IGF-1 LR3 is a research compound studied for its role in performance & hormone research. This page covers mechanism of action, published studies, preclinical protocols, and analytical specifications.
Quick Reference: IGF-1 LR3
CAS Number
206658-92-6
Molecular Formula
C400H625N111O115S9
Molecular Weight
9117.5 g/mol
Sequence / Structure
83-aa analog of IGF-1: Arg at position 3 (R3) + 13-aa N-terminal extension (Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Val-Leu-Val)
Physical Form
Lyophilized powder
Purity (QSC)
β₯99%
Storage
Store lyophilized at -20Β°C. Reconstituted: 4Β°C, use within 28 days. Some protocols use 10mM acetic acid for reconstitution.
Reconstitution
Add bacteriostatic water or 10mM acetic acid per protocol. Swirl gently β do not shake. For in vitro work, dilute in PBS or culture medium.
Mechanism of Action
IGF-1 LR3 (Long-R3 IGF-1) is a recombinant analog of insulin-like growth factor 1 (IGF-1) engineered for extended plasma half-life and reduced IGFBP binding β properties that make it a superior research tool compared to native IGF-1 for studying IGF-1 receptor (IGF-1R) biology in sustained-exposure experimental designs.
Structural Modifications: Two changes distinguish IGF-1 LR3 from native IGF-1. First, an arginine substitution at position 3 (R3) reduces affinity for IGF-binding proteins (IGFBPs) by approximately 1000-fold. Since IGFBPs sequester ~99% of circulating native IGF-1, this modification dramatically increases the proportion of free (bioavailable) peptide. Second, a 13-amino acid N-terminal extension (Long) further reduces IGFBP binding and slightly increases IGF-1R binding affinity. Together, these modifications extend half-life from ~15 minutes (native IGF-1) to approximately 20β30 hours.
IGF-1 Receptor (IGF-1R) Activation: IGF-1 LR3 binds and activates the IGF-1R β a receptor tyrosine kinase. Ligand binding causes receptor dimerisation and autophosphorylation of the intracellular kinase domain. This activates two major downstream pathways: PI3K-Akt-mTOR (promoting protein synthesis, cell survival, glucose uptake) and MAPK-ERK1/2 (promoting cell proliferation and differentiation). These pathways mediate IGF-1’s anabolic, anti-apoptotic, and mitogenic effects in muscle, bone, and other tissues.
Insulin Receptor Cross-Reactivity: At high concentrations, IGF-1 LR3 can activate the insulin receptor (IR) due to structural homology with insulin. This cross-reactivity is concentration-dependent and is an important consideration in research designs examining metabolic endpoints β studies requiring pure IGF-1R selectivity should use selective IGF-1R agonists or design around IR co-activation.
Research Applications
Skeletal Muscle Hypertrophy Research: IGF-1 LR3 is the standard research compound for studying IGF-1R-mediated satellite cell activation, myoblast proliferation, myotube differentiation, and protein synthesis in skeletal muscle cell models and animal studies.
IGF-1R Signalling Pathway Studies: The PI3K-Akt-mTOR and MAPK-ERK pathways activated by IGF-1 LR3 are studied using selective inhibitors alongside IGF-1 LR3 stimulation to dissect pathway contributions to specific cellular responses.
Cancer Biology Research: IGF-1R overexpression in cancer cell lines is studied using IGF-1 LR3 as the receptor activator in proliferation, survival, and resistance studies β particularly relevant in breast, prostate, and colorectal cancer research.
Bone Biology: Osteoblast proliferation and differentiation research uses IGF-1 LR3 to study IGF-1R’s role in bone formation, mineralisation, and the GH-IGF-1-bone axis.
Comparison with Native IGF-1: The extended half-life of IGF-1 LR3 vs native IGF-1 allows researchers to study how sustained vs pulsatile IGF-1R activation produces different downstream signalling outcomes β analogous to the pulsatile vs sustained GH secretion question.
Key Published Research
Primary publications relevant to IGF-1 LR3 research. Full citations available via PubMed. QSC does not endorse or make claims based on this research.
Francis et al. (1992)
“Characterisation of a Truncated Form of IGF-I (des(1-3)IGF-I) and its Analogue (Long R3 IGF-I)” β Journal of Molecular Endocrinology
Original characterisation paper for IGF-1 LR3, establishing its IGFBP binding profile, receptor affinity, and extended half-life relative to native IGF-1.
Tomas et al. (1993)
“Long-R3 IGF-I Retains Anabolic Effects on Skeletal Muscle” β Journal of Endocrinology
Documents IGF-1 LR3’s sustained anabolic activity in muscle tissue and establishes the research framework for its use in body composition studies.
LeRoith & Roberts (2003)
“The Insulin-like Growth Factor System and Cancer” β Cancer Letters
Reviews IGF-1R biology and the use of IGF-1 analogs including LR3 in cancer research, establishing the pathway framework.
Daily injection for 2β4 weeks; endpoints: muscle mass, cross-sectional area, IGF-1R phosphorylation, protein synthesis rate
Cancer Cell Proliferation Assay
0.1β100 ng/ml
Added to culture medium
72β96 hour MTT/CCK-8 assay; proliferation and survival endpoints
Frequently Asked Questions
What is IGF-1 LR3?
IGF-1 LR3 (Long-R3 IGF-1) is a recombinant analog of IGF-1 with two modifications β an N-terminal 13-aa extension and Arg3 substitution β that reduce IGFBP binding by ~1000x and extend plasma half-life to ~20β30 hours vs ~15 minutes for native IGF-1. Used in research requiring sustained IGF-1 receptor activation.
What is the difference between IGF-1 and IGF-1 LR3?
Native IGF-1 is rapidly sequestered by IGFBPs in plasma, with only ~1% free at any time and a ~15-minute half-life. IGF-1 LR3 has drastically reduced IGFBP affinity, dramatically increasing free bioavailable fraction and extending half-life to ~20β30 hours β making it the preferred research tool for sustained IGF-1R activation studies.
Can IGF-1 LR3 activate insulin receptors?
At high concentrations, IGF-1 LR3 can cross-activate insulin receptors due to structural homology with insulin. This is concentration-dependent and should be accounted for in research designs with metabolic endpoints. At research-relevant concentrations in most cellular models, IGF-1R selectivity is maintained.
How should IGF-1 LR3 be reconstituted?
Add bacteriostatic water or 10mM acetic acid per vial. For in vitro work, dilute in PBS or culture medium to working concentration. Swirl gently β do not shake. Some protocols use acetic acid for initial solubilisation then dilute in PBS.
What purity is QSC IGF-1 LR3?
β₯99% by HPLC and mass spectrometry. COA published on product page, verifiable via Janoshik.
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