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Insulin-like growth factor 1 and insulin-like growth factor 2 are evolutionarily conserved peptide hormones instrumental in regulating cell growth, differentiation, survival, and metabolism. IGF-1 is mainly active in childhood growth and adulthood metabolism, whereas IGF-2 is a major growth factor during fetal development. Both function via type 1 IGF receptor (IGF-1R), insulin receptor isoforms (IR-A, IR-B), and for IGF-2, IGF2R. Ligand binding activates autophosphorylation and downstream signaling cascades—primarily PI3K-Akt and MAPK pathways—critical for anabolic growth, mitogenesis, and anti-apoptosis. Dysregulated IGF signaling is implicated in cancer, metabolic and endocrine disorders, and abnormal growth syndromes. Multiple therapeutic approaches target IGF pathways in oncology and metabolic disease, and serum IGF levels serve as biomarkers for diagnosis, monitoring, and therapeutic selection[1][2][3][4][5][7].
Blockade of IGF-1R or IGF2R signaling to inhibit downstream mitogenic and anti-apoptotic effects Inhibition of ligand binding to IGF-1R or IR-A Modulation of IGFBPs to affect IGF bioavailability
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