What Is IGF-1 LR3?

IGF-1 LR3 demonstrates significantly enhanced potency over native IGF-1 due to reduced binding protein affinity and extended half-life, promoting dose-dependent muscle growth.

Philippou & Barton (Growth Hormone & IGF Res.): Comprehensive review of IGF-1's role in muscle satellite cell activation, myoblast proliferation, and skeletal muscle regeneration.

Bowers et al.: Meta-analysis of epidemiological studies examining positive correlation between circulating IGF-1 levels and prostate, breast, and colorectal cancer risk.

A 2025 study found that a novel plant-based nerve conduit featuring controlled release of IGF-1 LR3 significantly improved axonal regeneration in a rat model of sciatic nerve injury. The conduit demonstrated performance comparable to autologous nerve grafts without inducing systemic toxicity.

A 2025 study found that a one-week infusion of IGF-1 LR3 did not improve growth or insulin secretion in growth-restricted fetal sheep. However, the treatment demonstrated a reduction in circulating amino acids, suggesting increased amino acid utilization.

A 2025 study found that intranasal LR3-IGF-1 promoted amyloid plaque remodeling and reduced low molecular weight Aβ oligomers in the cerebral cortex of an Alzheimer's mouse model. However, the treatment failed to preserve cognitive function or memory in the mice.

A 2024 study demonstrated a simplified, validated chromatographic-mass spectrometric method for efficiently extracting and detecting prohibited peptides, including insulins and GHRHs, in doping control urine samples. The approach successfully met World Anti-Doping Agency requirements and was verified using authentic post-administration samples.

A 2023 study found that an IGF1 analog mitigated age-related loss of gastric pacemaker cells in mice by activating ERK1/2 signaling. This preservation demonstrated improved gastric compliance, increased food intake, and prevented impaired body weight gain in the animal model.

In a 2023 study, researchers demonstrated that high levels of bioactive human IGF-1 and its analog LR3 IGF-1 can be successfully produced in a Pichia pastoris expression system by fusing them with xylanase. The purified recombinant proteins exhibited excellent cell proliferation bioactivity comparable to standard IGF-1.

A 2023 study demonstrated that acute IGF-1 LR3 infusion in fetal sheep suppressed in vivo glucose-stimulated insulin secretion. However, researchers found that isolated islets retained the ability to recover insulin secretion in vitro, indicating beta-cells can overcome acute suppression.

A 2022 in-vitro study demonstrated that proper N-linked glycosylation is critical for insulin-like growth factor 1 (IGF-1) signaling in Chinese hamster ovary cells. Researchers found that defective glycosylation significantly reduced IGF-1 receptor levels and impaired IGF-1-dependent ERK signaling pathways.

A 2021 study demonstrated that a one-week infusion of IGF-1 LR3 in fetal sheep lowered plasma insulin and glucose concentrations and reduced glucose-stimulated insulin secretion. Researchers found this impaired insulin release persisted in isolated islets, indicating an intrinsic islet defect.

In a 2021 preclinical study, researchers demonstrated that a novel mass spectrometry method successfully detected IGF-I analogs like Des(1-3)-IGF-I for up to 24 hours in rats. The study also identified new degradation products of LongR3-IGF-I in both rat models and human blood in vitro.

A 2021 study in fetal sheep demonstrated that LR3 IGF-1 infusion increased specific organ growth and skeletal muscle myoblast proliferation. Researchers found that the peptide efficiently utilized available nutrients to support organ-specific growth rather than stimulating placental nutrient transfer.

IGF-1 administration stimulates myocardial growth accompanied by appropriate expansion and function of the coronary vasculature, a 2020 study in fetal sheep demonstrated. Researchers found that coronary conductance and hypoxia-mediated vasodilation were preserved alongside the increased heart mass.

The ALK4/5 receptor blocker GW788388 prevented cancer-associated muscle wasting and downregulated Atrogin-1 expression in mice, according to a 2019 study. Additionally, researchers demonstrated that while LR3 IGF-I limited muscle mass loss, it accelerated tumor growth.

A 2011 study demonstrated that the IGF-1 analog Long R3 IGF-1 reduced stenosis, increased vascular smooth muscle cell content, and decreased intraplaque hemorrhage in atherosclerotic mice. These findings suggest IGF-1 alters cell phenotypes to promote plaque stability in preclinical models.

A 2010 case report identified His-tagged Long-R³-IGF-I, a protein typically used for biochemical studies, within a confiscated black market injection vial. The analysis demonstrated that the protein retained its His-tag, highlighting the unknown physiological effects of such illicitly manufactured peptides.

A 2009 preclinical study demonstrated that a novel insulin-like growth factor-methotrexate conjugate inhibited prostate and breast tumor growth in mouse models more effectively than methotrexate alone at lower dosages. The conjugate also exhibited higher binding affinity to cancer cells in vitro.

A 2009 study demonstrated that NKX3.1 activates insulin-like growth factor binding protein-3 expression to suppress prostate cancer cell proliferation. Researchers found this activation attenuates IGF-I signaling in both cell cultures and mouse models.