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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
 Fluoropyrimidine Despite the improved OS, systemic toxicity and tumor resistance are limitations of this therapy [121] NA
Targeted therapy
1. Monoclonal antibodies
  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®)