Humanized anti-CD20 IgG1 monoclonal antibody administered subcutaneously; depletes CD20+ B cells mainly via ADCC and apoptosis, with less CDC activity compared with ofatumumab.
Humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B to mature B cells and depletes them primarily via antibody-dependent cellular cytotoxicity (ADCC) and apoptosis, with lower complement-dependent cytotoxicity; spares stem cells and plasma cells, reducing antigen presentation and proinflammatory cytokines.
YES
DIRECT
Anti-CD20 IgG1 binds CD20 on B cells and triggers their depletion via Fc-mediated ADCC (NK cells/macrophages), with some complement-dependent cytotoxicity and apoptosis.
IGM-2323; an intravenously administered bispecific IgM monoclonal antibody (T-cell engager) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity and activate complement, depleting CD20+ B cells to reduce pathogenic autoantibody production in SLE.
Imvotamab is a bispecific IgM antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to redirect T-cell cytotoxicity against CD20+ B cells. Its multivalent IgM format confers high-avidity CD20 binding and strong complement activation, inducing complement-dependent cytotoxicity in addition to T-cell–mediated killing, resulting in depletion of CD20+ B cells and reduction of pathogenic autoantibody production.
YES
DIRECT
Imvotamab bridges CD3+ T cells to CD20+ cells to trigger T‑cell–mediated killing (perforin/granzyme apoptosis) and, via its IgM format, activates complement to induce complement-dependent cytotoxicity (CDC) of CD20-expressing cells.
IGM-2323; an intravenously administered bispecific IgM monoclonal antibody (T-cell engager) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity and activate complement, depleting CD20+ B cells to reduce pathogenic autoantibody production in SLE.
Imvotamab is a bispecific IgM antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to redirect T-cell cytotoxicity against CD20+ B cells. Its multivalent IgM format confers high-avidity CD20 binding and strong complement activation, inducing complement-dependent cytotoxicity in addition to T-cell–mediated killing, resulting in depletion of CD20+ B cells and reduction of pathogenic autoantibody production.
NO
INDIRECT
Imvotamab binds CD3 on T cells to engage and activate them; the activated T cells and complement kill CD20+ B cells. CD3+ T cells are not directly targeted for killing.
A fully humanized IgG1 antibody–drug conjugate targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, it is internalized and releases a cytotoxic payload, leading to selective killing of B7‑H3–expressing cells.
Fully humanized IgG1 ADC targeting B7-H3 (CD276); upon binding to B7-H3 on tumor cells, the complex is internalized and releases a cytotoxic payload, selectively killing B7-H3–expressing tumor cells.
YES
DIRECT
The ADC binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload inside the cell, leading to target-cell death (e.g., via DNA damage or microtubule disruption).
Autologous, gene-modified T cells engineered to express a chimeric antigen receptor targeting CD7; antigen engagement triggers T-cell activation, expansion, cytokine release, and cytolytic killing of CD7+ malignant cells, with on-target effects on normal CD7+ T cells and NK cells.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting CD7. Upon binding CD7 on target cells, CAR signaling activates the T cells, driving expansion, cytokine release, and perforin/granzyme-mediated killing of CD7+ malignant cells, with on-target depletion of normal CD7+ T cells and NK cells.
YES
DIRECT
CAR engagement of CD7 activates the engineered T cells to form a cytolytic synapse and kill CD7+ cells via perforin/granzyme–mediated apoptosis (and potentially death-receptor pathways).