Autologous anti-CD19 CAR T‑cell therapy with a CD28 costimulatory domain; engineered patient T cells target CD19+ B cells to drive cytotoxicity and cytokine release in relapsed/refractory B‑cell malignancies.
Autologous T cells engineered to express an anti‑CD19 CAR with CD28 costimulatory and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR activates T‑cell signaling, leading to T‑cell expansion, cytokine release, and cytotoxic killing of CD19‑expressing malignant B cells.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, and kill via T-cell cytotoxic pathways (perforin/granzyme-mediated lysis and apoptosis).
An oral small-molecule BCL-2 inhibitor (BH3 mimetic) that blocks the antiapoptotic BCL-2 pathway, restoring intrinsic mitochondrial apoptosis in CLL cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocks its antiapoptotic function, and restores intrinsic mitochondrial apoptosis in malignant B cells; spares BCL-XL.
Venetoclax directly inhibits anti‑apoptotic BCL‑2 (BH3 mimetic), freeing pro‑apoptotic factors to activate BAX/BAK, causing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL‑2–dependent cells.
Autologous anti-CD19 CAR T‑cell therapy with a CD28 costimulatory domain; engineered patient T cells target CD19+ B cells, leading to T‑cell activation, cytolysis, and cytokine release in relapsed/refractory B‑cell malignancies.
Autologous T cells are engineered to express an anti‑CD19 chimeric antigen receptor with a CD28 costimulatory domain and CD3ζ signaling. After infusion, CAR T cells bind CD19 on B cells, become activated, proliferate, release cytokines, and mediate cytolytic killing of CD19‑positive malignant B cells.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and directly induce cytolysis via perforin/granzyme and death-receptor pathways.
An antibody–drug conjugate (ADC) also known as iza-bren/izalontamab brengitecan (BMS-986507). The antibody binds a tumor-associated antigen on cancer cells, is internalized, and releases the topoisomerase I inhibitor payload brengitecan to induce DNA damage and apoptosis.
Dual-targeted anti-EGFR/anti-HER3 antibody-drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan to cause DNA damage and apoptosis.
The ADC binds EGFR on target cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis.
An antibody–drug conjugate (ADC) also known as iza-bren/izalontamab brengitecan (BMS-986507). The antibody binds a tumor-associated antigen on cancer cells, is internalized, and releases the topoisomerase I inhibitor payload brengitecan to induce DNA damage and apoptosis.
Dual-targeted anti-EGFR/anti-HER3 antibody-drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan to cause DNA damage and apoptosis.
The ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis.