Novel benzoxazines as inhibitors of angiogenesis

Invest New Drugs. 2015 Feb;33(1):45-52. doi: 10.1007/s10637-014-0172-8. Epub 2014 Oct 23.

Abstract

Dysregulation of angiogenesis has been associated with many pathological disorders, including cancer; where angiogenesis has been found to be critical for the maintenance and metastasis of tumours. One of the pathways involved in the regulation of angiogenesis is the phosphatidylinositol3-kinase (PI3K) signalling pathway. The PI3K family consists of enzymes that phosphorylate the 3-OH of the inositol ring of phosphatidyl inositol. There are four isoforms, PI3Kα, PI3Kβ, PI3Kγ and PI3Kδ, that are signalling intermediaries involved in numerous pathways that sustain and maintain the tumours. In this study, we screened eight novel benzoxazine inhibitors of both PI3K isoforms and the related DNA-PK, for their anti-angiogenic effects. Our findings identified the novel benzoxazine (7, 8 (substituted)-2-morpholino-benz (1,3) oxazine: LTUSI122) to be non-toxic at concentrations up to 5 μM, while exhibiting significant inhibition of various aspects of angiogenesis including endothelial proliferation, migration and tube formation. The molecular mechanisms were examined using an angiogenesis array, revealing inhibition of several proliferative and migratory angiogenic factors, including VEGFR, MMP, IL-8, uPAR and MCP; and stimulation of the endogenous inhibitor, endostatin. We hypothesize that these anti-angiogenic effects are mediated by targeting an important signaling intermediary, PI3Kα, and subsequently its action on vascular endothelial growth factor (VEGF, a key growth factor in the process of angiogenesis). If used in combination with more targeted therapies, LTUSI122 could reduce tumour growth and increase the efficacy of these treatments.

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Benzoxazines / pharmacology*
  • Cell Movement / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Chemokine CXCL5 / metabolism
  • Endostatins / metabolism
  • Human Umbilical Vein Endothelial Cells / drug effects*
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Human Umbilical Vein Endothelial Cells / physiology
  • Humans
  • Interleukin-8 / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Monocyte Chemoattractant Proteins / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Receptors, Urokinase Plasminogen Activator / metabolism
  • Thrombopoietin / metabolism
  • Transforming Growth Factor beta / metabolism
  • Vascular Endothelial Growth Factor Receptor-2 / metabolism

Substances

  • Angiogenesis Inhibitors
  • Benzoxazines
  • CCL13 protein, human
  • CXCL5 protein, human
  • CXCL8 protein, human
  • Chemokine CXCL5
  • Endostatins
  • Interleukin-8
  • Monocyte Chemoattractant Proteins
  • Receptors, Urokinase Plasminogen Activator
  • Transforming Growth Factor beta
  • Thrombopoietin
  • Phosphatidylinositol 3-Kinases
  • KDR protein, human
  • Vascular Endothelial Growth Factor Receptor-2
  • MMP9 protein, human
  • Matrix Metalloproteinase 9