Table 3 Actions of modificed tetrac in combination with clinical anti-cancer agents Drug
From: Role of thyroid hormone-integrin αvβ3-signal and therapeutic strategies in colorectal cancers
Clinical agents | Efficacy and deficiency | Tetrac/NDAT combination |
|---|---|---|
Chemotherapy | ||
Fluoropyrimidine | Despite the improved OS, systemic toxicity and tumor resistance are limitations of this therapy [121] | NA |
Oxaliplatin | ||
Targeted therapy | ||
1. Monoclonal antibodies | ||
Anti-VEGF/VEGFR: | ||
Bevacizumab (Avastin®) | Chemo-combination therapy is superior to single agent. PIGF or angiopoietin-2 were upregulated in CRC cases resistant to antiangiogenic therapy [39, 54] | NA |
Aflibercept (Eylea® and Zaltrap®) | ||
Regorafenib (Stivarga®) | ||
Ramucirumab (Cyramza®) | ||
Anti- EGFR: | ||
Cetuximab (Erbitux®) | Cetuximab (Erbitux®) inhibited K-Ras WT but not K-Ras-mutant CRC cell growth[58] | NDAT potentiated cetuximab-induced antiproliferation in both K-Ras WT and K-Ras mutant CRC cells[58]. They also showed potentiation effect in vivo |
Panitumumab (Vectibix®) | ||
Immune checkpoint inhibitor: | ||
Pembrolizumab (Keytruda®) | Pembrolizumab and Nivolumab displayed good efficacy for high levels of microsatellite instability (MSI-H) or MMR deficiency (dMMR) but unsatisfactory results for MS stable and MMR proficient cases. [57, 94] | NA |
Nivolumab (Opdivo®) | ||
Ipilimumab (Yervoy®) | ||
2. Small molecules | ||
EGFR inhibitor: | ||
Gefitinib (Iressa®) | Gefitinib was shown less effective in CRC compared to other cancer types[45] | NDAT enhanced gefitinib-induced antiproliferation via a mechanism involving inhibition of ST6Gal1 activity and PI3K activation[5, 45] |
Erlotinib (Tarceva®) | ||