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TNF receptor superfamily-induced cell death: Redox-dependent execution

Takei et al., 2017a, b

All studies included in the review treated cases and controls equally

9th Advances in CRC: Controversies and Emerging Approaches Symposium

Additional structural modifications included (i) substitution with aminoisobutyric acid at position 2 to increase resistance to DPP-4-mediated cleavage and inactivation, (ii) the addition of a C-terminal extension with 9 amino acids from exendin-4 to enhance structural stability, and (iii) acylation with a C16:0 fatty acid or PEGylation with 40 kDA PEG to extend in vivo activity, thus enabling daily or weekly administration, respectively [69]