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IGF-1 LR3

IGF Axis & Muscle
Insulin-like Growth Factor 1 LR3Long R3 IGF-1

Overview

IGF-1 LR3, also known as Insulin-like Growth Factor 1 Long R3, is a synthetic analog of human IGF-1. It is engineered to have an extended half-life and increased potency compared to native IGF-1. The modification involves the substitution of arginine for glutamic acid at position 3 and the addition of 13 amino acids to the N-terminus, resulting in a 83-amino acid peptide. Researchers synthesize IGF-1 LR3 using recombinant DNA technology, typically in E. coli expression systems. IGF-1 LR3 is primarily studied in the context of muscle growth and repair, as well as its potential role in metabolic regulation. Researchers have observed that IGF-1 LR3 can stimulate muscle cell proliferation and differentiation, making it of interest in muscle-wasting conditions and athletic performance enhancement. Additionally, its effects on glucose metabolism and insulin sensitivity are under investigation. The mechanism of action of IGF-1 LR3 involves binding to the IGF-1 receptor with high affinity, initiating intracellular signaling cascades such as the PI3K/Akt and MAPK pathways. These pathways are crucial for cellular growth, survival, and metabolism. IGF-1 LR3's pharmacokinetic properties are characterized by a significantly extended half-life compared to native IGF-1, due to reduced binding to IGF-binding proteins. Researchers have reported a half-life of approximately 20-30 hours, allowing for less frequent administration in experimental settings. The compound is stable under physiological conditions, with bioavailability dependent on the route of administration. Current research on IGF-1 LR3 is focused on its therapeutic potential in muscle-wasting diseases and metabolic disorders. However, it is not approved for clinical use by major regulatory agencies, and its use is restricted to research settings. The compound's regulatory status varies by country, and it is often considered a research chemical with limited legal clarity for non-research applications.

Mechanism of Action

IGF-1 LR3 exerts its effects by binding to the IGF-1 receptor, activating the PI3K/Akt and MAPK signaling pathways. These pathways promote cellular growth, proliferation, and survival, contributing to its anabolic effects on muscle tissue.

Half-Life

Subcutaneous20-30 hours
Intramuscular20-30 hours
OralPoor bioavailability

The extended half-life is due to reduced affinity for IGF-binding proteins.

Storage

Lyophilized

Stable for 2+ years at -20°C, 12 months at 4°C

Reconstituted

Use within 14 days when refrigerated at 4°C

Avoid

Avoid repeated freeze-thaw cycles, direct light

Solvent

Bacteriostatic water or sterile saline recommended

Solubility

IGF-1 LR3 is soluble in water and aqueous buffers.

Legal Status

🇩🇪DE

Not approved as a medicinal product. Not a controlled substance. Sale as research chemical is a legal grey area.

🇺🇸US

Not approved by the FDA for human use. Not scheduled by the DEA.

🇦🇺AU

Not approved by the TGA for therapeutic use.

🇬🇧UK

Not approved by the MHRA for medicinal use.

Legal status information is provided for general reference only and may not reflect the most current regulatory changes. Always verify with official government sources before making any decisions.

10 Research Publications

Intranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice.

Animal

Journal of Alzheimer's disease : JAD · 2025

Researchers studied the effects of intranasal long R3 insulin-like growth factor-1 (LR3-IGF-1) on cognitive decline and brain pathology in a mouse model of Alzheimer's disease. They found that while LR3-IGF-1 improved certain brain features related to amyloid plaques, it did not significantly enhance memory or cognitive function in the mice.

  • LR3-IGF-1 treatment improved body composition in male 5XFAD mice.
  • The treatment reduced filamentous amyloid plaques and increased inert plaques in the brain.
  • Despite these changes in brain pathology, LR3-IGF-1 did not preserve cognitive function or memory.
PubMed

IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.

Unknown

American journal of physiology. Endocrinology and metabolism · 2025

Researchers studied the effects of IGF-1 LR3, a growth hormone, on fetal sheep that were growth-restricted due to pregnancy complications. They found that IGF-1 LR3 did not promote growth in these late-gestation fetal sheep, suggesting that this treatment may not be effective in addressing growth issues in similar conditions.

  • Researchers observed that IGF-1 LR3 did not enhance growth in late-gestation fetal sheep with growth restrictions.
  • The study highlighted low levels of IGF-1 and insulin in growth-restricted fetuses due to complications like placental insufficiency.
  • Findings suggest that IGF-1 LR3 may not be a viable option for improving growth in fetuses affected by growth restriction.
PubMed

Recombinant expression of IGF-1 and LR3 IGF-1 fused with xylanase in Pichia pastoris.

Human

Applied microbiology and biotechnology · 2023

Researchers found a way to produce human insulin-like growth factor-1 (IGF-1) and its variant LR3 IGF-1 in a yeast system called Pichia pastoris. The study observed that these proteins exhibited strong biological activity and were produced in higher quantities than traditional methods, making them potentially useful for clinical and scientific applications.

  • Researchers observed that human IGF-1 and LR3 IGF-1 were successfully produced using the Pichia pastoris expression system.
  • The purified IGF-1 and LR3 IGF-1 showed bioactivity comparable to standard IGF-1.
  • High levels of these proteins were achieved through fermentation in a bioreactor, reaching significant concentrations.
PubMed

Attenuated glucose-stimulated insulin secretion during an acute IGF-1 LR3 infusion into fetal sheep does not persist in isolated islets.

Unknown

Journal of developmental origins of health and disease · 2023

Researchers studied how an infusion of insulin-like growth factor-1 (IGF-1) affects insulin secretion in fetal sheep. They found that while the infusion reduced insulin secretion in response to glucose, this effect did not continue when the islets were isolated from the body. This suggests that the impact of IGF-1 on insulin secretion may be temporary and dependent on the surrounding environment.

  • Researchers observed that IGF-1 LR3 infusion decreased glucose-stimulated insulin secretion in fetal sheep.
  • The reduced insulin secretion effect did not persist when the islets were isolated from the body.
  • This indicates that the influence of IGF-1 on insulin secretion is likely influenced by the fetal environment.
PubMed

N-Linked Glycosylation in Chinese Hamster Ovary Cells Is Critical for Insulin-like Growth Factor 1 Signaling.

Unknown

International journal of molecular sciences · 2022

Researchers studied the role of N-linked glycosylation in Chinese hamster ovary cells, which are important for cell communication and function. They found that changes in the glycosylation process can significantly affect how these cells respond to insulin-like growth factor 1, which is crucial for cell growth and development.

  • Researchers observed that N-glycans on cell surface proteins are essential for proper signaling of insulin-like growth factor 1.
  • The study highlighted that disruptions in glycosylation can lead to changes in cell behavior and may be linked to various diseases.
  • Findings suggest that understanding glycosylation could provide insights into disease mechanisms and potential therapeutic targets.
PubMed

IGF-1 infusion to fetal sheep increases organ growth but not by stimulating nutrient transfer to the fetus.

Unknown

American journal of physiology. Endocrinology and metabolism · 2021

Researchers studied the effects of insulin-like growth factor-1 (IGF-1) on fetal sheep to understand its role in growth. They found that while IGF-1 infusion increased organ growth in the fetuses, it did not enhance the transfer of nutrients from the placenta to support this growth.

  • Researchers observed that IGF-1 infusion led to increased organ growth in fetal sheep.
  • The study found that IGF-1 did not stimulate increased placental blood flow.
  • Nutrient transfer from the placenta to the fetus was not improved by IGF-1 infusion.
PubMed

Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep.

Unknown

FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020

Researchers studied how insulin-like growth factor 1 (IGF-1) affects heart and blood vessel growth in fetal sheep. They found that IGF-1 treatment not only increased heart muscle cells but also ensured that the blood vessels supplying the heart grew appropriately, maintaining their function during stress.

  • Researchers found that IGF-1 treatment preserved coronary blood flow efficiency in relation to heart weight.
  • The study observed that the mechanisms for blood vessel dilation during low oxygen levels were similar in both IGF-1-treated and control fetuses.
  • Researchers concluded that IGF-1 stimulates both heart muscle and coronary blood vessel growth, suggesting its potential for improving heart development before birth.
PubMed

Action of long(R3)-insulin-like growth factor-1 on protein metabolism in beef heifers.

Unknown

Domestic animal endocrinology · 1999

Researchers studied the effects of a specific insulin-like growth factor (Long(R3)-IGF-1) on protein metabolism in beef heifers that were losing weight due to limited feeding. They found that this treatment tended to preserve muscle and overall body protein, suggesting it could help reduce weight loss during challenging feeding conditions.

  • Long(R3)-IGF-1 infusion tended to conserve whole-body and skeletal muscle protein in beef heifers on a low-quality diet.
  • The treatment significantly reduced plasma levels of amino acids and glucose in the heifers.
  • Plasma concentrations of IGF-2 decreased dramatically in the treated group compared to the control group.
PubMed

Involvement of insulin-like growth factor-1 and its binding proteins in proliferation and differentiation of murine bone marrow-derived macrophage precursors.

Unknown

Endocrine · 1998

Researchers studied the role of insulin-like growth factor-1 (IGF-1) and its binding proteins in the development of immune cells called macrophages from bone marrow. They found that IGF-1 promotes the growth of these cells, but different forms of IGF-1 have varying effects on their maturation.

  • Researchers observed that the levels of IGF-1 increased as bone marrow-derived macrophages developed.
  • The study found that different forms of IGF-1 influenced the proliferation and differentiation of macrophages in distinct ways.
  • Researchers noted that the accumulation of IGFBP-4 might limit the effectiveness of IGF-1 during macrophage development.
PubMed

Insulin-like growth factor-1 (IGF-1) receptor-insulin receptor substrate complexes in the uterus. Altered signaling response to estradiol in the IGF-1(m/m) mouse.

Animal

The Journal of biological chemistry · 1998

Researchers studied how the hormone estradiol affects signaling pathways in the uterus of mice, specifically looking at the insulin-like growth factor-1 (IGF-1) receptor. They found that estradiol enhances the interaction between key proteins involved in cell growth, suggesting that these interactions play a significant role in how estradiol influences uterine function.

  • Researchers observed that estradiol stimulates the binding of insulin receptor substrate proteins to the IGF-1 receptor in the uterus.
  • The study found that the absence of IGF-1 significantly weakens the signaling response to estradiol in the uterus.
  • Researchers noted that estradiol decreases levels of IRS-2, indicating different roles for IRS-1 and IRS-2 in hormone signaling.
PubMed

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This page is for informational and research purposes only. All information is based on published scientific literature. Nothing on this page constitutes medical advice or replaces consultation with a qualified healthcare professional.