📈IGF-1 LR3
Long-acting IGF-1 analogue with 20–30h half-life. Activates mTORC1, suppresses FOXO atrophy genes, and drives satellite cell proliferation. 1000× reduced IGFBP binding vs native IGF-1.
Modified IGF-1 with N-terminal Met extension + Arg3 substitutionWhat Is IGF-1 LR3?
IGF-1 LR3 is a recombinant analogue of endogenous IGF-1 with two modifications: N-terminal methionine extension and glutamic acid→arginine (R3) substitution. The R3 change reduces IGFBP binding affinity >1000×, extending half-life from ~12 minutes to 20–30 hours.
Key Mechanisms
- PI3K→Akt→mTORC1 — phosphorylates S6K1 and 4E-BP1, driving ribosomal biogenesis and protein translation
- Ras→MEK→ERK — cell cycle progression (G1→S via cyclin D1), DNA replication, differentiation
- FOXO suppression — phosphorylates FOXO1/3a, blocking MuRF1 and Atrogin-1 transcription — prevents muscle proteolysis
- Satellite cell activation — drives skeletal muscle stem cell proliferation and myofibre formation
Key References
- Coleman ME et al. "IGF-I stimulates muscle cell differentiation and myofiber hypertrophy." J Biol Chem, 1995;270:12109–12116.
- Foulstone EJ et al. "Role of IGFBP-3 in the IGF axis of human skeletal muscle." J Cell Physiol, 2003;196:229–240.
Frequently Asked Questions
"Long Arg3" — it refers to the two structural modifications (an N-terminal extension and an Arg-for-Glu substitution at position 3) that give this IGF-1 analogue its dramatically reduced IGFBP binding and extended half-life versus native IGF-1.
No — it's a deliberately modified analogue. Native IGF-1 has a half-life of only a few minutes because IGFBPs sequester it almost immediately; LR3's modifications reduce that binding by roughly 1000-fold, which is the entire point of using the analogue in research instead of native IGF-1.
Refrigerate the lyophilized vial at 2–8°C. Once reconstituted, keep refrigerated and use within the standard stability window, protected from light and repeated freeze-thaw cycles.