Angiogenesis is a fundamental process in which new blood vessels are formed from pre-existing vessels. It is important in growth, development, and regeneration after injury. Inflammation causes an imbalance in the regulation of angiogenesis leading to unregulated pathological neovascularisation that exacerbates diseases such as cancer and atherosclerosis. Current anti-angiogenic therapies for the treatment of these diseases inhibit both pathological and physiological angiogenesis causing side effects such as hypertension, bleeding, severe weight loss, diarrhoea and nausea in a large percentage of patients. Increasing evidence suggests the CC-chemokine class promote inflammatory-driven angiogenesis, with little-to-no effect in hypoxia-mediated angiogenesis. Inhibition of the CC-chemokine class may therefore regulate angiogenesis differently depending on the pathophysiological context. The main objectives of the present studies were to compare the role of CC-chemokines in both inflammatory-driven and ischaemia-mediated angiogenesis using a broad-spectrum CC-chemokine specific inhibitor "35K". The studies presented in this thesis demonstrate for the first time that broad-spectrum CC-chemokine inhibition by 35K attenuates inflammatory-driven pathological angiogenesis whilst preserving ischaemia-mediated neovascularisation in vitro and in vivo.