Humanized monoclonal antibody that binds all VEGF-A isoforms with high affinity, blocking VEGFR1/2 engagement and tumor angiogenesis. SDH deficiency provides a direct mechanistic rationale for VEGF blockade: impaired succinate oxidation causes intracellular succinate accumulation, which competitively inhibits PHD prolyl hydroxylases (α-KG-dependent dioxygenases), preventing VHL-mediated HIF-1α/2α ubiquitination and constitutively activating transcription of VEGF-A, PDGFB, and downstream angiogenic targets independent of oxygen tension. This pseudohypoxic VEGF overexpression is the same upstream lesion targeted by sunitinib (Phase 2 RCT FIRSTMAPPP, NCT01371201) and by belzutifan at the HIF-2α level (LITESPARK-015, NCT04924075). Bevacizumab has been combined with temozolomide in metastatic PPGL based on complementary mechanisms — temozolomide exploiting CIMP-driven MGMT silencing, bevacizumab neutralising HIF-driven tumor vasculature — in clinical practice prior to the availability of approved options.