Anti-CD79b antibody–drug conjugate delivering MMAE, a microtubule-disrupting agent.
CD79b-directed antibody–drug conjugate; the anti-CD79b mAb binds B-cell malignancies, is internalized, and releases MMAE via a protease-cleavable linker. MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptotic death of the tumor cell.
YES
DIRECT
The anti-CD79b ADC binds CD79B on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cell.
Anti-CD79b antibody–drug conjugate delivering MMAE, a microtubule-disrupting agent.
CD79b-directed antibody–drug conjugate; the anti-CD79b mAb binds B-cell malignancies, is internalized, and releases MMAE via a protease-cleavable linker. MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptotic death of the tumor cell.
NO
INDIRECT
Polatuzumab vedotin binds CD79b on B cells, is internalized, and releases MMAE, which binds beta-tubulin to disrupt microtubules causing G2/M arrest and apoptosis. Beta-tubulin expression alone does not determine killing; CD79b targeting is required.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-cell lymphoblasts and CD3 on T cells, redirecting cytotoxic T cells to lyse CD19-positive leukemia cells.
Blinatumomab is a bispecific antibody that simultaneously binds CD19 on B cells and CD3 on T cells, bringing T cells into close proximity with CD19+ leukemia cells to trigger TCR/CD3-mediated activation and perforin/granzyme-dependent cytotoxic killing of the target B cells.
YES
DIRECT
Blinatumomab links CD19 on target cells to CD3 on T cells, activating T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-cell lymphoblasts and CD3 on T cells, redirecting cytotoxic T cells to lyse CD19-positive leukemia cells.
Blinatumomab is a bispecific antibody that simultaneously binds CD19 on B cells and CD3 on T cells, bringing T cells into close proximity with CD19+ leukemia cells to trigger TCR/CD3-mediated activation and perforin/granzyme-dependent cytotoxic killing of the target B cells.
NO
INDIRECT
Blinatumomab binds CD3 on T cells and CD19 on B cells, activating T cells to release perforin/granzymes that kill CD19+ cells; CD3+ T cells are not directly killed.
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
YES
DIRECT
NKG2D-based CAR NK cells bind MICB on tumor cells, activating NK cytotoxicity and degranulation (perforin/granzyme) to induce apoptosis/lysis of the target cells.