Autologous anti‑CD19 CAR T‑cell therapy with a 4‑1BB co‑stimulatory domain and CD3ζ signaling, engineered to recognize and kill CD19‑positive B cells.
Autologous T cells genetically engineered to express an anti‑CD19 chimeric antigen receptor with a 4‑1BB co‑stimulatory domain and CD3ζ signaling. Upon binding CD19 on B cells, the CAR activates T‑cell cytotoxicity, proliferation, and cytokine release to eliminate CD19‑positive malignant B cells and promote persistence.
Anti-CD19 CAR T cells bind CD19 on B cells, become activated via CD3ζ/4-1BB signaling, and directly kill target cells through perforin/granzyme-mediated lysis and death-receptor pathways.
HER2-directed antibody–drug conjugate composed of trastuzumab linked to the microtubule inhibitor DM1; after HER2 binding and internalization, DM1 is released to disrupt microtubules in HER2-positive cells.
HER2-directed antibody-drug conjugate in which trastuzumab binds HER2 on tumor cells and is internalized; intracellular processing releases the maytansinoid payload DM1, which inhibits microtubule assembly leading to mitotic arrest and apoptosis. The trastuzumab component also blocks HER2 signaling and can mediate ADCC.
Trastuzumab binds HER2 and is internalized; intracellular release of the DM1 payload inhibits microtubules, causing mitotic arrest and apoptosis. The Fc can also mediate ADCC.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity, and apoptosis signaling.
Anti-CD22 antibody–drug conjugate that delivers calicheamicin to CD22-positive B cells, causing DNA double-strand breaks.
Humanized anti-CD22 antibody-drug conjugate that binds CD22 on B cells, is internalized, and releases the calicheamicin payload intracellularly; calicheamicin binds the DNA minor groove and induces double-strand breaks, triggering apoptosis.
Anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin intracellularly; the payload binds DNA’s minor groove, causes double‑strand breaks, and triggers apoptosis.
Bispecific T-cell engager (CD19xCD3) that redirects T cells to kill CD19-positive B-ALL blasts.
Blinatumomab is a CD19xCD3 bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and form an immunologic synapse, resulting in perforin/granzyme-mediated killing of CD19-positive B-lymphoblasts.
Blinatumomab links CD3 on T cells to CD19 on target cells, activating T cells to kill CD19-positive cells via perforin/granzyme-mediated cytotoxicity.