An intravenous, novel asymmetric trivalent, tri-specific humanized antibody (biologic immunotherapy) designed to bind three targets simultaneously to enhance immune-mediated killing of malignant plasma cells in relapsed/refractory multiple myeloma; specific antigen targets and precise mechanism are not disclosed.
Asymmetric trispecific humanized antibody that binds BCMA and GPRC5D on multiple myeloma cells and CD3 on T cells, crosslinking to redirect and activate cytotoxic T cells to form an immune synapse and kill BCMA/GPRC5D-expressing malignant plasma cells.
The trispecific T-cell engager binds GPRC5D on tumor cells and CD3 on T cells, crosslinking to activate T cells that form an immune synapse and kill GPRC5D+ cells via perforin/granzyme-mediated apoptosis.
A nectin‑4–targeted antibody–drug conjugate that binds nectin‑4 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death.
CRB-701 is a nectin-4–targeted IgG1 antibody-drug conjugate linked via a cleavable linker to monomethyl auristatin E (MMAE). After binding nectin-4 on tumor cells, it is internalized and releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis; the antibody component may also mediate ADCC and CDC against nectin-4–expressing cells.
The ADC binds nectin-4, is internalized, and releases MMAE, which inhibits tubulin (G2/M arrest) leading to apoptosis; the IgG1 Fc can also mediate ADCC/CDC against nectin-4–expressing cells.
Anti-CD38 IgG1 monoclonal antibody (administered subcutaneously with rHuPH20) that mediates CDC, ADCC, and ADCP to deplete CD38-positive plasma cells.
Human IgG1κ monoclonal antibody targeting CD38 on plasma cells; binding triggers complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and antibody-dependent cellular phagocytosis to deplete CD38-positive tumor cells, and also reduces CD38-expressing immunosuppressive cells (Tregs, B cells, MDSCs).
Daratumumab binds CD38 on target cells and triggers complement-dependent cytotoxicity, NK cell–mediated ADCC, and macrophage ADCP; it can also induce apoptosis upon cross-linking.
Autologous genetically modified T-cell therapy expressing a chimeric antigen receptor targeting B7-H3 (CD276); antigen engagement activates T-cell cytotoxicity and cytokine release to kill B7-H3–positive tumor cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting B7-H3 (CD276). Upon binding B7-H3 on tumor cells, CAR signaling activates T-cell cytotoxicity and cytokine release, leading to selective killing of B7-H3–positive tumor cells.
CAR-T cells bind B7-H3 on target cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated lysis and Fas/FasL), with cytokine release contributing.
Chimeric anti-CD20 monoclonal antibody that mediates complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induces apoptosis of CD20-positive B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Rituximab binds CD20 on B cells and mediates killing via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) through Fcγ receptor–bearing effectors, and can induce apoptosis.