Evidence is limited to animal or in-vitro work. No human pharmacokinetics. Any human dose in circulation is extrapolated, and extrapolation across species routinely fails.
No human pharmacokinetic half-life exists. The widely repeated "20-30 hour half-life" could NOT be traced to any retrievable primary source. Contradicting it, an anti-doping study found LongR3-IGF-I disappeared rapidly after 4 hours in rats, while Des(1-3)-IGF-I remained detectable to 24 hours, the opposite of the usual community claim that LR3 is the long-acting variant. Detection windows are not half-lives, so neither is reported as one here.
No human dosing data. LongR3-IGF-1 is manufactured and sold as a cell-culture reagent, not a human therapeutic. Community protocols (20-50 mcg/day) are anecdotal with no published human basis.
SERIOUS RISK. The Arg3 substitution plus 13-amino-acid N-terminal extension markedly reduces affinity for IGF-binding proteins while retaining IGF-1R binding, it circulates unbuffered by the IGFBP system that normally constrains free IGF-1. Hypoglycaemia is a real and potentially severe acute risk via IGF-1R/insulin receptor cross-reactivity. Guinea pig infusion caused organ growth alongside suppression of endogenous IGF-I, IGF-II and IGFBPs, evidence of axis disruption. Unopposed IGF-1R signalling is mitogenic, with theoretical risk of promoting occult malignancy. No human safety data exist at any dose.