DES(1-3)IGF has less affinity for the IGF receptor than IGF-1, the net result of a much lower affinity for IGFBPs is that a lower dose is more potent, although it binds indiscriminately.
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