Intravenous monoclonal antibody against endoglin (CD105) on proliferating endothelial cells; anti-angiogenic via blockade of TGF-β/BMP9/10–ALK1/endoglin signaling with potential ADCC.
Chimeric monoclonal antibody targeting endoglin (CD105) on proliferating endothelial cells; blocks TGF-β/BMP9/10–ALK1/endoglin signaling to inhibit angiogenesis and endothelial proliferation, with potential Fc-mediated ADCC, leading to anti-tumor effects via vascular targeting.
YES
DIRECT
Anti-endoglin IgG engages Fc receptors to trigger ADCC against endoglin-positive endothelial cells; it also blocks TGF-β/ALK1 signaling to inhibit proliferation/angiogenesis.
A bispecific T‑cell–engaging IgG antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting and activating T cells to kill BCMA-positive cells via TCR/CD3 signaling and cytotoxic effector functions.
Teclistamab is a bispecific IgG antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate TCR/CD3 signaling and redirect polyclonal T-cell cytotoxicity to kill BCMA-positive myeloma cells.
YES
DIRECT
Teclistamab bridges CD3 on T cells to BCMA on target cells, activating TCR/CD3 signaling and redirecting T-cell cytotoxicity (perforin/granzyme-mediated lysis) to kill BCMA-positive cells.
A bispecific T‑cell–engaging IgG antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting and activating T cells to kill BCMA-positive cells via TCR/CD3 signaling and cytotoxic effector functions.
Teclistamab is a bispecific IgG antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate TCR/CD3 signaling and redirect polyclonal T-cell cytotoxicity to kill BCMA-positive myeloma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to activate and redirect them to kill BCMA-positive myeloma cells; the CD3e-expressing T cells are not the cytotoxic target.
Autologous T cells genetically modified to express a chimeric antigen receptor that binds mesothelin on tumor cells, triggering T-cell activation, cytokine release, and cytotoxic killing; evaluated via IV or local delivery, with lymphodepleting chemotherapy used to enhance expansion and optional combination with immune checkpoint inhibitors.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes mesothelin on tumor cells. CAR engagement triggers T-cell activation, cytokine release, proliferation, and targeted cytotoxic killing of mesothelin-expressing cancer cells; lymphodepleting chemotherapy may be used to enhance expansion.
YES
DIRECT
CAR-T cells bind mesothelin on target cells and, upon CAR engagement, directly kill them via perforin/granzyme-mediated cytolysis and Fas–FasL–mediated apoptosis.
Autologous, gene-modified T cells expressing a cooperative/dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) to mediate cytotoxic killing of AML blasts/LSCs while aiming to spare normal myeloid cells.
Autologous T cells engineered to express a cooperative dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) on AML blasts and leukemic stem cells; antigen binding activates CAR signaling leading to T-cell activation and cytotoxic killing of malignant cells while aiming to spare normal myeloid cells.
YES
DIRECT
CAR T cells recognize ADGRE2 (with CLEC12A co-recognition) and directly lyse target cells via perforin/granzyme-mediated cytotoxicity.