An anti-CD22 × anti-CD28 costimulatory bispecific monoclonal antibody that binds CD22 on B cells and CD28 on T cells to deliver CD28 costimulation without independent T-cell activation; a costimulatory T-cell–engager.
Costimulatory bispecific IgG4 antibody that binds CD22 on B cells and CD28 on T cells to deliver CD28 costimulation without independent T-cell activation. By crosslinking T cells to CD22+ tumor cells, it provides CD28 costimulatory signaling in the context of TCR engagement, enhancing cytotoxic T-lymphocyte activation and killing of CD22-expressing B-cell malignancies.
The bispecific binds CD22 on tumor cells and CD28 on T cells to provide CD28 costimulation; with concurrent TCR/CD3 engagement, this activates cytotoxic T cells to kill CD22+ cells via perforin/granzyme-mediated apoptosis.
Oral HER2-selective tyrosine kinase inhibitor that blocks HER2 phosphorylation and downstream PI3K/AKT and RAS/RAF/MEK/ERK signaling; designed to spare EGFR.
Oral, irreversible HER2-selective tyrosine kinase inhibitor that binds and inhibits HER2 and HER2 mutants (including exon 20 insertions), blocking HER2 phosphorylation and downstream PI3K/AKT and RAS/RAF/MEK/ERK signaling, while sparing wild‑type EGFR; this suppresses proliferation and can induce death in HER2-expressing tumor cells.
Irreversible HER2 kinase inhibition blocks HER2 phosphorylation and downstream PI3K/AKT and RAS/RAF/MEK/ERK signaling, leading to growth arrest and apoptotic death of HER2-expressing tumor cells.
Oral HER2-selective tyrosine kinase inhibitor that blocks HER2 phosphorylation and downstream PI3K/AKT and RAS/RAF/MEK/ERK signaling; designed to spare EGFR.
Oral, irreversible HER2-selective tyrosine kinase inhibitor that binds and inhibits HER2 and HER2 mutants (including exon 20 insertions), blocking HER2 phosphorylation and downstream PI3K/AKT and RAS/RAF/MEK/ERK signaling, while sparing wild‑type EGFR; this suppresses proliferation and can induce death in HER2-expressing tumor cells.
Irreversible small‑molecule HER2 TKI that binds and inhibits mutant HER2 (including exon 20 insertions), blocking PI3K/AKT and RAS/RAF/MEK/ERK signaling and inducing growth arrest and apoptosis of HER2‑mutant tumor cells.
Intravenous anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates ADCC in HER2-overexpressing tumors.
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the extracellular domain to block HER2 signaling and dimerization, inhibiting downstream PI3K/AKT and MAPK pathways, and recruits immune effector cells to induce antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptors on NK cells/macrophages to mediate antibody-dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells; it may also inhibit signaling and modestly activate complement.
Obrixtamig; an intravenous bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to activate T-cell–mediated cytotoxicity.
Obrixtamig (BI 764532) is a bispecific T-cell–engaging antibody that binds DLL3 on tumor cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill DLL3-expressing cancer cells.
The bispecific T-cell engager binds DLL3 on target cells and CD3 on T cells, forming an immune synapse that activates T cells to kill DLL3-expressing cells via perforin/granzyme-mediated cytotoxicity.