Table 3: Antiproliferative activity of natural, synthetic, and recombinant avenanthramides.

YearCompoundEffectsRef.

1994–1996TranilastBlockage of PDGF-induced cell-cycle progression at the G1/S checkpoint, inhibition of VSMC proliferation, and suppression of intimal hyperplasia after photochemically induced endothelial injury in the rat[31]
1994–1997TranilastProposed as a putative therapeutic agent for prevention and treatment of diseases associated with neovascularization, such as diabetic retinopathy, senile discoid macular degeneration, neovascular glaucoma, and rheumatoid arthritis[5962]
2001TranilastInhibition of migration and invasiveness of human malignant glioma cells[37]
2002TranilastInhibition of pancreatic cancer cell proliferation and tumor angiogenesis[58]
2003TranilastInhibition of oral squamous cell carcinoma growth and invasion[76]
2006Avn-C and CH3-Avn-CInhibition of VSMC proliferation[31]
2006Avn-CInhibition of SMC proliferation by upregulating the p53-p21cip1 pathway and inhibiting pRB phosphorylation[30, 31]
2009TranilastInhibition of human prostate adenocarcinoma cell proliferation[74]
2009TranilastInhibition of neurofibroma cell growth[81]
2010TranilastEffectiveness in the treatment of desmoid tumor of the chest wall and inhibition of breast cancer stem cells[73]
2010TranilastInhibition of murine and human breast cancer cell proliferation and migration[79, 80]
2010Avn-enriched extracts of oats, Avn-C, and CH3-Avn-CAntiproliferative effects on distinct colon cancer cell lines[25]
2011DH Avn-DInhibition of human breast cancer cell invasion through downregulation of MAPK/NF-κB and MAPK/AP-1 pathways and suppression of MMP-9 expression[32]
2015YAvnsStronger antiproliferative properties than natural Avns, including Avn-B, due to enhanced capacity of reducing intracellular ROS levels and cyclin D1 expression[40]
2017AvnsAntiproliferative effect on breast cancer cells through an antiapoptotic mechanism as revealed by annexin V and caspase activities[57]
2018Natural and synthetic AvnsCytotoxic and proapoptotic effects on CaCo-2 and Hep3B cancer cells[83]

Avns: avenanthramides; CH3-Avn-C: methyl ester of Avn-C; DH Avn-D: dihydro-avenanthramide D; PDGF: platelet-derived growth factor; ROS: reactive oxygen species; VSMC: vascular smooth muscle cells; YAvns: yeast avenanthramides.