Long-acting IGF-1 analogue (research)
IGF-1 LR3
IGF-1 analogue with reduced IGFBP binding and longer half-life, activating IGF-1 receptors and PI3K/AKT/ growth signalling.
Primary Mechanism of Action
Clinical / Scientific
IGF-1 LR3 binds IGF-1R (and hybrids), activating –– and pathways that control growth and metabolism. The LR3 modification reduces affinity for IGF-binding proteins. Research use is not a licensed anabolic indication; IGF-1R signalling is also an oncology-relevant pathway.
Pathway Targets
IGF-1 receptor
Scientific explanation
Tyrosine- agonism.
PI3K/AKT
Scientific explanation
Downstream growth/metabolic signalling.
mTOR
Scientific explanation
Downstream protein-synthesis signalling.
Pathway Convergence
Clinical / Scientific
Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.
Receptor to physiology
Target to downstream effect: IGF-1 receptor → PI3K/AKT → mTOR
Mechanistically Relevant Repurposed & Adjunctive Applications
Research peptide context
PreclinicalMechanistic rationale
Catalogued as a research peptide. Mechanistic statements below describe known or pathway biology and do not establish a licensed therapeutic indication.
Mechanistic Application Matrix
| Biological Target | Mechanism | Potential Relevance | Evidence Level |
|---|---|---|---|
| IGF-1R | Agonism | Growth signalling | Established mechanism |
| PI3K/AKT/mTOR | Downstream activation | Protein synthesis / mitogenic signalling | Established mechanism |
Mechanistic Interaction Considerations
Hypoglycaemia risk (-like activity). Theoretical mitogenic concerns in IGF-1R-expressing tumours.
In Plain Language
IGF-1 LR3 is a long-lasting copy of -like growth factor-1. It turns on growth receptors that also sit on many cell types, which is why it is biologically powerful and not a casual supplement.
Compounds Sharing Pathways
Other library compounds whose structured pathway data overlap this ingredient. Shared pathways are not combination recommendations.
IGF-1 receptor
Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.