IGF-1 LR3
experimentalAlso known as: Long R3 IGF-1, Long Arg3 IGF-1
**Mechanism of Action** IGF-1 LR3 (Long R3 IGF-1) is a synthetic analog of insulin-like growth factor-1 engineered with an arginine substitution at position 3 and a 13-amino-acid N-terminal extension. This modification significantly reduces binding to insulin-like growth factor-binding proteins (IGFBPs), thereby prolonging its half-life and enhancing bioavailability. The peptide acts primarily by activating the IGF-1 receptor (IGF-1R), a tyrosine kinase receptor that initiates downstream signaling cascades, including the PI3K/Akt and MAPK/ERK pathways. These pathways promote protein synthesis, satellite cell activation, and myonuclear accretion, leading to muscle hypertrophy and reduced catabolism. **Key Research Findings** Preclinical studies demonstrate that IGF-1 LR3 induces greater myotube hypertrophy and proliferation in vitro compared to native IGF-1, attributed to sustained receptor activation. In rodent models, systemic administration increases lean body mass, muscle fiber cross-sectional area, and functional strength, with effects observed in both skeletal and cardiac muscle. However, prolonged activation of IGF-1R raises concerns regarding mitogenic potential, as elevated IGF-1 signaling is linked to accelerated tumor growth in certain cancer models. Limited human data exist, with most evidence derived from animal studies or anecdotal reports. **Clinical Relevance** IGF-1 LR3 remains an experimental compound with no approved therapeutic indications. Its potent anabolic effects have attracted interest for conditions involving muscle wasting (e.g., cachexia, sarcopenia), but safety concerns—including hypoglycemia, acromegalic-like effects, and potential carcinogenicity—preclude clinical use. Regulatory status varies, but it is not approved for human consumption by major health authorities. For research purposes only — not medical advice.
Key data
Research & studies
IGF-1 LR3 treatment did not increase fetal body weight in growth-restricted sheep.; Plasma insulin, glucose, oxygen, and glucose-stimulated insulin secretion were unchanged between groups.; Circulating amino acids decreased significantly in the IGF-1 LR3 group, possibly indicating increased utilization.
Human IGF-1 and LR3 IGF-1 were produced in the P. pastoris expression system using xylanase fusion.; Purified IGF-1 and LR3 IGF-1 showed bioactivity comparable to standard IGF-1 in cell proliferation assays.; High heterologous expression levels of 0.5 g/L for XynCDBFV-IGF-1 and 1 g/L for XynCDBFV-TEV-LR3 IGF-1 were achieved via bioreactor fermentation.
Fetal plasma insulin decreased during IGF-1 LR3 infusion.; In vivo GSIS was 66% lower with IGF-1 LR3 versus control.; Insulin secretion from isolated fetal islets did not differ by infusion group.; Acute IGF-1 LR3 may directly suppress insulin secretion, but islets retain recovery capacity.
Frequently asked questions
What is IGF-1 LR3?
**Mechanism of Action** IGF-1 LR3 (Long R3 IGF-1) is a synthetic analog of insulin-like growth factor-1 engineered with an arginine substitution at position 3 and a 13-amino-acid N-terminal extension. This modification significantly reduces binding to insulin-like growth factor-binding proteins (IGFBPs), thereby prolon
How does IGF-1 LR3 work?
Long-acting IGF-1 analog with reduced IGFBP binding, prolonging activation of the IGF-1 receptor to drive muscle hypertrophy.
What is the research status of IGF-1 LR3?
IGF-1 LR3 is currently classified as experimental, with 15 research references on record. This is for research purposes only and is not medical advice.
Related peptides
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Activin-binding glycoprotein that antagonizes myostatin (GDF-8) to release the brake on skeletal muscle growth.
Soluble ActRIIB-Fc decoy receptor that sequesters myostatin and related ligands; trialed in muscular dystrophy before discontinuation.
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