IGF-1 LR3

This page cites ten publications from 2006 to 2025, but only two study IGF-1 LR3 directly: a 2025 study in a mouse model of Alzheimer's disease and a 2023 study producing the analogue in the yeast Pichia pastoris. Five examine native IGF-1 or its receptor, in fetal sheep, food-restricted mice, a mammary tumour model, a panel of cell lines and colon cancer allografts in mice. The remaining three concern other agents acting on the growth hormone and IGF-1 axis: CJC-1295 in healthy adults, and cabergoline and pasireotide in acromegaly.

In male 5XFAD mice, LR3 was associated with remodelling of amyloid plaques in the cortex but did not preserve behaviour or memory, and the authors did not support it as a stand-alone approach. The production study reported that LR3 IGF-1 expressed as a xylanase fusion had bioactivity comparable to a standard IGF-1. The native IGF-1 studies reported organ-specific growth in fetal sheep given ovine IGF-1; lower serum IGF-1 alongside reduced cortical bone mass in food-restricted mice; shorter mammary tumour latency with chronic IGF-1 receptor activation, attributed to tumour progression rather than initiation; lower cyclin G2 levels after exposure to insulin, IGF-1 or an insulin analogue across several cell lines, proposed as a route to cell proliferation; and faster growth of colon cancer allografts in obese mice given IGF-1 or the insulin analogue X10. The papers on other agents describe growth hormone and IGF-1 levels in healthy adults and in acromegaly.

For IGF-1 LR3 itself the cited evidence is thin: one mouse study with a negative behavioural result, one production study, and no human data. Results for native IGF-1 cannot be assumed to hold for an engineered analogue, and the tumour and proliferation studies describe IGF-1 signalling in general rather than this compound. The three papers on other drugs say nothing about LR3.