IGF-1 LR3

A genetically lengthened analogue of IGF-1 with 83 amino acids, studied in animal models for growth effects and listed as a doping substance in competitive sport.

IGF-1 LR3 is a recombinant analogue of the naturally occurring insulin-like growth factor 1, originally developed for cell-culture research. It carries additional amino acids at the N-terminus and an altered position 3, which makes it largely unable to bind IGF-binding proteins. It is studied mainly in animal models of organ and cell growth, but outside research it is also widely used for purported performance enhancement without solid human data.

Facts

• Molecular weight: 9111.4 g/mol
• Amino acids: 83
• Purity specification: ≥ 98 % (HPLC, commercial standard)

Evidence

• An infusion study in guinea pigs described increased organ growth under long R3 IGF-1, while at the same time plasma levels of endogenous IGF-1, IGF-2, and IGF-binding proteins declined. Conlon et al. 1995, Journal of Endocrinology, PMID 7561636
• A cell study in fetal sheep cardiomyocytes used IGF-1 LR3 as a stable receptor stimulus and described cell proliferation mediated through the ERK and PI3K pathways. Sundgren et al. 2003, American Journal of Physiology, PMID 12947030
• A 2026 review described a substantial gap between the clinical evidence base for growth-hormone-axis peptides such as IGF-1 LR3 and their widespread self-administration outside medical supervision. Dominikowski et al. 2026, Frontiers in Endocrinology, PMID 42395176

Frequently asked questions

What distinguishes IGF-1 LR3 from natural IGF-1?
IGF-1 LR3 carries additional amino acids at the N-terminus and an altered position 3, which means it barely binds IGF-binding proteins and therefore acts on the receptor longer and more strongly than native IGF-1.

Is IGF-1 LR3 allowed in sport?
No, it is listed as a growth factor on the WADA Prohibited List (category S2) and is banned at all times in organized sport.

Are there human studies on IGF-1 LR3?
Controlled human studies are not available, the existing evidence comes from cell and animal models, a 2026 review points to this evidence gap.

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