GH-axis research
IGF-1 LR3
Péptido de investigación de señalización endocrina liofilizado para revisión de sistemas
IGF-1 LR3 is a modified IGF-1 analog studied around IGF receptor signaling and altered binding-protein interaction.
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Contexto de investigación
Perfil de investigación de IGF-1 LR3
IGF-1 LR3 is a modified analog of insulin-like growth factor 1 designed with sequence changes that reduce interaction with IGF-binding proteins and alter experimental persistence. Cell and animal studies use it to examine IGF-1 receptor signaling, PI3K-AKT and MAPK pathways, proliferation, differentiation, glucose handling, and other growth-related endpoints. It is not interchangeable with endogenous IGF-1, full-length HGH, or upstream GH secretagogues. IGF-1 LR3 is generally selected for controlled cell-culture or receptor-pathway experiments that specifically require the long-R3 analog. Results can vary substantially with cell type, serum conditions, concentration, and exposure time, and the evidence base is primarily preclinical.
Molecular class
83-residue long-R3 IGF-1 analog
Sequence / composition
An IGF-1 analog with an Arg substitution at position 3 and a 13-residue amino-terminal extension.
Research design note
The long-R3 construct is used to alter binding-protein interaction relative to native 70-residue IGF-1.
Mecanismo propuesto
A modified IGF-1 analog with an N-terminal extension and an amino-acid substitution that reduce affinity for IGF-binding proteins. The proposed result is greater free analog availability and prolonged activation of IGF-1R, PI3K-AKT, and MAPK signaling.
Efectos reportados en estudios
- Cell studies report increased proliferation, survival signaling, differentiation, protein synthesis, and glucose uptake in responsive cell types.
- Animal and agricultural-model studies report growth and metabolic effects that vary with tissue, dose, and exposure.
- Prolonged mitogenic signaling, hypoglycemia-related effects, and uncontrolled cell growth are important experimental concerns.
Criterios de investigación comunes
IGF-1R phosphorylation, AKT and ERK signaling, proliferation, apoptosis, differentiation, protein synthesis, glucose uptake, binding-protein interaction, and exposure duration.
Evidencia y limitaciones
Evidence is predominantly cell and animal based. IGF-1 LR3 is not equivalent to endogenous IGF-1, and established human safety data are lacking.
External reading
Literature for context—not product proof.
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