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Its defining structural feature is the gamma-glutamyl linkage: the glutamate residue is joined through its side-chain carboxyl rather than the usual alpha-peptide bond, which makes the molecule resistant to most intracellular peptidases and means it is cleaved almost exclusively by gamma-glutamyl transpeptidase at the outer cell surface (Zhang, Forman and Choi, Methods in Enzymology, 2005)

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Tumor cells with mesenchymal phenotype are resistant to the dual IGF-IR/InsR inhibitor linsitinib, due to the decreased expression of IGF2 and InsR, and phosphorylation of IGF-IR/InsR in these cells [182]

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