A subcutaneous, T-cell–redirecting bispecific IgG4 monoclonal antibody (JNJ-64007957) that binds BCMA on myeloma/plasma cells and CD3 on T cells, bridging them to activate TCR/CD3 signaling and induce cytotoxic killing and apoptosis of multiple myeloma cells.
Bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, bridging them to form an immune synapse, activate TCR/CD3 signaling, and drive T cell-mediated cytotoxicity and apoptosis of BCMA-positive multiple myeloma cells.
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme-mediated apoptosis) to kill BCMA-expressing cells.
HER2-targeted antibody–drug conjugate; an anti-HER2 monoclonal antibody linked to MMAE (microtubule inhibitor) that is released after internalization to induce mitotic arrest and apoptosis, with potential ADCC/bystander effects.
HER2‑targeted antibody–drug conjugate: the anti‑HER2 mAb binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE (microtubule inhibitor) after linker cleavage, disrupting tubulin polymerization to induce mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
Anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE after linker cleavage, disrupting microtubules to cause mitotic arrest and apoptosis; Fc-mediated ADCC and bystander killing can also contribute.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
ULBP3 engages NKG2D on allogeneic Vγ9Vδ2 T cells, activating them to kill target cells via perforin/granzyme-mediated cytotoxicity.
Recombinant SIRPα–IgG4 Fc fusion protein that binds CD47 to block the "don’t‑eat‑me" signal and enhance macrophage/monocyte phagocytosis.
Recombinant SIRPα–IgG4 Fc fusion protein that binds CD47 on tumor cells, blocking the CD47–SIRPα “don’t‑eat‑me” signal and thereby promoting macrophage/monocyte phagocytosis and innate anti-tumor activity.
Blocking CD47–SIRPα removes the ‘don’t‑eat‑me’ signal and, via the IgG4 Fc engaging Fcγ receptors, directly promotes macrophage/monocyte antibody‑dependent cellular phagocytosis of CD47+ cells.
SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
Blocks the CD47–SIRPα “don’t‑eat‑me” signal and engages Fcγ receptors, enabling macrophage/monocyte antibody‑dependent cellular phagocytosis of CD47+ cells, leading to their killing.