Combretastatin A-4 phosphate suppresses development and induces regression of choroidal neovascularization

Invest Ophthalmol Vis Sci. 2003 Aug;44(8):3650-5. doi: 10.1167/iovs.02-0985.

Abstract

Purpose: Combretastatin A-4 (CA-4) is a naturally occurring agent that binds tubulin and causes necrosis and shrinkage of tumors by damaging their blood vessels. In this study the effect of a CA-4 prodrug, combretastatin A-4-phosphate (CA-4-P), was tested in two models of ocular neovascularization.

Methods: The effect of CA-4-P was quantitatively assessed in transgenic mice with overexpression of vascular endothelial growth factor in the retina (rho/VEGF mice) and mice with choroidal neovascularization (CNV) due to laser-induced rupture of Bruch's membrane.

Results: In rho/VEGF mice, daily intraperitoneal injections of 4.0 mg/kg CA-4-P starting at postnatal day (P)7, the time of onset of transgene expression, resulted in a significant reduction in the number of neovascular lesions and total area of neovascularization per retina at P21, compared with vehicle-injected mice. In mice with laser-induced rupture of Bruch's membrane, daily intraperitoneal injections of 75 or 100 mg/kg CA-4-P resulted in a significant reduction in the area of CNV at rupture sites compared with vehicle-injected mice. In mice with established CNV, daily intraperitoneal injections of 100 mg/kg CA-4-P for 1 week resulted in a significant reduction in CNV area at rupture sites compared with the baseline area before treatment or the area of CNV in vehicle-treated mice.

Conclusions: These data indicate that CA-4-P suppresses the development of VEGF-induced neovascularization in the retina and both blocks development and promotes regression of CNV. Therefore, CA-4-P shows potential for both prevention and treatment of ocular neovascularization.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antineoplastic Agents, Phytogenic / therapeutic use*
  • Choroidal Neovascularization / chemically induced
  • Choroidal Neovascularization / drug therapy*
  • Choroidal Neovascularization / pathology
  • Choroidal Neovascularization / prevention & control
  • Disease Models, Animal
  • Endothelial Growth Factors
  • Female
  • Intercellular Signaling Peptides and Proteins
  • Lymphokines
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Prodrugs / therapeutic use*
  • Remission Induction
  • Rhodopsin / metabolism
  • Stilbenes / therapeutic use*
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Substances

  • Antineoplastic Agents, Phytogenic
  • Endothelial Growth Factors
  • Intercellular Signaling Peptides and Proteins
  • Lymphokines
  • Prodrugs
  • Stilbenes
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Rhodopsin
  • fosbretabulin