Endogenous inhibitors (as opposed to angiogenesis-inhibiting drugs) of angiogenesis play important roles in regulating the appropriate formation of new blood vessels from pre-existing ones. These inhibitors are part of a system that acts to maintain a balance between pro-angiogenic and anti-angiogenic factors, ensuring that angiogenesis occurs in a controlled and regulated manner. They therefore function to prevent excessive or aberrant blood vessel growth, which is often associated with various diseases, including cancer, inflammatory disorders, and ocular conditions. Several endogenous inhibitors of angiogenesis have been identified, each with distinct mechanisms of action and roles in regulating blood vessel formation. The Thrombospondin-1 (TSP-1) glycoprotein is a potent inhibitor of angiogenesis and prevents endothelial cell migration and proliferation by binding to specific cell surface receptors. TSP-1 exerts its anti-angiogenic effects primarily through interactions with the cell surface receptor CD36. CD36 is a multifunctional scavenger receptor that is expressed on various cell types, including endothelial cells, macrophages, and platelets. TSP-1 binds to CD36 and triggers signalling events that contribute to the inhibition of angiogenesis. TSP-1 is found in the extracellular matrix, and by inhibiting new vessel formation, helps to maintain vascular quiescence. Moreover, like TSP-1, TSP-2 is a member of the thrombospondin family and has anti-angiogenic properties. It affects endothelial cell behaviour and ECM interactions, inhibiting angiogenesis in different physiological and pathological contexts. Derived from the non-collagenous C-terminal domain of type XVIII collagen, endostatin inhibits endothelial cell adhesion, migration, and proliferation. It can also induce endothelial cell apoptosis, contributing to vessel regression. Endostatin can activate various pro-apoptotic signalling pathways within endothelial cells, for example, inducing the activation of caspases involved in executing the apoptotic process. A fragment of plasminogen, angiostatin inhibits endothelial cell migration and proliferation. It functions by targeting several components of the angiogenic pathway, including integrins, and interfering with signalling cascades that promote vessel growth. PTX3 is an acute-phase protein that regulates inflammation and innate immunity. It also has anti-angiogenic effects by inhibiting endothelial cell adhesion and migration. Both interferon-alpha (IFN-α) and interferon-beta (IFN-β) also exhibit anti-angiogenic properties. They interfere with the production of pro-angiogenic factors, such as VEGF and FGF, and thereby suppress endothelial cell growth and migration. TIMPs are molecular inhibitors of matrix metalloproteinases (MMPs), enzymes that degrade the extracellular matrix and are involved in the remodelling of the ECM in angiogenesis. By regulating MMP activity, TIMPs help maintain the integrity of the extracellular matrix and modulate angiogenesis. Finally, some endogenous isoforms of VEGF, such as VEGFxxxb, have anti-angiogenic effects. VEGFxxxb isoforms inhibit angiogenesis by interfering with the binding of pro-angiogenic VEGF isoforms such as VEGF to their receptors on endothelial cells. This competitive inhibition thereby reduces the pro-angiogenic signalling cascade and helps to maintain vascular quiescence in certain contexts. We offer a large product catalogue of research tools for investigating angiogenesis inhibitors, including TL1A antibodies, PEDF antibodies, EMAP II antibodies, IL17F ELISA Kits, and PF4 ELISA Kits. Explore our full angiogenesis inhibitors product range below and discover more, for less.