Neovascularization is a critical process in the pathophysiology of neovascular eye diseases. Although anti-VEGF therapy has achieved remarkable curative effects, complications, limited efficacy and drug resistance remain the prominent problems. DCZ3301, an aryl-guanidino compound, was reported to have anti-tumor activity in the previous studies. Here, we demonstrated the effects of DCZ3301 on human umbilical vein endothelial cell (HUVEC) in vitro, and performed choroid microvascular sprouting assay ex vivo and alkali-burn induced corneal neovascularization mouse model in vivo. We found that DCZ3301 inhibited the proliferation, migration, and tube formation of HUVECs, while inducing the spontaneous apoptosis of HUVECs by suppressing the activation of PI3K/AKT and ERK1/2 pathways. Furthermore, DCZ3301 inhibited the choroid microvascular sprouting, diminished the area of corneal neovascularization and attenuated the edema of corneal stroma after alkali burn. Together, these results suggested that DCZ3301 exerted anti-angiogenic properties, and might be regarded as a potential candidate for ocular neovascularization.

新血管形成是新血管眼疾病的病理生理学中的关键过程。尽管抗VEGF疗法已经取得了显着的疗效，但是并发症，有限的疗效和耐药性仍然是突出的问题。在以前的研究中，DCZ3301是一种芳基胍基化合物，据报道具有抗肿瘤活性。在这里，我们证明了DCZ3301对人的影响脐静脉内皮细胞（HUVEC）在体外，和进行脉络膜微血管出芽测定离体和碱烧伤诱导角膜新生血管形成的小鼠模型在体内。我们发现DCZ3301通过抑制PI3K / AKT和ERK1 / 2途径的激活，抑制HUVEC的增殖，迁移和管形成，同时诱导HUVEC的自发凋亡。此外，DCZ3301抑制了碱烧伤后脉络膜微血管的发芽，减少了角膜新生血管的面积并减弱了角膜基质的水肿。在一起，这些结果表明DCZ3301发挥抗血管生成特性，并可能被认为是眼新血管形成的潜在候选者。