IGF1-LR3

Storage. Store dry lyophilized powder desiccated at -20^°C to -80^°C, protected from atmospheric moisture and direct light.

Solubility. Reconstitute initially in sterile dilute acetic acid (10--100 mM, pH 3.0--4.0) or sterile deionized water at a concentration of ≥ 0.1 mg/mL. Subsequent dilutions into cell culture media should contain 0.1% carrier protein (such as laboratory-grade BSA or HSA) to prevent non-specific surface adsorption.

• Handling Warnings: Contains three tertiary disulfide bridges; *do not* introduce reducing agents (e.g., DTT, TCEP, β-mercaptoethanol) into storage or assay buffers, as reduction of disulfide bonds abolishes tertiary conformation and receptor binding affinity. Avoid vigorous mechanical agitation or vortexing.

Agonist of the Type 1 Insulin-like Growth Factor Receptor (IGF-1R, a receptor tyrosine kinase), inducing downstream autophosphorylation of the β-subunit kinase domain.

Biochemical Modification Rationale: Engineered to overcome the rapid sequestration of native IGF-1 by Insulin-like Growth Factor-Binding Proteins (IGFBP-1 through IGFBP-6). The Glu³ → Arg³ substitution and the 13-amino-acid N-terminal leader peptide reduce binding affinity for inhibitory IGFBPs by >100-fold while retaining full agonist affinity for the IGF-1R, yielding high free-ligand bioavailability in serum-containing or serum-free in vitro assay systems.

Cellular Pathways Investigated: Extensively documented in in vitro mammalian cell cultures (including C2C12 skeletal myoblasts, primary satellite cells, and CHO bioprocess systems) to analyze IRS-1/PI3K/Akt and Ras/Raf/MAPK/ERK signal transduction, protein synthesis upregulation via mTORC1/p70S6K signaling, and inhibition of apoptosis via Bad/FoxO1 phosphorylation.