Intraocular angiogenesis mediated by vascular endothelial growth factor (VEGF) and the related ocular disease, age-related macular degeneration (AMD), is the leading cause of loss of vision worldwide. Though anti-VEGF antibodies are used to control AMD, administration of high doses or frequent dosing, and poor ocular retention of the drug adversely affect the patient outcomes. Herein, we report the synthesis of anti-angiogenic carbon nanovesicles (CNVs) through one-step mild carbonization of Brij L76 for loading and sustained release of anti-VEGF antibody [bevacizumab (Avastin)] to treat VEGF-induced angiogenesis. Compared to liposomes and polymersomes, the preparation of CNVs is relatively quick, straightforward, and cost-effective. The bevacizumab loading efficiency of the CNVs is 24.4%, with an encapsulation efficiency of 56.4%. With negligible cytotoxicity toward human umbilical vein endothelial cells and retinal pigment epithelial cells, the bevacizumab-loaded CNVs (BVZ@CNVs) effectively inhibit VEGF-induced cell proliferation and suppress HUVEC migration. In vivo studies show that BVZ@CNVs has superior efficacy to bevacizumab in treating pathological angiogenesis of rabbit eyes as a result of increased bioavailability of the drug through sustained release combined with the anti-angiogenic effect of CNVs. Our findings indicate that BVZ@CNVs hold great potential as a therapeutic anti-angiogenic agent for clinical AMD treatment. [Display omitted] • Anti-angiogenic carbon nanovesicles (CNVs) were synthesized for loading and sustainable release of bevacizumab (BVZ). • BVZ@CNVs inhibit the VEGF-induced cell proliferation and suppress migration of HUVECs. • BVZ@CNVs relieve the symptoms of VEGF-induced angiogenesis in vivo in a rabbit model. • A combined therapeutic effect of CNVs and long-term release of BVZ has been demonstrated. [ABSTRACT FROM AUTHOR]