Igf 1 Lr3 Research
Product image coming soon
IGF-1 LR3: Insulin-Like Growth Factor Research Profile
IGF-1 LR3 (Insulin-like Growth Factor 1 Long Arg3) is a synthetic analogue of human IGF-1 with an N-terminal 13 amino acid extension and an Arg3 substitution. It is studied in laboratory settings for its role in IGF-1 receptor (IGF-1R) signalling, cellular growth pathway research, and comparative pharmacokinetics versus native IGF-1.
Chemical and Molecular Data
| Property | Value |
|---|---|
| Molecular formula | C400H625N111O115S9 |
| Molecular weight | 9117.5 g/mol |
| CAS number | 946870-92-4 |
| Amino acid count | 83 (native IGF-1 has 70) |
| N-terminal extension | 13 amino acid sequence |
| Key modification | Glu3 to Arg3 substitution |
| Purity | greater than or equal to 98% as verified by HPLC |
| Form | Lyophilised powder |
| Storage | -20 degrees C, protected from light and moisture |
| Reconstitution | Bacteriostatic water with 0.1% acetic acid recommended |
IGF-1 LR3: Reduced IGFBP Binding and IGF-1R Signalling
Design Rationale: Extended Half-Life and Reduced IGFBP Binding
Native IGF-1 has a plasma half-life of only 10-20 minutes when not bound to insulin-like growth factor binding proteins (IGFBPs). In biological fluids, approximately 99% of IGF-1 is bound to one of six IGFBPs, which dramatically extend its half-life but also modulate its bioavailability and tissue distribution.
IGF-1 LR3 was engineered to minimise IGFBP binding: the Glu3 to Arg3 substitution and the N-terminal 13 amino acid extension together reduce the affinity of IGF-1 LR3 for all six IGFBPs by approximately 1000-fold compared to native IGF-1. This results in a significantly longer free half-life (approximately 20-30 hours) and altered tissue distribution patterns, making it useful for studying IGF-1R signalling independently of IGFBP regulation.
IGF-1 Receptor Signalling Research
IGF-1R is a receptor tyrosine kinase belonging to the insulin receptor family. Binding of IGF-1 (or IGF-1 LR3) to the extracellular alpha subunits of IGF-1R triggers autophosphorylation of the intracellular beta subunits and activates downstream signalling through two major pathways.
PI3K/Akt/mTOR pathway. IGF-1R activation recruits IRS-1 and IRS-2 scaffold proteins, activating phosphatidylinositol 3-kinase (PI3K) and subsequently Akt (PKB). Akt activation promotes cell survival (through Bad and caspase-9 phosphorylation), protein synthesis (through mTORC1), and glucose uptake (through GLUT4 translocation). This pathway is central to anabolic signalling research.
Ras/MAPK/ERK pathway. IGF-1R also activates Ras through Shc-Grb2-SOS adaptor complexes, leading to ERK1/2 activation and transcriptional regulation of genes involved in cell proliferation and differentiation.
Research Applications
IGF-1 LR3 is used as a tool compound in IGF-1R binding studies (competitive binding assays), PI3K/Akt/mTOR pathway research, cell proliferation and survival assays, skeletal muscle hypertrophy signalling research (often studied alongside ACE-031 for complementary growth pathway coverage), and GH axis research downstream of Tesamorelin and CJC-1295 studies.
IGF-1 Analogue Comparison
| Property | Native IGF-1 | IGF-1 LR3 | Des(1-3)IGF-1 |
|---|---|---|---|
| Length | 70aa | 83aa | 67aa |
| Modification | None | +13aa N-extension, Arg3 | Deleted positions 1-3 |
| IGFBP-1 affinity | High | ~1000x lower | ~1000x lower |
| IGFBP-3 affinity | High | ~1000x lower | Moderate reduction |
| Free half-life | 10-20 min | 20-30 hr | ~30 min |
| IGF-1R affinity | High | High | High |
| IR cross-reactivity | Low | Low | Low |
IGF-1R Signalling Pathways
IGF-1 LR3 activates IGF-1R (a receptor tyrosine kinase) through the same receptor complex as native IGF-1, triggering autophosphorylation of the intracellular beta subunits. The two major downstream signalling cascades are:
PI3K/Akt/mTOR pathway:
IGF-1R phosphorylation recruits IRS-1 and IRS-2 scaffold proteins, which activate PI3K. PI3K generates PIP3 at the membrane, recruiting Akt (PKB). Akt has numerous substrates relevant to cell biology research including mTORC1 (activating protein synthesis via S6K1 and 4E-BP1), FOXO transcription factors (suppressing atrophy gene expression), BAD (promoting cell survival), and GSK3beta (regulating glycogen synthesis and cell cycle).
Ras/MAPK/ERK pathway:
IGF-1R also signals through Shc-Grb2-SOS complexes to activate Ras, leading to the MAPK cascade (Raf-MEK-ERK). ERK1/2 activation promotes cell proliferation and differentiation through transcriptional regulation of immediate early genes including c-Fos and c-Myc.
Frequently Asked Questions
Why is 0.1% acetic acid used for IGF-1 LR3 reconstitution?
IGF-1 LR3 has limited solubility in neutral or alkaline aqueous conditions due to its hydrophobic regions and tendency to aggregate. Mildly acidic conditions (0.1% acetic acid, approximately pH 3-4) improve solubility by protonating basic residues, reducing intermolecular electrostatic interactions that promote aggregation. After preparing the stock solution in 0.1% acetic acid, dilute into your buffer system to achieve the desired pH for your assay. Avoid repeated freeze-thaw cycles of the reconstituted solution.
How does IGF-1 LR3 differ from IGFBP-3 in research applications?
These are completely different types of research tools. IGF-1 LR3 is an IGF-1 receptor agonist — it activates IGF-1R signalling. IGFBP-3 (insulin-like growth factor binding protein 3) is a binding protein that sequesters native IGF-1 and modulates its bioavailability. Some researchers use IGF-1 LR3 precisely because it does not bind IGFBPs, allowing study of IGF-1R signalling without IGFBP regulation as a confounding variable — essentially studying the "free IGF-1" signalling state in isolation.
Published Research References
For laboratory and analytical research purposes only. Not for human or veterinary use. No dosage or administration guidance is provided or implied.
Related research peptides: Tesamorelin | ACE-031 | Ipamorelin