Learning Objectives

  • Recognize that bispecific antibody failure is the result of a complex interplay between patient factors, disease characteristics, and the immune system

  • Understand that future research should focus on optimal drug sequencing, responses in biological subgroups, and methods to reinvigorate exhausted T cells

A 35-year-old woman with stage III, diffuse large B-cell lymphoma (DLBCL) who relapsed within 12 months of frontline rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy, received second-line CD19-directed autologous chimeric antigen receptor T-cell (CAR-T) therapy with R-gemcitabine, dexamethasone, and cisplatin bridging. Day 30 post CAR-T positron emission tomography (PET) imaging demonstrated bulky stage IV disease progression. Secondary to tumor burden and prior therapy toxicity, the patient's Eastern Cooperative Oncology Group (ECOG) performance status was 2. She was considered for third-line CD3/CD20-directed bispecific antibody (BsAb) treatment.

CD3/CD20 BsAbs redirect and recruit T cells to their target;...

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