Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2007 Apr 23;96(8):1159-65.
doi: 10.1038/sj.bjc.6603694. Epub 2007 Mar 20.

Vascular disrupting agents in clinical development

P Hinnen  1 , F A L M Eskens
Affiliations
Review

Vascular disrupting agents in clinical development

P Hinnen et al. Br J Cancer. .

Abstract

Growth of human tumours depends on the supply of oxygen and nutrients via the surrounding vasculature. Therefore tumour vasculature is an attractive target for anticancer therapy. Apart from angiogenesis inhibitors that compromise the formation of new blood vessels, a second class of specific anticancer drugs has been developed. These so-called vascular disrupting agents (VDAs) target the established tumour vasculature and cause an acute and pronounced shutdown of blood vessels resulting in an almost complete stop of blood flow, ultimately leading to selective tumour necrosis. As a number of VDAs are now being tested in clinical studies, we will discuss their mechanism of action and the results obtained in preclinical studies. Also data from clinical studies will be reviewed and some considerations with regard to the future development are given.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Architectural difference between vasculature in normal (small arrows) and tumour tissue (thick arrows).
Figure 2
Figure 2
Typical example of a tumour with a viable rim (V) and central necrosis (N) following exposure to a vascular disrupting agent.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Baguley BC, Zhuang L, Kestell P (1997) Increased plasma serotonin following treatment with flavone-8-acetic acid, 5,6-dimethylxanthenone-4-acetic acid, vinblastine, and colchicines: relation to vascular effects. Oncol Res 9: 55–60 - PubMed
    1. Beauregard DA, Thelwall PE, Chaplin DJ, Hill SA, Adams GE, Brindle KM (1998) Magnetic resonance imaging and spectroscopy of combretastatin A4 prodrug-induced disruption of tumour perfusion and energetic status. Br J Cancer 77: 1761–1767 - PMC - PubMed
    1. Beerepoot LV, Radema SA, Witteveen EO, Thomas T, Wheeler C, Kempin S, Voest E (2006) Phase I clinical evaluation of weekly administration of the novel vascular-targeting agent, ZD6126, in patients with solid tumors. J Clin Oncol 24: 1491–1498 - PubMed
    1. Bilenker JH, Flaherty KT, Rosen M, Davis L, Gallagher M, Stevenson JP, Sun W, Vaughn D, Giantonio B, Zimmer R, Schnall M, O'Dwyer PJ (2005) Phase I trial of combretastatin a-4 phosphate with carboplatin. Clin Cancer Res 11: 1527–1533 - PubMed
    1. Chaplin DJ, Dougherty GJ (1999) Tumour vasculature as a target for cancer therapy. Br J Cancer 80(Suppl 1): 57–64 - PubMed

MeSH terms