Fc‑engineered anti‑CD19 monoclonal antibody that enhances ADCC/ADCP against CD19+ B cells (IV).
Humanized, Fc‑engineered anti‑CD19 monoclonal antibody that binds CD19 on malignant and normal B cells and engages Fcγ receptors on effector cells to enhance antibody‑dependent cellular cytotoxicity (ADCC) and antibody‑dependent cellular phagocytosis (ADCP), leading to depletion of CD19+ B cells.
NO
INDIRECT
Tafasitamab binds CD19 on B cells and engages CD16A on NK/macrophages via its Fc to trigger ADCC/ADCP against CD19+ cells; CD16A-expressing effector cells are not targeted or killed by the drug.
Fc‑engineered anti‑CD19 monoclonal antibody that enhances ADCC/ADCP against CD19+ B cells (IV).
Humanized, Fc‑engineered anti‑CD19 monoclonal antibody that binds CD19 on malignant and normal B cells and engages Fcγ receptors on effector cells to enhance antibody‑dependent cellular cytotoxicity (ADCC) and antibody‑dependent cellular phagocytosis (ADCP), leading to depletion of CD19+ B cells.
NO
INDIRECT
Tafasitamab binds CD19 on B cells; its Fc engages CD32A (FcγRIIA) on effector cells to trigger ADCC/ADCP, leading to killing of CD19+ B cells. CD32A-expressing cells serve as effectors, not targets, and are not directly killed.
Autologous T cells engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells, mediating cytotoxicity via perforin/granzyme and cytokine release.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells. Antigen engagement activates the T cells to proliferate and kill BCMA-expressing cells via perforin/granzyme-mediated cytotoxicity and cytokine release.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells, become activated, and kill them via T cell cytotoxicity—primarily perforin/granzyme-mediated lysis (with possible Fas/FasL and cytokine-mediated apoptosis).
Investigational intravenous antibody-drug conjugate (ADC) that binds a tumor-associated surface antigen and delivers an intracellular cytotoxic payload to kill antigen-expressing cancer cells.
Human anti–folate receptor alpha (FRa) antibody-drug conjugate that binds FRa on tumor cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor (AZ14170132). The payload inhibits TOP1, causing DNA replication stress and single- and double-strand breaks, leading to cell-cycle arrest and apoptosis in FRa-expressing cancer cells.
YES
DIRECT
An FRa-targeted antibody-drug conjugate binds FRa on tumor cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor that induces DNA damage, causing cell-cycle arrest and apoptosis of FRa-expressing cells.
Investigational intravenous antibody-drug conjugate (ADC) that binds a tumor-associated surface antigen and delivers an intracellular cytotoxic payload to kill antigen-expressing cancer cells.
Human anti–folate receptor alpha (FRa) antibody-drug conjugate that binds FRa on tumor cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor (AZ14170132). The payload inhibits TOP1, causing DNA replication stress and single- and double-strand breaks, leading to cell-cycle arrest and apoptosis in FRa-expressing cancer cells.
NO
INDIRECT
AZD5335 targets folate receptor alpha on tumor cells, is internalized, and releases a camptothecin payload that inhibits topoisomerase I, causing DNA damage and apoptosis. Killing is directed by FRα expression; DNA topoisomerase I is the intracellular payload target, not the direct targeting antigen.