Insulin-like growth factors (IGFs) are pivotal in cellular processes contributing to normal physiology as well as certain pathologies (e.g., cancer).[3] The IGF family of proteins, also known as the IGF axis, consists of three ligands (insulin, IGF1, IGF2), three cell surface receptors (insulin receptor [IR], IGF1 receptor [IGF1R], IGF2 receptor [IGF2R]), and seven IGF binding proteins (IGFBP1-7).[5] Notably, IGF1R serves as the primary receptor within the IGF axis.[5] The IGF1R is a receptor tyrosine kinase (RTK) with a heterotetrameric structure composed of two extracellular α subunits and two transmembrane β subunits.[3][5] Upon ligand-induced activation of this receptor, cytoplasmicadaptor proteins, Src-homology collagen (Shc) and insulin receptor substrate (IRS), are phosphorylated and, in turn, trigger the activation of the Ras/Raf/MEK/Erk and phosphoinositide 3-kinase (PI3K)/Akt signaling pathways, respectively.[3] These signaling pathways are involved in the regulation of cell survival and cell cycle progression.[3]
Furthermore, IGF1R amplification and overexpression have been observed in the formation of tumors and metastasis of various human cancers.[5] These findings justified the development of anti-IGF1R therapies with the goal of inhibiting aberrant receptor activity and potentially yielding anticancer effects.[3] Among said therapies, Dalotuzumab, a humanized monoclonal antibody, was designed to target and bind the extracellular domains of IGF1R, effectively blocking ligand activation of the receptor and preventing downstream signaling.[3] Moreover, the binding of Dalotuzumab to IGF1R, as seen with other anti-IGF1R antibodies, downregulates the expression of the receptors by prompting the internalization and degradation of IGF1R.[3]
History
There are more than 30 different anti-IGF1R candidate drugs involved in over 70 industry and academic-initiated clinical trials.[6]
^"Dalotuzumab". SEER*Rx Interactive Antineoplastic Drugs Database. National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services. Retrieved 2023-01-01.