Vascular disrupting cancer therapy is aimed at causing a rapid shut-down of the established tumour blood supply, sufficient to induce secondary tumour cell death. It is conceptually distinct from anti-angiogenic therapy, which aims to prevent neo-vascularization of solid tumours. Several low molecular weight drugs have recently entered clinical trial as vascular disrupting agents or VDAs. The lead compound is the tubulin-binding, microtubule depolymerising agent, disodium combretastatin A4 3-O-phosphate (CA-4-P). Tissue blood flow rate (F) is a critical parameter for assessing functional efficiency of a blood vessel network following VDA treatment. CA-4-P causes almost complete cessation of blood flow in many tumour models within I hour of a moderate single dose of CA-4-P. Significant tumour blood flow shut-down has also been observed in clinical trials, without vascular damage in normal tissues. However, reasons for tumour selectivity of VDAs such as CA-4-P remain unclear. Here, we describe methods for evaluating vascular effects of VDAs in pre-clinical models of cancer and the current status of VDA treatments.