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Obinutuzumab (OBI) is a humanized glycoengineered type 2 anti-CD20 mAb. Compared to RTX or OFA, OBI-induced B-cell depletion is not related to complement-dependent cytotoxicity, mostly operating through antibody-dependent cell-mediated cytotoxicity, antibody-dependent phagocytosis, and direct cell death. These characteristics could play a pivotal role in the development of new anti-rejection strategies, enabling the simultaneous administration of complement inhibitors and B-cell-depleting agents. OBI has also demonstrated more powerful peripheral and central B-cell depletion capacities than RTX, with enhanced effects on memory B cells and plasmablasts. In patients with autoimmune glomerulopathies or multidrug-dependent nephrotic syndrome, OBI has shown encouraging results, representing a potential evolution of the treatment of post-transplant relapsing PRD. 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